2-OH estrogens bind to the estrogen receptor (ER) with affinity equivalent to or greater than estradiol
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α-Lipoic Acid and Cardiovascular Disease - 0 views
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cardiovascular disease CVD alpha alpha lipoic acid ALA antioxidant antioxidants ROS reactive oxygen species
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Nutrition Journal | Full text | Homocysteine and reactive oxygen species in metabolic s... - 0 views
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homocysteine contributes to atherogenesis and CVD via: increased ROS, induces endothelial dysfunction, increases platelete adhesion and thrombosis, increases smooth muscle cell proliferation, endothelial cell cytotoxicity, increases LDL oxidation, vasoconstriction, increased MCP-1 and IL-8, and induces endothelial HMG CoA reductase.
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Radical changes in multiple sclerosis pathogenesis - 0 views
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Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxida... - 0 views
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blood-brain barrier MS multiple sclerosis ROS reactive oxygen species antioxidants antioxidant SOD superoxide disumutase catalase
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This article proposes that increased antioxidant enzymatic activity is an adaption to the increased ROS found in MS. This increased ROS disrupts the blood-brain barrier.
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Levothyroxine and lung cancer in females: the importance of oxidative stress - 0 views
www.rbej.com/...1477-7827-11-75.pdf
T4 synthroid lung cancer oxidative stress ROS reactive oxygenation species
shared by Nathan Goodyear on 13 Aug 13
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Study links synthetic T4, synthroid, to increased risk of Lung cancer. The authors acknowledge that the limitations of this study are large. Yet, the association is evident. The proposed mechanism is likely the overdosing and the resultant ROS as a result.
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Molecular Mechanism of Heavy Metal Toxicity and Tolerance in Plants: Central Role of Gl... - 0 views
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Study looked at the action of glutathione in plants with high metal exposure.
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Circulating 2-hydroxy and 16-α hydroxy estrone levels and risk of breast canc... - 1 views
www.ncbi.nlm.nih.gov/...PMC2562592
estrogen metabolism menopause post-menopause post menopause estrogen metabolite 2-OH-estrone 16-alpha-OH-estrone 2:16alpha-OH estrone breast cancer risk hormone hormones
shared by Nathan Goodyear on 21 Aug 14
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previous prospective studies have not observed any significant associations with either 2-OH or 16α-OH estrone or the ratio of the two metabolites and breast cancer risk overall.
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it has been hypothesized that metabolism favoring the 2-OH over the 16α-OH pathway may be inversely associated with breast cancer risk (28).
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they may act as only weak mitogens (14, 15), or as inhibitors of proliferation
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No significant associations have been observed between 2-OH estrone and breast cancer risk
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While 16α-OH estrone binds to the ER with lower affinity than estradiol, it binds covalently (18-20) and once bound, fails to down-regulate the receptor (21). Thus, 16α-OH estrone stimulates cell proliferation in a manner comparable to estradiol in ER+ breast cancer cell lines
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In this large prospective study of 2-OH and 16α-OH estrone metabolites and breast cancer risk, we did not observe any significant associations overall with either individual metabolite or with the ratio of the two metabolites
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we observed positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with lower BMI and women with ER-/PR-tumors,
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To date, several epidemiologic studies have examined the association between the 2-OH and 16α-OH estrogen metabolites and breast cancer risk with inconclusive results.
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circulating estrogen levels have been associated more strongly with ER+/PR+ tumors than with ER-/PR- tumors
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our results do not support the hypothesis that metabolism favoring the 2-OH estrone pathway is more beneficial to breast cancer risk than that favoring the 16α-OH estrone pathway
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we observed significant positive associations of both 2-OH estrone and the 2:16α-OH estrone ratio with ER-/PR-tumors
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Three (30, 32, 33) of four (30-33) studies observed RRs above 1 for the association between 16α-OH estrone and breast cancer risk (range of RRs=1.23-2.47); none of the point estimates was statistically significant though one trend was suggestive
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based on animal studies, 2-OH estrone and the 2:16α-OH estrone ratio have been hypothesized to be inversely associated with breast cancer risk
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No significant associations have been observed between 2-OH estrone, 16α-OH estrone, or the 2:16α-OH estrone ratio and breast cancer risk and the direction of the estimates is not consistent across studies.
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better worded is no consistent, significant associations. There are some studies that point to the 16 catecholestrogen and increased cancer risk; limited studies show negative effects of 2 catecholestrogens on cancer risk and prospective studies available pretty much dispel the idea that the 2:16 ratio has an risk predictability.
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we observed a suggestive inverse association with 16α-OH estrone and a significant positive association with the 2:16α-OH estrone ratio among lean women, suggesting possible associations in a low estrogen environment.
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16α-OH estrone increases unscheduled DNA synthesis in mouse mammary cells (27) and hence also may be genotoxic
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Although 2-OH estrogens are capable of redox cycling, the semiquinones and quinones (i.e., the oxidized forms) form stable DNA adducts that are reversible without DNA destruction
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In our population of PMH nonusers, we observed no associations with ER+/PR+ tumors, but significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with ER-/PR- tumors
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one of the few studies to find this association between 2 catecholestrogens and the 2:16 ratio and ER-/PR-tumors
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Animal and in vitro studies have shown that hydroxy estrogens can induce DNA damage either directly, through the formation of quinones and DNA adducts, or indirectly, through redox cycling and the generation of reactive oxygen species
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genotoxic via directe DNA adducts and indirectly via ROS; this is in addition to the proliferative effect
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we observed a significant positive association between the 2:16α-OH estrone ratio and breast cancer risk among lean women
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No significant associations have been observed with the 2:16α-OH estrone ratio
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In the Danish study, no associations were observed with either ER+ or ER- tumors among PMH nonusers
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significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio were observed among PMH users with ER+, but not ER-, tumors
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it is possible that the genotoxicity of 2-OH estrone plays a role in hormone receptor negative tumors
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4-OH estrogens have a greater estrogenic potential than 2-OH estrogens, given the lower dissociation rate from estrogen receptors compared with estradiol (61), and are potentially more genotoxic since the quinones form unstable adducts, leading to depurination and mutation in vitro and in vivo
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the balance between the catechol (i.e., 2-OH and 4-OH) and methoxy (i.e., 2-Me and 4-Me) estrogens may impact risk
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The risks of estrogen metabolism are not clear cut. Likely never will be due to the complexity of individual metabolism. This study found no correlation between 2OH-Estrone and 2OH:16alpha-Estrone and breast cancer risk in ER+/PR+ breast cancer. Translated: no benefit in breast cancer risk in 2OH-Estrone metabolism or increased 2OH:16alpha estrone metabolism. There was a positive association between 2OH-Estrone and 2:16alpha-Estrone in women with ER-/PR- tumors and low BMI.
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Multiple Myeloma Tumor Cells are Selectively Killed by Pharmacologically-dosed Ascorbic... - 0 views
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Recent reports indicate that a certain ROS concentration is required for high-dose vitamin C to induce cytotoxicity in cancer cells.
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The generation of ascorbyl- and H2O2 radicals by PAA increases ROS stress in cancer cells
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In this study, we report that PAA is efficacious in killing MM cells in vitro and in vivo models, which generated levels of 20–40 mM ascorbate and 500 nM ascorbyl radicals after intraperitoneal administration of 4 g ascorbate per kilogram of body weight (Chen et al., 2008Chen et al., 2008), in xenograft MM mice
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These data suggest that PAA may show a therapeutic advantage to blood cancers vs solid tumors because of the communication between tumor cells and blood plasma
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These results strongly suggest that the mechanism of PAA killing of MM cells is indeed iron-dependent
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These results suggest that PAA administration in SMM may be able to prevent progression to symtomatic MM
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A recent study by Yun and colleagues demonstrated that vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH, but spares normal cells
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RAS family genes show the most frequent mutations in MM. KRAS, NRAS and BRAF are mutated in 22%, 20% and 7% of MM samples
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the disease stage rather than the mutation of RAS and/or BRAF is the major predictive factor for PAA sensitivity in MM treatment
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Other molecular mechanisms including ATP depletion and ATM-AMPK signaling have been reported to explain PAA-induced cell death
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our pilot study also suggested that PAA could overcome drug resistance to bortezomib in MM cells
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Our findings complement reported studies and further address the mechanism of action using clinical samples in which we observed that PAA killed tumor cells with high iron content, suggesting that iron might be the initiator of PAA cytotoxicity
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combination of PAA with standard therapeutic drugs, such as melphalan, may significantly reduce the dose of melphalan needed
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Combined treatment of reduced dose melphalan with PAA achieved a significantly longer progression-free survival than the same dose of melphalan alone.
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These data also suggest that the bone marrow suppression induced by high-dose melphalan can be ameliorated by the combination of PAA with lower dose of melphalan because of the lack of toxicity of PAA on normal cells with low iron content.
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if creatinine clearance is <30 mL/min, high dose ascorbic acid should be not administrated.
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In MM preclinical and clinical studies, ascorbate was used as an adjunct drug and showed controversial results (Harvey et al., 2009, Perrone et al., 2009, Held et al., 2013, Sharma et al., 2012, Nakano et al., 2011, Takahashi, 2010, Sharma et al., 2009, Qazilbash et al., 2008). However, none of these tests used pharmacological doses of ascorbate and intravenous administration
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Multiple myeloma (MM) is a plasma cell neoplasm.
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Cameron and Pauling reported that high doses of vitamin C increased survival of patients with cancer
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pharmacologically dosed ascorbic acid (PAA) 50–100 g (Chen et al., 2008, Padayatty et al., 2004, Hoffer et al., 2008, Padayatty et al., 2006, Welsh et al., 2013), administered intravenously, has potent anti-cancer activity and its role as anti-cancer therapy is being studied at the University of Iowa and in other centers
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In the presence of catalytic metal ions like iron, PAA administered intravenously exerts pro-oxidant effects leading to the formation of highly reactive oxygen species (ROS), resulting in cell death
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the labile iron pool (LIP) is significantly elevated in MM cells
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The survival of CD138+ cells in vitro was significantly decreased following PAA treatment in all 9 MM
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In contrast, no significant change of cell viability was observed in CD138− BM cells from the same patients
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The same effect of PAA was also observed in the SMM patients
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no response to PAA was detected in CD138+ cells from the 2 MGUS patients
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the combination of melphalan plus PAA showed greater tumor burden reduction than each drug alone, suggesting a synergistic activity between these two drugs
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Both catalase and NAC protect cells from oxidative damage
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cells pretreated with NAC and catalase became resistant to PAA even at high doses
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adding deferoxamine (DFO), an iron chelator, to OCI-MY5 cells before PAA treatment was also sufficient to prevent PAA-induced cellular death
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iron is essential for PAA to achieve its anti-cancer activity
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PAA induced early necrosis (Fig. 3Fig. 3A, 60 min) followed by late apoptosis
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results further indicated that PAA induced mitochondria-mediated apoptosis
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PAA by reacting with LIP and generating ROS induces mitochondria-mediated apoptosis in which AIF1 cleavage is important for cell death.
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ROS and H2O2 are well known factors mediating PAA-induced cancer cell death
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PAA was sensitive to all 9 MMs and 2 SMMs
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animal study finds high-dose, pharmacologic vitamin C found to kill multiple myeloma cells via pro-oxidant effect found in similar studies in dealing with different cancers.
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American Journal of Obstetrics &amp; Gynecology Home Page - 0 views
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M1 macrophages are characterized by the secretion of reactive oxygen species and proinflammatory cytokines and chemokines and can be identified via the cell surface marker CD86
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M2 macrophages secrete growth factors and antiinflammatory immune modulators and can be identified by the cell surface marker CD206
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an overzealous M2 response can also lead to excess tissue deposition and fibrosis
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Studies of similar meshes that are used in hernia repair have demonstrated that all polypropylene meshes induce a prolonged inflammatory response at the site of implantation
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the long-term presence of activated inflammatory cells, such as macrophages at the mesh tissue interface, can impact negatively the ability of the mesh to function as intended.
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All M1 proinflammatory and M2 proremodeling cytokines and chemokines were increased in mesh explants as compared with nonmesh tissue (Table 3Table 3), which indicated a robust, active, and ongoing host response to polypropylene long after implantation
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Comparison of the ratio of the M2 proremodeling cytokines (IL-10+IL-4) with the M1 proinflammatory cytokines (TNF-α+IL-12p70) revealed a decrease in mesh explants as compared with controls (P = .003), which indicated a shift towards a proinflammatory profile.
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Mesh explants contained a higher number of total cells/×200 field when compared with controls (682.46 ± 142.61 cells vs 441.63 ± 126.13 cells; P < .001) and a lower ratio of M2:M1 macrophages (0.260 ± 0.161 cells vs 1.772 ± 1.919; P = .001), which supported an ongoing proinflammatory response.
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the host response was proportional to the amount of material in contact with the host
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A persistent foreign body response was observed in mesh-tissue complexes that were excised from women who required surgical excision of mesh months to years after mesh implantation
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The host response was characterized by a predominance of macrophages with an increase in both proinflammatory and proremodeling cytokines/chemokines along with increased tissue degradation, as evidenced by increased MMP-2 and -9
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Mesh-tissue complexes removed for mesh exposure had increased pro–MMP-9 that indicated a proinflammatory and tissue destruction–type response
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The presence of macrophages, elevated cytokines, chemokines, and MMPs in tissue-mesh complexes that were excised from patients with exposure or pain suggests that polypropylene mesh elicits an ongoing host inflammatory response
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In the presence of a permanent foreign body, the implant is surrounded with a fibrotic capsule because it cannot be degraded
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For hernia meshes, if the fibers are too close (<1 mm), the fibrotic response to neighboring fibers overlaps, or “bridges,” and results in “bridging fibrosis” or encapsulation of the mesh
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Gynemesh PS has a highly unstable geometry when loaded that resulted in pore collapse and increasing stiffness of the product
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mesh shrinkage (50-70%) has been described to occur after transvaginal insertion of prolapse meshes
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Contribution of Reactive Oxygen Species to Ovarian Cancer Cell Growth Arrest and Killin... - 0 views
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Artesunate increased ROS in ovarian cancer cells that lead to G1 cell cycle arrest and halt in proliferation.
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Growth Inhibition of Ovarian Tumor-Initiating Cells by Niclosamide | Molecular Cancer T... - 0 views
mct.aacrjournals.org/...1703.long
Niclosamide Tumor-initiation cells TIC ovarian cancer cancer CSC cancer stem cells
shared by Nathan Goodyear on 16 Apr 18
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Ovarian cancer is the most lethal gynecologic malignancy and the fifth-most cause of overall cancer death of women in developed countries
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An increasingly accepted cancer stem cell hypothesis regards tumors as caricatures of normal organs, possessing a hierarchy of cell types, at various stages of aberrant differentiation, descended from precursor tumor-initiating cells (TIC) cells that are highly resistant to conventional cytotoxics
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Significant changes of gene expression in 2,928 genes were identified after niclosamide treatment for different time periods
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uncoupling of mitochondrial oxidative phosphorylation is believed to be its anti-helminthic mechanism of action
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we hypothesized that niclosamides antagonistic effects on OTICs could, in part, be due to its disruption of metabolism
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Our results showed that genes participating in protein complexes of oxidative phosphorylation were downregulated
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niclosamide treatment resulted in a more than 20% increase in reactive oxygen species (ROS) in cultured OTICs
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niclosamide, which has proved to be safe and effective for the past 2 decades against numerous parasites, inhibited OTIC growth both in vitro and in vivo
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niclosamide represses metabolic enzymes responsible for bioenergetics, biosynthesis, and redox regulation specifically in OTICs, presumably leading to mitochondrial intrinsic apoptosis pathways, loss of tumor stemness, and growth inhibition
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Niclosamide is believed to inhibit mitochondrial oxidative phosphorylation
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Niclosamide was reported to inactivate NF-κB, causing mitochondrial damage and the generation of ROS, leading to apoptosis of leukemic stem cells
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niclosamide were identified in a screen for mTOR-signaling inhibitors
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mTOR was reported to maintain stemness properties of HSCs by inhibiting mitochondrial biogenesis and ROS levels (39), implying that mTOR inhibitors (such as niclosamide) may interfere with mitochondria and various metabolic pathways in TICs via disruption of antioxidant responses
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We observed Wnt hyperactivity in OTICs, in agreement with previous hypotheses of Wnt inhibitor effectiveness as an ovarian cancer therapy
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niclosamide has now been independently identified in screens for Wnt inhibitors
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downregulation of the Wnt/β-catenin target oncogenes survivin and c-Myc
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ovarian carcinogenesis, the cell-to-cell signaling pathway Notch (8), were also suppressed by niclosamide (data not shown). These results agree with another recent niclosamide study in leukemia (49), and it has been widely hypothesized that disruption of Notch signaling may represent a highly effective therapy for ovarian and other solid tumors, via its essentiality to maintaining TIC stemness
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Niclosamide, common anti-parasitic medication, inhibits cellular metabolism and increases ROS; both of which provide powerful anti-proliferative, anti-cancer treatment mechanism in TICs. Powerful target therapy for cancer stem cells. Also shown to inhibit Wnt stimulated oncogenes survivin and c-Myc, disrupts Notch signaling, inactivates NF-kappaBeta, and inhibits mTOR-signaling. This has been found in in vitro and in vivo studies.
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Anti-helminth compound niclosamide downregulates Wnt Signaling and elicits antitumor re... - 0 views
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Others have reported that niclosamide inhibits the NF-κB pathway in leukemia cell lines (26) or mTOR signaling in MCF-7 breast cancer cells
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niclosamide enhances the anti-tumor effect of oxaliplatin
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In the more rapidly growing tumor (HCT116), a dose of 200 mg/kg of body weight was needed to suppress the tumor growth
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however, 100 mg/kg of niclosamide could suppress the growth of the relatively slow-growing tumor (CRC039) to the same level
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niclosamide was confirmed to inhibit the growth of human CRCs in NOD/SCID mice
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niclosamide can inhibit Wnt pathway activation in CRC
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The mechanism of action of the niclosamide in our studies is thought to be through internalization of Fzd1 and downregulation of Wnt pathway intermediaries
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Recently, Jin et al. (26) reported that niclosamide inhibited the NF-κB pathway and increased reactive oxygen species levels to induce apoptosis in AML cells. In contrast, we did not observe any inhibitory effect of niclosamide on NF-κB signaling in our CRC model
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oral administration of niclosamide does result in sufficient distribution of the drug into tumor tissue, to prove a prolonged inhibitory effect on Wnt/ß-catenin signaling, resulting in tumor growth inhibition
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we required higher doses (100 ~ 200 mg/kg body weight) of niclosamide in order to demonstrate significant inhibition of tumor growth in NOD/SCID mice
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niclosamide concentrations in tumor tissue showed good correlation with those in plasma, suggesting the efficient distribution of niclosamide from blood to tumor tissue
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we observed downregulation of Dvl2 and ß-catenin cytosolic expression in niclosamide-treated tumor cells in vivo
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One potential concern for the use of niclosamide as an anticancer therapy is the poor absorption of this drug
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The Wnt signaling pathway, fundamental to embryonic tissue patterning, is also activated in stem-like cells
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The canonical Wnt pathway is activated in approximately 80% of sporadic CRC primarily due to mutations in the APC gene
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recent observations reveal that Wnt ligands or inhibitors may affect the growth and survival of colon cancer cells in spite of the presence of APC or CTNNB1 mutations
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Niclosamide found to inhibit Wnt/B-catenin signaling pathway, and thus promotion of apoptosis, in colorectal cancer cells in Vivo study. It was also found to augment chemotherapeutic.
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Oncotarget | Preclinical evaluation of a nanoformulated antihelminthic, niclosamide, in... - 0 views
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Ovarian cancer is the most lethal gynecologic malignancy in the world
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paclitaxel represents a breakthrough in the treatment of ovarian cancer, the overall 5-year survival rate of patients with stage III disease is still approximately 40%
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Targeting cancer stem cells is an emerging concept in cancer therapy
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Ovarian cancer stem cells play an important role in chemoresistance and cancer recurrence
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Furthermore, recent studies indicate that niclosamide exhibits anticancer effects against various human cancer cells by acting on multiple cell signaling pathways and inducing mitochondrial uncoupling [16–21]
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has low systemic bioavailability (~10%) when administered orally, which is beneficial for treating local parasitic infections of the intestines while minimizing systemic exposure
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The nano-NI demonstrated significantly higher inhibitory effects on sphere formation than the original niclosamide did
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the nano-NI formulation decreased the metabolic activity of ovarian cancer cells and caused a metabolic shift from oxidative phosphorylation to glycolysis
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This toxicity evaluation showed that oral nano-NI had no toxic effect on either group of mice in terms of weight, plasma albumin levels, and blood cell counts, and revealed no adverse effects on vital organ function in the rodents, which suggests that nano-NI is safe for animals
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niclosamide inhibits tumor cell growth by interrupting multiple pathways (Wnt, Notch, STAT3, NF-κB, and mTORc1) and the generation of reactive oxygen species in several cancer cells
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The current standard therapy for ovarian cancer includes taxanes and platinum-based chemotherapy after cytoreductive surgery. Among treated patients, nearly 70 to 80% will experience disease recurrence
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nano-Niclosamide more effective than traditional Niclosamide in in vitro and in vivo ovarian cancer.
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Drug Screening Identifies Niclosamide as an Inhibitor of Breast Cancer Stem-Like Cells - 0 views
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cancer stem cells may also contribute to tumor formation, metastasis, and treatment resistance
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Studies have shown that some agents (such as metformin) can selectively target cancer stem cells and that dietary polyphenols, curcumin, peperine, and sulforaphane, which are derived from broccoli/broccoli sprouts, are able to target breast cancer stem cells via inhibition of the Wnt signaling, which affects mammosphere size and colony formation
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niclosamide inhibits tumor growth and reduces tumor weight
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Niclosamide treatment inhibited the expression of cyclin D1, Hes1, and PTCH by 33%, 57%, and 79%, respectively
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The mechanism via which niclosamide, a protonophoric anthelmintic drug, induces stem-like-cell-specific toxicity in breast cancer is interesting. It is an old drug that has been used to treat tapeworms in animals
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Niclosamide is known to uncouple mitochondrial oxidative phosphorylation during tapeworm killing
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A screening of autophagy modulators revealed that niclosamide is a novel inhibitor of mTORC1 signaling
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A recent work also demonstrated that niclosamide induces the apoptosis of myelogenous leukemic cells via the inactivation of NF-kappaB and reactive oxygen species generation
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Niclosamide was also reported to inhibit Wnt signaling [31]–[33] in colon cancer cells
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Our recent work demonstrated that niclosamide disrupts multiple metabolic pathways in ovarian-cancer-initiating cells
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The present study showed that niclosamide treatment resulted in the downregulation of target genes involved in the self-renewal of cancer stem-like cells and inhibited breast SPS
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Old ant-parasitic, niclosamide, found to down-regulate cancer stem cell activity.
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The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic... - 0 views
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orally active competitive opioid receptor antagonist
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4.5 mg, though the dosage can vary a few milligrams below or above that common value
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At the low dosage level, naltrexone exhibits paradoxical properties, including analgesia and anti-inflammatory actions
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LDN may be an effective treatment for FM
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In addition to the antagonist effect on mu-opioid and other opioid receptors, naltrexone simultaneously has an antagonist effect on non-opioid receptors (Toll-like receptor 4 or TLR4) that are found on macrophages such as microglia
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It is via the non-opioid antagonist path that LDN is thought to exert its anti-inflammatory effects
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Once activated, microglia produce inflammatory and excitatory factors that can cause sickness behaviors such as pain sensitivity, fatigue, cognitive disruption, sleep disorders, mood disorders, and general malaise
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The neuroprotective action appears to result when microglia activation in the brain and spinal cord is inhibited
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By suppressing microglia activation, naloxone reduces the production of reactive oxygen species and other potentially neuroexcitatory and neurotoxic chemicals
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suppressed TNF-alpha, IL-6, MCP-1, and other inflammatory agents in peripheral macrophages
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individuals with greater ESR at baseline experienced a greater drop in pain when taking LDN
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LDN has been reported to reduce not only self-reported pain in that condition but also objective markers of inflammation and disease severity
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Naltrexone has also shown some promise in improving disease severity in multiple sclerosis
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LDN maybe useful in treating chronic pain via anti-inflammatory effects on microglia.
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Contribution of reactive oxygen species to ovarian cancer cell growth arrest and killin... - 0 views
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Metformin Inhibits the Production of Reactive Oxygen Species from NADH:Ubiqui... - 0 views
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Metformin inhibits LPS induced IL-1beta stimulation. Interesting that metformin is a inhibitor of complex I in the electron transport chain.
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Curcumin decreases malignant characteristics of glioblastoma stem cells via induction o... - 0 views