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katherine-medina

Dandelion root extract affects colorectal cancer proliferation and survival through the... - 0 views

  • of an aqueous dandelion root extract
  • caspase-8 activation was not essential for the induction of cell death in colon cancer cells as an inhibition of caspase-8 activation did not alter the cytotoxicity of DRE
  • We have been able to identify four pharmacologically active components, α-amyrin, β-amyrin, lupeol and taraxasterol, in two out of the six bioactive fractions, but the anti-cancer activities of the individual compounds were not as strong as that of the unfractionated DRE indicating, clearly, the benefits of using the whole extract.
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  • which might represent a novel non-toxic alternative to conventional cancer therapy available today.
  • These results clearly indicate that dandelion root extract can inhibit the ability of colorectal cancer cells to migrate and invade, and therefore metastasize to secondary locations.
    • katherine-medina
       
      Wow. I like to see that in 3 different studies DRE was proven to selectively pick the cancer cells, and ignore the normal cells.
  • morphological differences in tissue slices between the control untreated and the DRE treated group
  • aken together, these results established that systemic oral intake of the DRE was safe and its anti-cancer efficacy should be further investigated.
    • katherine-medina
       
      I love the fact that they yet again state that I should look more into this topic.
  • , but the DRE treatment efficiently suppressed the growth of both p53 WT and p53 mutant tumors in-vivo (Figure 4B – 4C)
    • katherine-medina
       
      great, they suppressed the growth of the tumors.
  • with no difference between the control and DRE treated samples of NCM460
    • katherine-medina
       
      I would not have thought that the mitochondria would be left alone by the drug.
  • Others suggest that following activation, caspases re-localize to the mitochondria, where they interact with other pro-apoptotic proteins during the progression of apoptosis [15]. A third option, put forward by Qin and colleagues, suggests that inactive caspases are kept in the mitochondria, but following apoptotic stimuli and activation, they are released from the mitochondria into the cytoplasmic peri-nuclear space [
  • The results showed a progressive destabilization of the mitochondrial membrane following the DRE treatment, which was observed as early as 30 minutes post treatment (Figure ​6C). Pro-caspase-8 (green) was localized in the mitochondria (red) in control untreated cells; however, following the DRE treatment, activated caspase-8 was released from the mitochondria into cytoplasmic space, as indicated by the dispersed green fluorescence (Figure ​6C
    • katherine-medina
       
      Pro-capase-8 helps to fight against the cancer
  • suggesting that in HT-29 colorectal cancer cells the DRE-induced cell death was caspase-8 independent.
    • katherine-medina
       
      So essentially caspase 8 had nothing to do with it
  • We observed a decrease in the viability of cells treated with α-amyrin, with 10 μM as the most effective concentration.
    • katherine-medina
       
      Hmm. the beginnings of narrowing down what it is about the plant that is able to fight cancer.
  • However, these results indicate that DRE and its anti-cancer components must be absorbed and circulated, in order to reach the site of the tumor (in order to inhibit tumor growth).
    • katherine-medina
       
      So it needs to be drank, or swallowed in a pill form to work.
  • , we confirmed the vulnerability of cancer cell mitochondria by showing that the DRE treatment led to a decrease in the mitochondrial membrane potential and increase in ROS levels in the isolated mitochondria.
  • caspase-8 specific inhibitor, IETD-fmk, did not change the DRE response in these cells. This was in contrast to our previous study in leukemia and pancreatic cancer cells
    • katherine-medina
       
      For each different cancer a new slightly different result is produced
  • he pro-apoptotic genes including Caspase-1, Interferon gamma and the TNF ligands and receptors, were up-regulated in HT-29 cells, prior to the apoptosis induction, while the same genes were down-regulated in NCM460 cells.
  • Previous findings show that taraxasterol has anti-inflammatory and chemopreventive activit
  • suggesting its importance in the anti-cancer activity of dandelion root extract, especially on the expression levels of COX-2. Additionally, we show that 10 μM lupeol is not very effective on its own
  •  
    Yet another article about how DRE can fight against cancer.
katherine-medina

Sci-Hub | Dandelion Root and Lemongrass Extracts Induce Apoptosis, Enhance Chemotherape... - 1 views

    • katherine-medina
       
      They found cancer cell-fighting properties in the dandelion root, lemon grass, long pepper, and hibiscus extract. (I should probably look into what makes these plants prone to killing cancer cells.)
    • katherine-medina
       
      In order to further understand how these complex extracts exhibit their anticancer efects, the mechanism of apoptotic induction should be investigated. In order to determine if apoptosis is induced through oxidative stress, N-acetylcysteine (NAC) is used
    • katherine-medina
       
      Okay, so they made sure to have a control group of cancer cells, then a group of healthy cells that are being experimented on with the liquid, then they had the cancer-ridden cells.
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    • katherine-medina
       
      s. Tus, we have shown for the frst time that these NHPs can be used as adjuvants to chemotherapies and potentially enhance their effect.
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    I will likely come back to this if I so choose to look into how dandelion roots fight cancer.
  •  
    Yes. Another approach is often... once (if) you can find a suggested mechanism of action... you can often pivot with that action into looking for similar effects in other areas (doesn't have to be human or mammal cancer cells). That area isn't a no-go, but it does present feasibility issues to be tackled. If you can find a suggested mechanism, then you can think more widely about how else could you look to see if that effect can be leveraged in other areas. That is often how you can move toward an easily feasible model organism to test that effect on. Keep up the good work!
katherine-medina

The Efficacy of Dandelion Root Extract in Inducing Apoptosis in Drug-Resistant Human Me... - 0 views

  • 2. Materials and Methods
  • 2. Materials and Methods
    • katherine-medina
       
      If I plan on doing some sort of experiment with Dandelion root, I will likely need to come back and look at how this study did it.
  • After a long exposure of 96 hours, NHFs did not exhibit any reduction in cell viability
    • katherine-medina
       
      Wow, so even after 3 days the Dandelion Root did nothing to the NHF aka. normal human cells.
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  • With DRE having proven its efficacy in successfully killing this aggressive, chemoresistant form of skin cancer, DRE toxicity on normal cells had to be evaluated
    • katherine-medina
       
      Always remember to hav e a control.
  • DRE was found to reduce cell viability in a dose-dependent fashion, over time, in A375 melanoma cells as was measured by WST-1 assay. Based on metabolic activity of A375s, it was confirmed that treatment at 2.5 mg/mL DRE resulted in ~50% reduction in cell viability against control within 24 hours (Figure 1(a))
  • Higher doses were then used and a response was observed at a concentration of 10 mg/mL (
    • katherine-medina
       
      For different types of melanoma a different amount of DRE is needed.
  • Typical apoptotic morphology was observed in G361 cells treated with DRE starting at 5 mg/mL concentrations for 72 hours
  • . However, there has been little scientific advancement made in this field with regard to the effect of dandelion root extract on cancer, and even more so on chemoresistant, human malignant melanoma skin cancer.
    • katherine-medina
       
      I do so love it when the author identifies the fact that there is so few research papers about DRE.
  • ) is more than a worthy chemopreventative, it is fast-acting, nontoxic, and therefore specific in its targeting of human melanoma cancer cells, making it a valuable chemotherapeutic. We have investigated the induction of apoptosis in human malignant melanoma cells and observed its long-term effects in human melanoma cancer.
    • katherine-medina
       
      alrighty then.
  • We are yet to determine the effect of each of the individual components (such as the family of triterpene alcohols and phenolic acids—found in the roots—and cinnamic acids, flavinoids and coumarins—that are found in the leaves
    • katherine-medina
       
      Maybe I could look into the specific component that kills the cancer, so that in future years after I had figured this out I could put it into practice.
  • Given that DRE has traditionally been used naturopathically for a variety of ailments, we assume that it would be relatively nontoxic to healthy cells. Our results show that the Normal Human Fibroblasts (NHFs) (which were treated at a low population doubling where NHFs have the best proliferation rate) and Peripheral Blood Mononuclear Cells remained unaffected and healthy after a 96-hour and 48- hour exposure to DRE, respectively (Figures 2(a)–2(d)).
  • Lupeol,
    • katherine-medina
       
      What is Lupeol. (I should probably look into that.)
  • taraxasterol
  • More importantly, an increase in ROS production indicates prooxidant behaviour of DRE on cancer cell mitochondria, which is contrary to the antioxidant convictions of traditional medicine and previous studies on Taraxacum extracts citing reductions in NO, ROS, RNS, and COX-2 [10, 11] in mouse macrophages.
    • katherine-medina
       
      That is very important and interesting.
  • There are two main points that must be stated here: firstly, that noncancerous cells are unaffected by DRE treatment, and secondly, melanoma cells retain the signals to commit suicide long after DRE has been removed from the system
    • katherine-medina
       
      Good to restate.
  • Metformin acts as a metabolism interfering compound that debilitates cancer cells, and the case of G361-resistant melanoma cells, combining DRE with metformin reduces cell viability at even lower doses (Figures 9(a) and 9(b)).
  • By 48 hours, human melanoma A375 cells uncharacteristically showed susceptibility to apoptosis induction by DRE
  • We believe that this nontoxic extract can undergo precipitous translation from bench top to bedside, with dandelion products that are already commercially available in the form of tea and supplements.
  •  
    Essentially it is an article that figured out that DRE can induce apoptosis in melanoma cells, and it also proved that DRE is non-toxic to normal human cells.
katherine-medina

Anti-Oxidative and Anti-Inflammatory Effects of Ginger in Health and Physical Activity:... - 1 views

  • the rhizome
  • Ginger has staring potential for treating a number of ailments including degenerative disorders (arthritis and rheumatism), digestive health (indigestion, constipation and ulcer), cardiovascular disorders (atherosclerosis and hypertension), vomiting, diabetes mellitus, and cancer.
    • katherine-medina
       
      It has the potential for it, so there may not be many studies on these different things that ginger can supposedly do. So it makes me Infinitely more curious to look and see if there are other studies that actually have information about these said claims.
  • Furthermore, it has antimicrobial potential as well which can help in treating infectious diseases.[2
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  • The bioactive molecules of ginger like gingerols have shown antioxidant activity in various modules
  • Inflammatory disorders such as gastritis, esophagitis, and hepatitis, which are caused not only by infectious agents such as viruses, bacteria, and parasites but also by physical and chemical agents like heat, acid, cigarette smoke, and foreign bodies, are recognized as risk factors for human cancer
  • This study aimed to review the current evidence on ginger effects as an anti-inflammatory and anti-oxidative.
  • es.[2
  • 6-Shogaol has exhibited the most potent antioxidant and anti-inflammatory properties in ginger, which can be attributed to the presence of alpha, beta-unsaturated ketone moiety
  • Furthermore, feeding ginger to rats at 1% w/w during administration of malathion
    • katherine-medina
       
      Wow, so they fed the rats pesticides than ginger
  • so it can possibly value in treatment of Parkinson's disease.[17]
    • katherine-medina
       
      Really cool
  • This effect was improved by a treatment with 1% dietary ginger 1 month in rats which suggest that ginger may have protective role against the ethanol induced hepatotoxicity.
  • could be useful in preventing acute liver injury
  • Habib et al. showed that ginger extract can reduce the elevated expression of NFκB and TNF-α in rats with liver cancer
  • howed that gingerols can inhibit LPS-induced COX-2 expression while shogaol containing extracts has no effect on COX-2 expression
  • Ginger and its bioactive molecules are effective in controlling the extent of colorectal, gastric, ovarian, liver, skin, breast, and prostate cancers
    • katherine-medina
       
      Wow it can do a lot.
  • They observed that [6]-gingerol inhibits TRAIL-induced NF-κB activation by impairing the nuclear translocation of NF-κB, suppresses cIAP1 expression, and increases TRAIL-induced caspase-3/7 activation
  • Inhibition of angiogenesis in the mouse skin is the mechanism of ginger for treating of skin cancer.
  • However, ginger significantly lowered blood glucose, serum total cholesterol, LDL, VLDL, and triglycerides, and raised HDL in hyperglycemic rats, in models that are diabetic, deficient in the apolipoprotein E gene or those that have been fed a high lipid diet.
  • ethanolic extract of ginger reduced body weights and levels of glucose, insulin, total cholesterol, LDL cholesterol, triglycerides, free fatty acids, and phospholipids in high-fat diets.
  • CONCLUSIONS
    • katherine-medina
       
      Overall a good synopsis on what ginger can do.
katherine-medina

In Vitro and In Vivo Evaluation of the Effectiveness and Safety of Amygdalin as a Cance... - 0 views

  • ]. Approximately 80% of all medications approved by the FDA in the last three decades have been derived from natural sources
  • Transdermal drug delivery is a promising route for cancer treatment compared with the oral route due to its low side effects and improved efficacy and selectivity
  • All ALN formulations containing DDP exhibited a higher percent of EE and smaller particle size and PDI than those that did not have DDP at the molar ratio investigated.
    • katherine-medina
       
      If I am to do my research project over the affects of amygdalin patches on cancer, I will need to keep this section of text in mind.
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  • The optimum ALN gel formulation reduced mean relative carcinoma volume (MCV) at a higher rate (p < 0.05) compared with free amygdalin solution and free tamoxifene suspension.
  • that the optimum ALN gel formulation reduced mean relative carcinoma volume (MCV) compared with the DMBA control.
    • katherine-medina
       
      reduced carcinoma in comparison to control group
  • . The value of the zeta potential indicated a negative surface charge, which is considered advantageous for transdermal drug delivery and for electrostatic stabilization due to the electrostatic repulsions between vesicles
    • katherine-medina
       
      Good to note.
  • 3. Materials and Methods3.1. MaterialsAmygdalin was attained from Nature’s Only Choice Company (Tbilisi, GA, USA). Sigma Aldrich (Agitech Company, Cairo, Egypt) provided Tween 60, Span 60, cholesterol, 7, 12-dimethylbenz[a] anthracene (DMBA), triethanolamine, and dihexadecyl phosphate. Carbopol 934, methanol, acetone, and chloroform were attained from Corner-Lab Company (Cairo, Egypt).
  • Histological examination of the oral tamoxifen suspension treated group (Figure 7C) revealed the presence of hyperkeratosis and acanthosis in the surface epithelium of the epidermis with signs of a diffuse inflammatory response and edema in the dermis and sub-cutaneous tissue.
  • Histological examination of the optimum ALN gel treated group (Figure 7F) showed clearly healed skin with normal covering epithelium and marked improvement in all signs of the epidermis and dermis that were better than those of the oral amygdalin solution. These results confirmed the effectiveness of amygdalin loaded niosomes gel as a cancer therapy in vivo.
    • katherine-medina
       
      Cool, so they tested and confirmed that ALN gel does work to treat cancer of the skin.
  • Histological examination of the optimum ALN gel-treated group (Figure 8B) showed clearly healed skin with normal covering epithelium.
  • The group treated with plain niosomes gel showed MCV nearly similar to that of the DMBA control group.
    • katherine-medina
       
      SO the niosome gel doesn't do much.
  • The optimum ALN gel enhanced the permeation of amygdalin into deep skin layers and showed significant anti-tumor activity compared with oral tamoxifen.
    • katherine-medina
       
      I think that Amygdalen could be one of my research topics for this upcoming year.
  •  
    A really cool study that showed that Amygdalin in a gel form can prove to be very sucsessful at healing tumors from the epidermis.
katherine-medina

Frontiers | Dietary Polyphenols and Their Role in Oxidative Stress-Induced Human Diseas... - 1 views

  • phenolic acids, flavonoids, catechins, tannins, lignans, stilbenes and anthocyanidins
  • They possess antioxidant, chemopreventive and a wide range of pharmacological properties (
  • Over 8,000 polyphenols have been reported from plants, out of several hundreds of polyphenols exist in human diets
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  • Organic compounds bearing an aromatic ring with at least one hydroxyl group are termed as “phenolics”. In case, a compound possesses one or more aromatic rings having more than one hydroxyl group are called polyphenols (or polyphenolic compounds).
  • As per the C1-C6 or C3-C6 backbone, they are usually referred to as derivatives of benzoic acid or cinnamic acid
  • However, the role of the dietary polyphenols of their antioxidant abilities is still unclear.
    • katherine-medina
       
      How exactly is the role of antioxidants unclear?
  • Increased intake of foods containing polyphenols (for example, quercetin, epigallocatechin-3-gallate, resveratrol, cyanidin etc.) has been claimed to lower the incidence of a majority of chronic oxidative cellular damage, DNA damage, tissue inflammations, various cancers, viral/bacterial infections, and neurodegenerative diseases
    • katherine-medina
       
      So an increase of foods with natural extracts, so just plain vegetables that are not processed.
  • This review specifically focuses a current understanding on the dietary sources of polyphenols and their protective effects including mechanisms of action against various major human diseases.
  • γ rays
    • katherine-medina
       
      I had no idea these were a thing.
  • ROS when increased or excessively produced can cause oxidative changes/damages to all cellular macromolecules
  • Several antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) aid in the removal of free radicals
  • Peroxynitrite can also destroy lipoproteins and causes lipid peroxidation of cell membranes
  • ROS can also affect protein synthesis and protein functions. Protein oxidation can result in amino acid modifications
  • Flavonoids are further classified into different subgroups based on their structures such as flavan-3-ols (examples: catechin, epicatechin, epigallocatechin), isoflavones (examples: genistein, genistin, daidzenin, daidzin, biochanin A, formononetin), flavones (examples: luteolin, apigenin, chrysin), flavonones (examples: hesperetin, naringenin), flavonols (examples: quercetin, kaempferol, galangin, fisetin, myricetin), flavononol (example: taxifolin), flavylium salts (examples: cyanidin, cyanin, pelargonidin), and flavanones (examples: hesperetin, naringenin, eriodictyol, isosakuranetin)
    • katherine-medina
       
      WOW so flavonoids have a large variety and classes.
  • Polyphenols are found naturally in fruits and vegetables such as cereals, pulses, dried legumes, spinach, tomatoes, beans, nuts, peppermint, cinnamon, pears, cherries, oranges, apples, red wine, tea, cocoa, coffee and so on (Arts and Hollman, 2005; Scalbert et al., 2005). Polyphenols are classified into different groups depending on the number of aromatic (phenolic) rings they contain and the structural elements that connect these rings. They are broadly grouped into phenolic acids, flavonoids, stilbenes and lignans
    • katherine-medina
       
      SO each polyphenol has a different number of phenolic rings. What is the difference between the different polyphenols such as phenolic acid, flavonoids, stilbenes and lignans. I think that I should look at which of these groups are more effective when working with antibiotics as a way to aid them in the fight against resistant bacterias.
  • urther, OS exerts deleterious effects on DNA leading to the formation of DNA lesions, which can result in genomic instability and consequently lead to cell death.
  • In plant derived polyphenolic compounds, flavonoids comprise the largest group with an approximately 10,000 natural analogues
  • Dietary supplements containing elevated amounts of flavonoids from strawberries, lettuce, or blueberries aid in the reversal of age-related discrepancies in the brain and behavioral control in aged rats
  • Tea catechins
    • katherine-medina
       
      I ha e looked into these a bit, but I did not know that they can help with neurodegenerative diseases.
  • reduced glutathione (GSH), and on membrane sulphydryl (-SH) group in humans has been reported by Maurya and Rizvi (2009).
  • OS can be the primary or secondary reason for various CVDs. Preclinical evidence support that OS is linked to a variety of CVDs, including atherosclerosis, ischemia, stroke, cardiomyopathy, cardiac hypertrophy, and hypertension, as well as congestive heart failure
  • Dietary flavonoids may reduce endothelial disorders linked with various risk factors for atherosclerosis before plaque creation
  • The polyphenols of Hibiscus sabdariffa weaken diabetic nephropathy in terms of serum lipid profile and kidney oxidative markers
  • . Studies suggest that a diet that includes regular consumption of fruits and vegetables (rich in polyphenols such as catechins, resveratrol, ellagic acid, naringenin, quercetin etc.) significantly lowers the risk of developing many cancers.
  • Black tea polyphenols like EGCG, theaflavins and thearubigins have potent anticancer properties
  • Anti-carcinogenic effects of resveratrol are due to the antioxidant function, which inhibits hydroperoxidase, Akt (PI3K-Akt) signaling pathway, matrix metalloprotease-9, NF-kB, protein kinase C, cyclooxygenase, focal adhesion kinase and Bcl-2 (B cell lymphoma 2) biomarkers/enzymes (Athar et al., 2007)
  • Increased OS may lead to the vulnerability of the infection and also triggers the malfunctioning of cellular metabolism
  • Resveratrol shows its anti-rheumatoid arthritis properties with reduced RA patients’ swelling, tenderness, and disease activity by lowering the biochemical indicators of inflammation like MMP-3, IL-6, ESR, C-reactive protein, and undercarboxylated osteocalcin
  •  
    A good overview about polyphenols.
katherine-medina

IJMS | Free Full-Text | Antioxidant Versus Pro-Apoptotic Effects of Mushroom-Enriched D... - 0 views

  • In addition, the gut microbiota has also been described to be modulated by mushroom bioactive molecules, with implications in reducing liver inflammation during NAFLD progression.
  • non-alcoholic steatohepatitis (NASH)
    • katherine-medina
       
      I like the abbreviation
  • NASH is currently the third most common indication for liver transplantation in the United States and accounts for 10% of all HCC cases in Europe
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  • The increase in nutrient availability causes systemic metabolic alterations that lead to an increase in hepatic mitochondrial respiration as well as changes in the mitochondrial lipid membrane composition.
  • They are also rich in phenolic acids, such as hydroxybenzoic and hydroxycinnamic acid, flavonoids, tocopherols, ascorbic acid and carotenoids that are known for their antioxidant activity
    • katherine-medina
       
      They are high in polyphenols, just like I had thought, I do wonder if they have tried to single out a certain flavonoid or stilbene in order to determine whether or not it was the mechanism that caused the positive reaction.
  • Of note, indeed NAFLD patients present a “metabolic inflexibility”, that is, a reduced capacity to switch back from
    • katherine-medina
       
      I did not know that
  • The increased levels of β-oxidation seem to result in an increase in citrate within the mitochondrial matrix that can be transported to the cytosol via the citrate-malate shuttle and converted to acetyl-CoA and oxaloacetate by the enzyme ATP-citrate lyase [90,106]. Indeed, NAFLD patients present increased citrate levels in plasma
  • An alternative explanation for the deficient mitochondrial respiration might be the alterations in the mitochondria lipid composition, which are already present in steatosis.
  • As defined by mitohormesis, ROS production is physiological at low levels, acting as a crucial effector in proliferation, expression of antioxidant enzymes and insulin signalling. However, high levels of ROS formation causes oxidative stress and cell damage by reacting with its different components [90,114,115]. Oxidative stress occurs when the antioxidant capacity of the cell is not sufficient to neutralize the overproduction of ROS. ROS generation causes the peroxidation of phospholipids and cardiolipin at the mitochondrial membrane
  • All these mechanisms seem to be involved in the progression from NAFL to NASH. Indeed, NASH patients present increased ROS production, DNA damage, as measured by 8-Oxo-2’-deoxyguanosine (8OHdG) levels, and hepatic lipid peroxidation coupled with decreased expression of ETC Com
    • katherine-medina
       
      So essentially NASH patients have a higher level of ROS which damages their DNA. increase of ROS = DNA damage
  • In parallel, the negative regulation on the inhibitor of apoptosis proteins (IAPs) mediated by the translocation of a series of IAP antagonists such as Smac, HTRA2/Omi and apoptosis-related protein in the TGF-ß signalling pathway (ARTS) to the cytosol, results in the release and activation of caspases
  • Aiming at weight loss, calorie-restricted diets and regular physical activity can improve hepatic mitochondria dysfunction by decreasing FFA liver input and alleviating oxidative stress.
  • New therapies need to be developed to target NAFLD and NASH,
    • katherine-medina
       
      Are there any new therapies to treat NASH and NAFLD
  • showed lipid metabolism-modulating properties in the liver
  • This may lead to a decrease in lipogenesis and a concomitant increase in β-oxidation that could explain the reduction in IHTG content [203]. Similarly, the supplementation with a 1% aqueous extract of A. cinnamomea for 8 weeks reduced the expression of leptin and increased the expression of adiponectin, which was accompanied by an increase of AMPK and PGC-1α and a reduced expression of ACC, FAS and SREBP
  • IHTG content that was similar to the positive control group, treated with rosiglitazone, a PPAR-agonist antidiabetic drug
    • katherine-medina
       
      Interesting, I wonder if there is more that can be done with this extract with these types of effects.
  • herefore, these studies suggest a pivotal capacity of mushroom extracts to counteract the detrimental oxidative damage of mitochondria in NAFLD.
  • which seems to exacerbate NASH. H2O2 over-production may open the mPTP, while its transmembrane diffusion to the cytoplasm may even result in highly detrimental OH• formation. [93,131,132]. In contrast, the capacity of mushroom extracts from species such as Pleurotus ostreatus (Jacq.) P. Kumm. (oyster mushroom) or G. lucidum to elevate the entire antioxidant defence system of hepatocytes, seems a more promising therapeutic effect against the oxidative stress in NASH.
  • . Such evidence further supports the potential of G. lucidum extracts in reversing mitochondrial dysfunction in NAFLD.
  • In this line of research, novel therapies aim to target apoptosis via mitochondria, using molecules that mimic BH3 proteins and disrupt the interactions of pro-apoptotic and anti-apoptotic proteins.
  • Both aqueous and ethanol extracts, or isolated compounds (GL22 from Ganoderma leucocontextum T.H Li, W.Q. Deng, Dong M. Wang & H.P. Hu) increased the pro-apoptotic Bax to anti-apoptotic Bcl-2/Bcl-xL ratio
  • The antitumorigenic effects of mushroom extracts and isolated compounds have also been demonstrated in in-vivo xenograft models, resulting in tumour size reduction and increased animal survival rates (Table 2). Furthermore, in the HCC Huh7 xenograft mice model, fatty acid binding proteins
  • Therefore, the mechanisms by which mushroom extracts or isolated compounds induce mitochondrial-related apoptosis pathways are diverse and may be related with specific bioactive compounds. Modulation of pathways crucial for cell survival and alterations in lipid homeostasis seem to be related with the pro-apoptotic effects observed in HCC cell lines and in in-vivo xenograft models.
    • katherine-medina
       
      Cool
  • To sum up, mitochondria play a central role in the pathophysiology and progression of NAFLD as well as in the development of HCC, which can be a late-stage consequence of NASH. Hepatic mitochondria undergo bioenergetic remodelling to face the metabolic burden imposed by the increased FFAs load secondary to systemic IR. In turn, a decompensation of these processes may result in ROS formation and mitochondrial dysfunction, contributing to the development of NASH. Lastly, hepatic mitochondria also seem to be involved in anti-apoptotic oncogenic processes driving HCC. Targeting mitochondrial dysfunction is thus a promising approach for the treatment of the NAFLD continuum. The following section describes some of the in-vitro and in-vivo studies on the beneficial effects of mushroom-enriched diets or mushroom-derived compounds/extracts (Box 2) in preventing/reverting such liver damage.
  • This distinct property of mushroom-based therapy or -containing diet is especially relevant in the multifactorial context of NAFLD and especially NASH, where systemic synergistic metabolic alterations need to be addressed.
  •  
    An article detailing a bit of the effects that mushrooms can have on the liver's mitochondrial cells.
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