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Anticancer properties of Ganoderma lucidum methanol extracts in vitro and in vivo. Harhaji Trajković LM, Mijatović SA, Maksimović-Ivanić DD, Stojanović ID, Momcilović MB, Tufegdzić SJ, Maksimović VM, Marjanović ZS, Stosić-Grujicić SD. Nutr Cancer. 2009;61(5):696-707. PMID: 19838944 DOI: 10.1080/01635580902898743 Anticancer activities of various extracts of the medicinal mushroom, Ganoderma lucidum, have been widely demonstrated and are mainly associated with the presence of different bioactive polysaccharides and triterpenoids. We have evaluated and compared in vitro and in vivo the antitumor effects of two preparations from Ganoderma lucidum: a methanol extract containing total terpenoids (GLme) and a purified methanol extract containing mainly acidic terpenoids (GLpme). Both extracts inhibited tumor growth of B16 mouse melanoma cells inoculated subcutaneously into syngeneic C57BL/6 mice and reduced viability of B16 cells in vitro, whereby GLme exhibited stronger effect. Furthermore, anticancer activity of GLme was demonstrated for the first time against two other rodent tumor cell lines, L929-mouse fibrosarcoma and C6-rat astrocytoma. The mechanism of antitumor activity of GLme comprised inhibition of cell proliferation and induction of caspase-dependent apoptotic cell death mediated by upregulated p53 and inhibited Bcl-2 expression. Moreover, the antitumor effect of the GLme was associated with intensified production of reactive oxygen species, whereas their neutralization by the antioxidant, N-acetyl cysteine, resulted in partial recovery of cell viability. Thus, our results suggest that GLme might be a good candidate for treatment of diverse forms of cancers.

Berberine and Coptidis rhizoma as novel antineoplastic agents: a review of traditional use and biomedical investigations. Tang J, Feng Y, Tsao S, Wang N, Curtain R, Wang Y. J Ethnopharmacol. 2009 Oct 29;126(1):5-17. Epub 2009 Aug 15. PMID: 19686830 doi:10.1016/j.jep.2009.08.009 Conclusions The modern evidences of treating cancer with Huanglian and berberine have a strong linkage with traditional concept and rules of using Huanglian in CM practice. As anticancer candidates with low toxicity, berberine and its altered structure, as well as Huanglian and its formulae, will attract scientists to pursue the potential anticancer effects and the mechanisms by using technologies of genomics, proteomics and other advanced approaches. On the other hand, relatively few in vivo studies have been conducted on anticancer effects of Huanglian and berberine. The clinical application of berberine or Huanglian as novel cancer therapeutic agents requires in vivo validations and further investigations of their anticancer mechanisms.

n vivo assessment of herb-drug interactions: possible utility of a pharmacogenetic approach? Tomlinson B, Hu M, Lee VW. Mol Nutr Food Res. 2008 Jul;52(7):799-809. Review. PMID: 18618477DOI: 10.1002/mnfr.200700454

Lucock MD, Wild J, Smithells RW, Hartley R. In vivo characterization of the absorption and biotransformation of pteroylmonoglutamic acid in man: a model for future studies. Biochem Med Metab Biol. 1989 Aug;42(1):30-42. PMID: 2505816 [PubMed - indexed

Short-term fish oil supplementation improved innate immunity, but increased ex vivo oxidation of LDL in man--a pilot study. Turini ME, Crozier GL, Donnet-Hughes A, Richelle MA. Eur J Nutr. 2001 Apr;40(2):56-65. PMID: 11518200 DOI: 10.1007/s003940170016

In vivo threshold for cutaneous synthesis of vitamin D3. Matsuoka LY, Wortsman J, Haddad JG, Hollis BW. J Lab Clin Med. 1989 Sep;114(3):301-5. PMID: 2549141

Ultrastructural changes in regressing equine sarcoid tumours--mysterious role of mitochondria. Hallamaa RE. In Vivo. 2008 Jul-Aug;22(4):519-23. PMID: 18712182

Macroscopical and histopathological changes in regressing primary and recurrent equine sarcoids during active specific bio-immunotherapy. Hallamaa RE, Saario E, Tallberg T. In Vivo. 2005 Jul-Aug;19(4):761-7. PMID: 15999546

2: Selenium and the immune response: 2. Enhancement of murine cytotoxic T-lymphocyte and natural killer cell cytotoxicity in vivo. Petrie HT, Klassen LW, Klassen PS, O'Dell JR, Kay HD. J Leukoc Biol. 1989 Mar;45(3):215-20. PMID: 2564412

Neuroprotective effects of berberine on stroke models in vitro and in vivo. Zhou XQ, Zeng XN, Kong H, Sun XL. Neurosci Lett. 2008 Dec 5;447(1):31-6. Epub 2008 Sep 30. PMID: 18838103 doi:10.1016/j.neulet.2008.09.064 Findings of this study suggest that berberine protects against ischemic brain injury by decreasing the intracellular ROS level and subsequently inhibiting mitochondrial apoptotic pathway.

[Vitamin K and Bone Update. In vivo Metabolism of Vitamin K. - In relation to the conversion of vitamin K(1) to MK-4 -] Okano T, Nakagawa K, Kamao M. Clin Calcium. 2009 Dec;19(12):1779-87. Japanese. PMID: 19949269 Phylloquinone is a major form (>90%) of dietary vitamin K, but the form of vitamin K that exists at the highest concentrations in tissues of animals and humans is menaquinone-4 (MK-4) . Despite this great difference, the origin of tissue MK-4 had not been clarified until recently. We demonstrated that deuterium-labeled phylloquinone was converted into deuterium-labeled MK-4 in mice and this conversion occurred following an oral or enteral administration, but not parenteral administration. By the oral route, the phylloquinone with the deuterium-labeled side chain (phytyl side-chain) was clearly converted into menaquinone-4 with a non-deuterium-labeled side chain (geranylgeranyl side-chain) , implying that phylloquinone was converted into menaquinone-4 via integral side-chain removal. Our results suggest that cerebral menaquinone-4 originates from phylloquinone intake and the release of menadione from phylloquinone in the intestine followed by the prenylation of menadione into menaquinone-4 in the intestine or tissues

Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo.\nChen Q, Espey MG, Sun AY, Lee JH, Krishna MC, Shacter E, Choyke PL, Pooput C, Kirk KL, Buettner GR, Levine M.\nProc Natl Acad Sci U S A. 2007 May 22;104(21):8749-54. Epub 2007 May 14.\nPMID: 17502596 \n doi: 10.1073/pnas.0702854104\n

Berberine inhibits human tongue squamous carcinoma cancer tumor growth in a murine xenograft model. Ho YT, Yang JS, Lu CC, Chiang JH, Li TC, Lin JJ, Lai KC, Liao CL, Lin JG, Chung JG. Phytomedicine. 2009 Sep;16(9):887-90. Epub 2009 Mar 20. PMID: 19303753 Our primary studies showed that berberine induced apoptosis in human tongue cancer SCC-4 cells in vitro. But there is no report to show berberine inhibited SCC-4 cancer cells in vivo on a murine xenograft animal model. SCC-4 tumor cells were implanted into mice and groups of mice were treated with vehicle, berberine (10mg/kg of body weight) and doxorubicin (4mg/kg of body weight). The tested agents were injected once per four days intraperitoneally (i.p.), with treatment starting 4 weeks prior to cells inoculation. Treatment with 4mg/kg of doxorubicin or with 10mg/kg of berberine resulted in a reduction in tumor incidence. Tumor size in xenograft mice treated with 10mg/kg berberine was significantly smaller than that in the control group. Our findings indicated that berbeirne inhibits tumor growth in a xenograft animal model. Therefore, berberine may represent a tongue cancer preventive agent and can be used in clinic.

Scientists have known that cruciferous vegetables contain a host of chemopreventive agents that act in many different ways to block cancer development.2 Key among these products are indole-3-carbinol (I3C) and sulforaphane.1,3 Cancer cells need a brisk blood supply to support their rampant growth and reproduction. Preliminary studies in vitro and in vivo have found that apigenin inhibits blood vessel growth (angiogenesis) in human ovarian cancer cells, blocking production of two main signaling molecules required to stimulate vessel growth.20,21 Scientists confirmed this effect in ovarian cancer cells, also finding that apigenin strongly inhibits cell proliferation.22 Apigenin and BITC: Complementary Cancer Protection Cancer cells also need energy to support their frenetic reproductive activity. Researchers applied apigenin to human pancreatic cancer cells in culture and studied the cells' uptake of glucose.14 Astonishingly, they found that apigenin deprived energy-hungry cancer cells of glucose to support their voracious appetites and aggressive growth. It did this by down-regulating vital glucose-transporting proteins in cancer cells. This approach could effectively starve deadly cancer cells and stop them in their tracks. Another cruciferous vegetable component receiving rave reviews is the sulfur-containing molecule benzyl isothiocyanate, or BITC (pronounced "bitsy"). As with apigenin, population studies have shown that higher intakes of BITC correlate with reduced risk of cancers of the lung, breast, and colon30 while blocking cancer development in a host of different ways. BITC induces breast cancer cell death by apoptosis (programmed cell death), interfering with cancer cells' energy utilization and causing them to die off before they can contribute to tumor growth.31,32 In human ovarian cancer cells, BITC induces apoptosis by a different mechanism. It stimulates "signaling" molecules that tell cancer cells it's time to close up shop.

Berberine inhibits growth, induces G1 arrest and apoptosis in human epidermoid carcinoma A431 cells by regulating Cdki-Cdk-cyclin cascade, disruption of mitochondrial membrane potential and cleavage of caspase 3 and PARP. Mantena SK, Sharma SD, Katiyar SK. Carcinogenesis. 2006 Oct;27(10):2018-27. Epub 2006 Apr 18. PMID: 16621886 doi:10.1093/carcin/bgl043 In the present investigation, we show that berberine, which is present abundantly in Berberis plant species, significantly inhibits the viability, proliferation and induces cell death in human epidermoid carcinoma A431 cells (Figure 1), but this effect was not found in normal human epidermal keratinocytes under the identical conditions, except for a non-significant reduction in cell viability at higher concentrations of berberine (50 and 75 µM) and treatment of cells for a longer period of time (72 h). These data suggested that berberine may be examined as an effective chemotherapeutic agent against non-melanoma skin cancers. In conclusion, our study indicates that berberine inhibits growth, induces G1 arrest and apoptotic cell death of human epidermoid carcinoma A431 cells. We also provide mechanistic evidences that berberine-induced apoptosis in human epidermoid carcinoma cells is mediated through disruption of mitochondrial membrane potential and activation of caspase 3 pathway, although other pathways may have a role and that require further investigation. Moreover, further in vivo studies are required to determine whether berberine could be an effective chemotherapeutic agent for the prevention of non-melanoma skin cancers.

Bioactive vitamin D or calcitriol is a steroid hormone that has long been known for its important role in regulating body levels of calcium and phosphorus, and in mineralization of bone. More recently, it has become clear that receptors for vitamin D are present in a wide variety of cells, and that this hormone has biologic effects which extend far beyond control of mineral metabolism. The active form of vitamin D binds to intracellular receptors that then function as transcription factors to modulate gene expression. Like the receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has hormone-binding and DNA-binding domains. The vitamin D receptor forms a complex with another intracellular receptor, the retinoid-X receptor, and that heterodimer is what binds to DNA. In most cases studied, the effect is to activate transcription, but situations are also known in which vitamin D suppresses transcription. Each of the forms of vitamin D is hydrophobic, and is transported in blood bound to carrier proteins. The major carrier is called, appropriately, vitamin D-binding protein. The halflife of 25-hydroxycholecalciferol is several weeks, while that of 1,25-dihydroxycholecalciferol is only a few hours. The vitamin D receptor binds several forms of cholecalciferol. Its affinity for 1,25-dihydroxycholecalciferol is roughly 1000 times that for 25-hydroxycholecalciferol, which explains their relative biological potencies