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Berberine inhibits human tongue squamous carcinoma cancer tumor growth in a murine xenograft model. - [Phytomedicine. 2009] - PubMed result
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.
Treatment of Type 2 Diabetes and Dyslipidemia with the Natural Plant Alkaloid Berberine -- Zhang et al. 93 (7): 2559 -- Journal of Clinical Endocrinology & Metabolism
Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine.
Zhang Y, Li X, Zou D, Liu W, Yang J, Zhu N, Huo L, Wang M, Hong J, Wu P, Ren G, Ning G.
J Clin Endocrinol Metab. 2008 Jul;93(7):2559-65. Epub 2008 Apr 8.
PMID: 18397984
doi:10.1210/jc.2007-2404
Conclusions: Berberine is effective and safe in the treatment of type 2 diabetes and dyslipidemia.
NEJM -- Low-Carbohydrate-Diet Score and the Risk of Coronary Heart Disease in Women
Low-carbohydrate-diet score and the risk of coronary heart disease in women.
Halton TL, Willett WC, Liu S, Manson JE, Albert CM, Rexrode K, Hu FB.
N Engl J Med. 2006 Nov 9;355(19):1991-2002.
PMID: 17093250
Conclusions Our findings suggest that diets lower in carbohydrate and higher in protein and fat are not associated with increased risk of coronary heart disease in women. When vegetable sources of fat and protein are chosen, these diets may moderately reduce the risk of coronary heart disease.
Hypercalcemia in advanced head and neck squamous cell carcinoma: prevalence and potential impact on palliative care. - [J Support Oncol. 2009 Sep-Oct] - PubMed result
Hypercalcemia in advanced head and neck squamous cell carcinoma: prevalence and potential impact on palliative care.
Alsirafy SA, Sroor MY, Al-Shahri MZ.
J Support Oncol. 2009 Sep-Oct;7(5):154-7.
PMID: 19831158
Dietary composition modulates brain mass and amyloid beta levels in a mouse model of aggressive Alzheimer's amyloid pathology - Molecular Neurodegeneration | Full text
Dietary composition modulates brain mass and solubilizable Abeta levels in a mouse model of aggressive Alzheimer's amyloid pathology.
Pedrini S, Thomas C, Brautigam H, Schmeidler J, Ho L, Fraser P, Westaway D, Hyslop PS, Martins RN, Buxbaum JD, Pasinetti GM, Dickstein DL, Hof PR, Ehrlich ME, Gandy S.
Mol Neurodegener. 2009 Oct 21;4:40.
PMID: 19845940
doi:10.1186/1750-1326-4-40
INTERPRETATION: Dissociation of Abeta changes from brain mass changes raises the possibility that diet plays a role not only in modulating amyloidosis but also in modulating neuronal vulnerability. However, in the absence of a study of the effects of a high protein/low carbohydrate diet on nontransgenic mice, one cannot be certain how much, if any, of the loss of brain mass exhibited by high protein/low carbohydrate diet-fed TgCRND8 mice was due to an interaction between cerebral amyloidosis and diet. Given the recent evidence that certain factors favor the maintenance of cognitive function in the face of substantial structural neuropathology, we propose that there might also exist factors that sensitize brain neurons to some forms of neurotoxicity, including, perhaps, amyloid neurotoxicity. Identification of these factors could help reconcile the poor clinicopathological correlation between cognitive status and structural neuropathology, including amyloid pathology.
A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer's disease - Nutrition & Metabolism | Full text
A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer's disease.
Van der Auwera I, Wera S, Van Leuven F, Henderson ST.
Nutr Metab (Lond). 2005 Oct 17;2:28.
PMID: 16229744
doi:10.1186/1743-7075-2-28
CONCLUSION: Previous studies have suggested that diets rich in cholesterol and saturated fats increased the deposition of Abeta and the risk of developing AD. Here we demonstrate that a diet rich in saturated fats and low in carbohydrates can actually reduce levels of Abeta. Therefore, dietary strategies aimed at reducing Abeta levels should take into account interactions of dietary components and the metabolic outcomes, in particular, levels of carbohydrates, total calories, and presence of ketone bodies should be considered.
Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial - Br J Nutr. 2009 Sep 28:1-7. - CJO - Abstract -
Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.
von Hurst PR, Stonehouse W, Coad J.
Br J Nutr. 2009 Sep 28:1-7. [Epub ahead of print]
PMID: 19781131
In conclusion, improving vitamin D status in insulin resistant women resulted in improved IR and sensitivity, but no change in insulin secretion. Optimal vitamin D concentrations for reducing IR were shown to be 80-119 nmol/l, providing further evidence for an increase in the recommended adequate levels. Registered Trial No. ACTRN12607000642482.
Effect of glucosamine sulfate with or without omega-3 fatty acids in patients with osteoarthritis. - Adv Ther. 2009 Sep 4. - SpringerLink - Journal Article
Effect of glucosamine sulfate with or without omega-3 fatty acids in patients with osteoarthritis.
Gruenwald J, Petzold E, Busch R, Petzold HP, Graubaum HJ.
Adv Ther. 2009 Sep 4. [Epub ahead of print]
PMID: 19756416
DOI: 10.1007/s12325-009-0060-3
Serum 25-Hydroxyvitamin D Levels Among US Children Aged 1 to 11 Years: Do Children Need More Vitamin D? - [Pediatrics. 2009] - PubMed result
Serum 25-Hydroxyvitamin D Levels Among US Children Aged 1 to 11 Years: Do Children Need More Vitamin D?
Mansbach JM, Ginde AA, Camargo CA Jr.
Pediatrics. 2009 Nov;124(5):1404-1410.
PMID: 19951983
CONCLUSIONS: On the basis of a nationally representative sample of US children aged 1 to 11 years, millions of children may have suboptimal levels of 25(OH)D, especially non-Hispanic black and Hispanic children. More data in children are needed not only to understand better the health implications of specific serum levels of 25(OH)D but also to determine the appropriate vitamin D supplement requirements for children.
Vitamin D and mortality in older men and women. - Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. - Wiley InterScience :: Article :: HTML Full Text
Vitamin D and mortality in older men and women.
Pilz S, Dobnig H, Nijpels G, Heine RJ, Stehouwer CD, Snijder MB, van Dam RM, Dekker JM.
Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. Epub 2009 Feb 18.
PMID: 19226272
DOI: 10.1111/j.1365-2265.2009.03548.x
Conclusions Low 25(OH)D levels are associated with all-cause mortality and even more pronounced with cardiovascular mortality, but it remains unclear whether vitamin D deficiency is a cause or a consequence of a poor health status. Therefore, intervention studies are warranted to evaluate whether vitamin D supplementation reduces mortality and cardiovascular diseases.
Low serum 25-hydroxyvitamin D concentrations are associated with greater all-cause mortality in older community-dwelling women
Low serum 25-hydroxyvitamin D concentrations are associated with greater all-cause mortality in older community-dwelling women.
Semba RD, Houston DK, Ferrucci L, Cappola AR, Sun K, Guralnik JM, Fried LP.
Nutr Res. 2009 Aug;29(8):525-30.
PMID: 19761886
doi:10.1016/j.nutres.2009.07.007
Older community-dwelling women with low 25(OH)D levels are at an increased risk of death.
Induction of Ovarian Cancer Cell Apoptosis by 1,25-Dihydroxyvitamin D3 through the Down-regulation of Telomerase — JBC
Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase.
Jiang F, Bao J, Li P, Nicosia SV, Bai W.
J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12.
PMID: 15485861
doi: 10.1074/jbc.M410395200
Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression.
Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85–90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene.
It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chromosome ends and leads to the genomic instability a
Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000-2004 -- Looker et al. 88 (6): 1519 -- American Journal of Clinical Nutrition
Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000-2004.
Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA.
Am J Clin Nutr. 2008 Dec;88(6):1519-27.
PMID: 19064511
doi:10.3945/ajcn.2008.26182
Conclusions: Overall, mean serum 25(OH)D was lower in 2000–2004 than 1988–1994. Assay changes unrelated to changes in vitamin D status accounted for much of the difference in most population groups. In an adult subgroup, combined changes in BMI, milk intake, and sun protection appeared to contribute to a real decline in vitamin D status.
In summary, age-standardized mean serum 25(OH)D concentrations based on observed values were significantly lower in 2000–2004 than in 1988–1994 in all groups examined. Adjustment for assay changes noticeably reduced the difference between surveys. However, mean serum 25(OH)D concentrations remained significantly lower in males (except Mexican Americans) in NHANES 2000–2004 than in NHANES III, even after adjustment for assay differences. This remaining difference likely represents a real decline in vitamin D status. Changes in BMI, milk intake, and sun protection appeared to contribute to this decline in a subgroup of non-Hispanic white adults. The possibility that trends in overweight, sun protection, and milk intake may continue supports the need to continue monitoring the serum 25(OH)D status of the population
The Effect of Vitamin D2 and Vitamin D3 on Intestinal Calcium Absorption in Nigerian Children with Rickets -- Thacher et al. 94 (9): 3314 -- Journal of Clinical Endocrinology & Metabolism
The effect of vitamin D2 and vitamin D3 on intestinal calcium absorption in Nigerian children with rickets.
Thacher TD, Obadofin MO, O'Brien KO, Abrams SA.
J Clin Endocrinol Metab. 2009 Sep;94(9):3314-21. Epub 2009 Jun 30.
PMID: 19567516
Conclusions: Despite similar increases in 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D with vitamin D2 or vitamin D3, fractional calcium absorption did not increase, indicating that rickets in Nigerian children is not primarily due to vitamin D-deficient calcium malabsorption
Developmental toxicity evaluation of berberine in rats and mice. Gloria D. Jahnke. 2006; Birth Defects Research Part B: Developmental and Reproductive Toxicology - Wiley InterScience
Developmental toxicity evaluation of berberine in rats and mice.
Jahnke GD, Price CJ, Marr MC, Myers CB, George JD.
Birth Defects Res B Dev Reprod Toxicol. 2006 Jun;77(3):195-206.
PMID: 16634078
DOI: 10.1002/bdrb.20075
BACKGROUND: Berberine, a plant alkaloid, is found in some herbal teas and health-related products. It is a component of goldenseal, an herbal supplement. Berberine chloride dihydrate (BCD) was evaluated for developmental toxicity in rats and mice.
METHODS: Berberine chloride dihydrate was administered in the feed to timed-mated Sprague-Dawley (CD) rats (0, 3625, 7250, or 14,500 ppm; on gestational days [GD] 6-20), and Swiss Albino (CD-1) mice (0, 3500, 5250, or 7000 ppm; on GD 6-17). Ingested doses were 0, 282, 531, and 1313 mg/kg/day (rats) and 0, 569, 841, and 1155 mg/kg/day (mice).
RESULTS:There were no maternal deaths. The rat maternal lowest observed adverse effect level (LOAEL), based on reduced maternal weight gain, was 7250 ppm. The rat developmental toxicity LOAEL, based on reduced fetal body weight per litter, was 14,500 ppm. In the mouse study, equivocal maternal and developmental toxicity LOAELs were 5250 ppm. Due to scattering of feed in the high dose groups, a gavage study at 1000 mg/kg/day was conducted in both species.
CONCLUSIONS: In rats, maternal, but not fetal adverse effects were noted. The maternal toxicity LOAEL remained at 7250 ppm (531 mg/kg/day) based on the feed study and the developmental toxicity NOAEL was raised to 1000 mg/kg/day BCD based on the gavage study. In the mouse, 33% of the treated females died. Surviving animals had increased relative water intake, and average fetal body weight per litter decreased 5-6% with no change in live litter size. The maternal toxicity LOAEL remained at 5250 ppm (841 mg/kg/day) BCD, based on increased water consumption. The developmental toxicity LOAEL was raised to 1000 mg/kg/day BCD based on decreased fetal body weight.
Mechanisms of Berberine (Natural Yellow 18)-Induced Mitochondrial Dysfunction: Interaction with the Adenine Nucleotide Translocator -- Pereira et al. 105 (2): 408 -- Toxicological Sciences
Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator.
Pereira CV, Machado NG, Oliveira PJ.
Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3.
PMID: 18599498
doi: 10.1124/jpet.107.128017
The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study.
Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs.
In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.
Mitochondrially Targeted Effects of Berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 Mouse Melanoma Cells: Comparison with Direct Effects on Isolated Mitochondrial Fractions - JPET
Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions.
Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ.
J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17.
PMID: 17704354
doi: 10.1124/jpet.107.128017
The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic “natural” over-the-counter medication.
Berberine Inhibits Metastasis of Nasopharyngeal Carcinoma 5-8F Cells by Targeting Rho Kinase-mediated Ezrin Phosphorylation at Threonine 567 - JBC
Berberine inhibits metastasis of nasopharyngeal carcinoma 5-8F cells by targeting Rho kinase-mediated Ezrin phosphorylation at threonine 567.
Tang F, Wang D, Duan C, Huang D, Wu Y, Chen Y, Wang W, Xie C, Meng J, Wang L, Wu B, Liu S, Tian D, Zhu F, He Z, Deng F, Cao Y.
J Biol Chem. 2009 Oct 2;284(40):27456-66. Epub 2009 Aug 3.
PMID: 19651779
Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells — Mol Cancer Ther
Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells.
Mantena SK, Sharma SD, Katiyar SK.
Mol Cancer Ther. 2006 Feb;5(2):296-308.
PMID: 16505103
doi: 10.1158/1535-7163.MCT-05-0448
The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy.
The evaluation of ancient herbal medicines may indicate novel strategies for the treatment of prostate cancer, which remains the leading cause of cancer-related deaths in American men (1). In our present investigation, we show that a naturally occurring isoquinoline alkaloid, berberine, significantly inhibits the proliferation and reduces the viability of DU145 and PC-3 as well as LNCaP cells (Fig. 1), which suggests that berberine may be an effective chemotherapeutic agent against both androgen-sensitive and androgen-insensitive prostate cancer cells. Importantly, we found that berberine did not exhibit toxicity to nonneoplastic human prostate epithelial cells under the conditions used, except for a moderate reduction in cell viability at higher concentrations when cells were treated in vitro for an extended period of time.
In conclusion, the results of the present study indicate that berberine inhibits proliferation and induces G1-phase arrest and apoptosis in human prostate cancer cells but not in normal human prostate epithelial cells. In addition, we provide mechanistic evidence that berberine-induced apoptosis in prostate carcinoma cells, particularly hormone-refractory prostate carcinoma cells, is mediated through enhanced expression of Bax, disruption of the mitochondrial membrane potential, and activation of caspase-3.
Jonathan Treasure’s Herblog » Berberine and cancer - recent research.
"Berberine, the yellow alkaloid ingredient of several traditional anticancer herbs such as Oregon grape root has an expanding literature confirming its anticancer properties. Here are a few recent studies…Oregon grape root was an ingredient of the controversial Hoxseys formula, and berberine herbs were included in Eclectic anticancer formula. Click Links for PubMed"
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