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Wednesday, April 16, 2014

Studies of ECGC and Lycopene in endometriosis

ECGC from green tea has been investigated as to its effect on endometriosis. ECGC, by reducing the effects on estrogen-2 receptors, *may* help decrease the stimulation of estrogen on endo lesions, causing them to not be as big bad and ugly. I haven't been able to find the actual study (nor could I find any other studies) about lycopene, but it supposedly works by reducing proteins that contribute to adhesions.



"Green tea epigallocatechin-3-gallate (EGCG) can inhibit angiogenesis and development of an experimental endometriosis model in mice, but it suffers from poor bioavailability. A prodrug of EGCG (pro-EGCG, EGCG octaacetate) is utilized to enhance the stability and bioavailability of EGCG in vivo. In this study, the potential of pro-EGCG as a potent anti-angiogenesis agent for endometriosis in mice was investigated. Homologous endometrium was subcutaneously transplanted into mice to receive either saline, vitamin E, EGCG or pro-EGCG treatment for 4 weeks. The growth of the endometrial implants were monitored by IVIS(®) non-invasive in vivo imaging during the interventions. Angiogenesis of the endometriotic lesions was determined by Cellvizio(®) in vivo imaging and SCANCO(®) Microfil microtomography. The bioavailability, anti-oxidation and anti-angiogenesis capacities of the treatments were measured in plasma and lesions. The implants with adjacent outer subcutaneous and inner abdominal muscle layers were collected for histological, microvessel and apoptosis examinations. The result showed that EGCG and pro-EGCG significantly decreased the growth of endometrial implants from the 2nd week to the 4th week of intervention. EGCG and pro-EGCG significantly reduced the lesion size and weight, inhibited functional and structural microvessels in the lesions, and enhanced lesion apoptosis at the end of interventions. The inhibition by pro-EGCG in all the angiogenesis parameters was significantly greater than that by EGCG, and pro-EGCG also had better bioavailability and greater anti-oxidation and anti-angiogenesis capacities than EGCG. Ovarian follicles and uterine endometrial glands were not affected by either EGCG or pro-EGCG. Vitamin E had no effect on endometriosis. In conclusion, pro-EGCG significantly inhibited the development, growth and angiogenesis of experimental endometriosis in mice with high efficacy, bioavailability, anti-oxidation and anti-angiogenesis capacities. Pro-EGCG could be a potent anti-angiogenesis agent for endometriosis." http://www.ncbi.nlm.nih.gov/pubmed/22948799

"In the mouse model, both treatments significantly reduced the mean number (P < 0.05 versus control) and the volume of established lesions (P < 0.05 versus control). Treatments consistently statistically significantly diminished cell proliferation (resveratrol P < 0.01 and EGCG P < 0.05, versus control), reduced vascular density (resveratrol P < 0.01 and EGCG P < 0.001, versus control) and increased apoptosis within the lesions (resveratrol P < 0.01 and EGCG P < 0.05, versus control). Both compounds induced reduction in human EEC proliferation (P < 0.05 versus basal) and increased apoptosis (P < 0.05 versus basal) in primary cultures." http://www.ncbi.nlm.nih.gov/pubmed/23081870

 "RESULTS We found that EGCG suppresses E2-stimulated activation, proliferation and VEGF expression of endometrial cells in vitro (all P < 0.05). Furthermore, EGCG selectively inhibited angiogenesis and blood perfusion (P < 0.05) of endometriotic lesions in vivo without affecting blood vessel development in ovarian follicles. Histology confirmed that EGCG-treatment induces regression of the endometriotic lesions." http://humrep.oxfordjournals.org/content/23/10/2308.full

"'One of the major complications of endometriosis is that it causes inflammation which induces adhesions. The inflammation basically causes scarring.

'What we did was to look at protein markers that could help us trace the activity of the abnormal ce
lls that cause these adhesions. The lycopene worked to reduce the abnormal activity of these cells.

'This means that you would not get the adhesions which suggests that lycopene could work to mitigate the complications and ailments of endometriosis. So, hypothetically speaking, we might be able to reduce the adhesion effects of endometriosis.'

Dr Dbouk said it was not possible at this stage to advise women on the amount of lycopene they should eat, but levels used in the study were similar to those that could be got from a diet packed with tomatoes and other lycopene-rich foods.

'There are many studies showing it plays a positive role in cancer and chronic inflammation, it's a nutrient and it can't do any harm,' he added.

The latest finding follows evidence that lycopene may protect against some forms of cancer, heart disease and male infertility.

The typical daily intake of a British adult is less than one milligram of lycopene, about 25 times less than the amount found by studies to protect against disease." http://www.dailymail.co.uk/.../Eating-tomatoes-fights...