Green Tea Extract has a Protective Effect on Leptin and Lipid Profile Levels Due to the Induction of Depot Medroxyprogesterone Acetate.

Background: Depot medroxyprogesterone acetate (DMPA) is a progesterone derivative synthesized in the laboratory. This substance has the ability to suppress ovulation, induce endometrial shrinkage, and even affect the hypothalamic-pituitary-gonadal axis in the reproductive system. Objective: The purpose of this study was to investigate the effects of administration of green tea extract on reducing visceral fat, increasing leptin levels, and improving the lipid profile in female rats injected with depot medroxyprogesterone acetate (DMPA). Results: This study was to look into the effects of green tea extract administration on visceral fat reduction, leptin levels, and lipid profile improvement as a result of DMPA administration. Analysis of HDL and LDL levels was performed by spectrophotometry. DMPA induced a significant increase in leptin levels compared with the control group (p 0.05). All doses of green tea extract can reduce this increase, with the highest doses reaching levels comparable to the control group (p > 0.05). DMPA significantly increased LDL levels compared to the control group (p < 0.05), and the highest green tea extract dose restored levels similar to the control group. DMPA triggered a decrease in HDL level that was significantly different from the control group (p < 0.05). The first dose of green tea extract can achieve HDL levels comparable to the control group (p > 0.05). Conclusion: It was concluded that green tea extract can protect the metabolic status through decreased leptin and an improvement of the lipid profile induced by DMPA.

Genistein modulates the estrogen receptor and suppresses angiogenesis and inflammation in the murine model of peritoneal endometriosis.

The purpose of this study was to investigate the effect of genistein administration on the modulation of the estrogen receptor, inhibition of inflammation and angiogenesis in the murine model of peritoneal endometriosis. A total of thirty-six mice (Mus musculus) were divided into six groups (n = 6), including the control group, endometriosis group, endometriosis group treated with various doses of genistein (0.78; 1.04; 1.3 mg/day), and endometriosis group treated with leuprolide acetate (0.00975 mg/day every 5 days for 15 days). Analysis of estrogen receptor-α, estrogen receptor-ß, TNF-α, IL-6, VEGF, and HIF-1α were performed immunohistochemically. Expression of estrogen receptor-α, estrogen receptor-ß, TNF-α, IL-6, VEGF and HIF-1α increased significantly compared with the control group (p < 0.05). All doses of genistein decreased the expression of estrogen receptor-α, increased estrogen receptor-ß, lowered VEGF and HIF-1α significantly compared with endometriosis group (p > 0.05). Genistein also decreased the expression of TNF-α and IL-6 (1.04 and 1.3 mg/day) compared with the endometriosis group, reaching level comparable to that of the control group (p > 0.05). It was concluded that genistein is able to modulate estrogen receptor-α and estrogen receptor-ß and inhibit the development of inflammation and angiogenesis in the murine model of peritoneal endometriosis. Thus, genistein can be a candidate in the treatment of endometriosis.

The effects of Eucheuma cottonii on alveolar macrophages and malondialdehyde levels in bronchoalveolar lavage fluid in chronically particulate matter 10 coal dust-exposed rats.

OBJECTIVES: To investigate the effect of Eucheuma cottonii on alveolar macrophages (AM) and malondialdehyde (MDA) levels in bronchoalveolar lavage fluids (BALF) in particulate matter 10 (PM10) coal dust-exposed rats. MATERIALS AND METHODS: Ten groups, including a non exposed group and groups exposed to coal dust at doses of 6.25 (CD6.25), 12.5 (CD12.5), or 25 mg/m(3) (CD25) an hour daily for 6 months with or without supplementation of ethanolic extract of E. cottonii at doses of 150 (EC150) or 300 mg/kg BW (EC300). The number of macrophages was determined using a light microscope. MDA levels were measured by TBARS assay. RESULTS: EC150 insignificantly (P > 0.05) reduces the AM in CD groups compared to non treatment groups. EC150 and EC300 significantly (P < 0.05) decreased MDA levels in CD12.5 and CD25 groups relative to non treatment groups. CONCLUSION: E. cottonii attenuated oxidative stress in chronic exposure of PM10 coal dust.

The Effects of Eucheuma cottonii on Signaling Pathway Inducing Mucin Synthesis in Rat Lungs Chronically Exposed to Particulate Matter 10 (PM10) Coal Dust.

This study was aimed at investigating the effects of Eucheuma cottonii (EC) in oxidative stress and the signaling for mucin synthesis in rat lungs chronically exposed to coal dust. Coal dust with concomitant oral administration of ethanolic extract of EC at doses of 150 (EC150) or 300 mg/kg BW (EC300) compared to exposed to PM10 coal dust at doses of 6.25 (CD6.25), 12.5 (CD12.5), or 25 mg/m(3) (CD25) (an hour daily for 6 months) and nonexposure group (control). The malondialdehyde (MDA), epidermal growth factor (EGF), transforming growth factor (TGF)- α , epidermal growth factor receptor (EGFR), and MUC5AC levels were determined in the lung. The administration of EC300 significantly (p < 0.05) reduced the MDA levels in groups exposed to all doses of coal dust compared to the respective coal dust-exposed nonsupplemented groups. Although not statistically significant,EC reduced the EGF levels and EGFR expressions in CD12.5 and CD25 groups and decreased the TGF- α , level and MUC5AC expression in CD25 group compared to the respective coal dust-exposed nonsupplemented groups. EC was able to decrease oxidative stress and was also able to decrease signaling for mucin synthesis, at least a part, via reducing the ligand in chronic coal dust exposure.