Jiawei Erzhiwan improves menopausal metabolic syndrome by enhancing insulin secretion in pancreatic β cells
| Autor: | Mu Zhang, Pei Zhang, Xiao-Jun Xu, Shi-Ping Ma, Xie Zhishen, Feng-Guo Xu, Ping Zhou, Xiao-Meng Wan |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Estrogen receptor medicine.disease_cause Rats Sprague-Dawley 03 medical and health sciences Mice Internal medicine Insulin-Secreting Cells Drug Discovery Hyperlipidemia Insulin Secretion medicine Animals Humans Insulin Metabolic Syndrome geography geography.geographical_feature_category business.industry Antagonist General Medicine medicine.disease Islet Rats 030104 developmental biology Endocrinology Glucose Complementary and alternative medicine Ovariectomized rat Female Metabolic syndrome Menopause business Carcinogenesis Hormone Drugs Chinese Herbal |
| Zdroj: | Chinese journal of natural medicines. 14(11) |
| ISSN: | 1875-5364 |
| Popis: | Menopausal metabolic syndrome (MMS) is a series of syndrome caused by ovarian function decline and hormone insufficiency, and is a high risk factor for cardiovascular diseases (CVD) and type II diabetes mellitus (T2DM). Erzhiwan (EZW), composed of Herba Ecliptae and Fructus Ligustri Lucidi, is a traditional Chinese herbal formula that has been used to treat menopausal syndrome for many years. We added Herba Epimedii, Radix Rehmanniae, and Fructus Corni into EZW, to prepare a new formula, termed Jiawei Erzhiwan (JE). The present study was designed to determine the anti-MMS effects of JE using ovariectomized (OVX) adult female rats that were treated with JE for 4 weeks, and β-tc-6 cells and INS cells were used to detected the protect effectiveness of JE. Our results showed JE could increase insulin sensitivity and ameliorated hyperlipidemia. Metabolomics analysis showed that the serum levels of branched and aromatic amino acids were down-regulated in serum by JE administration. Moreover, JE enhanced the function of islet β cells INS-1 and β-tc-6, through increasing the glucose stimulated insulin secretion (GSIS), which was abolished by estrogen receptor (ER) antagonist, indicating that JE functions were mediated by ER signaling. Additionally, JE did not induce tumorigenesis in rat mammary tissue or promoted proliferation of MCF-7 and Hela cells. In conclusion, our work demonstrated that JE ameliorated OVX-induced glucose and lipid metabolism disorder through activating estrogen receptor pathway and promoting GSIS in islet β cells, thus indicating that JE could be a safe and effective medication for MMS therapy. |
| Databáze: | OpenAIRE |
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