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林安盈, 杨璐瑜, 杨正望, 余曦明.健脾化痰方通过调控PPAR信号通路改善PCOS-IR大鼠的机制研究[J].湖南中医药大学学报,2024,44(12):2157-2163[点击复制] |
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| 健脾化痰方通过调控PPAR信号通路改善PCOS-IR大鼠的机制研究 |
| 林安盈,杨璐瑜,杨正望,余曦明 |
| (湖南中医药大学, 湖南 长沙 410208;广州市花都区妇幼保健院, 广东 广州 510810;江西省中西医结合医院, 江西 南昌 330012;湖南中医药大学第一附属医院, 湖南 长沙 410007) |
| 摘要: |
| 目的 基于过氧化物酶体增殖物激活受体家族（peroxisome proliferators-activated receptors,PPAR）信号通路研究健脾化痰方对多囊卵巢综合征（polycystic ovary syndrome,PCOS）伴胰岛素抵抗（insulin resistance,IR）大鼠模型的作用机制。方法 40只SD大鼠随机分为两组，空白对照组10只和造模组30只，造模组采用来曲唑灌胃及高脂饲料喂养造模8周。将造模成功的大鼠随机分为模型对照组、二甲双胍组、健脾化痰方组，每组10只。健脾化痰方组和二甲双胍组分别予以健脾化痰方、二甲双胍干预，连续4周。采用HE染色法观察卵巢组织病理学改变；ELISA法测定卵泡刺激素（follicle-stimulating hormone,FSH）、黄体生成素（luteinizinghormone,LH）、雌二醇（estradiol,E2）、总睾酮（testosterone,T）、空腹血糖（fasti ng blood glucose,FBG）、空腹胰岛素（fasting serum lisulin,FINS）、脂联素的水平并计算胰岛素抵抗指数（homeostatic model assessment of insulin resistance,HMOR-IR）；PCR和Western blot分别检测卵巢组织PPARα、PPARγ的mRNA和蛋白表达水平。结果 与空白对照组比较，模型对照组大鼠体质量明显增加，血清LH、T、LH/FSH升高，E2、FSH降低，卵巢多囊性改变明显，糖脂代谢调控失常（P<0.01）；与模型对照组比较，健脾化痰方组大鼠可控制体质量增速，调节大鼠血清、血脂、血糖代谢环节，T、LH水平降低（P＜0.05），FSH、E2、脂联素水平升高（P＜0.05），卵巢组织多囊样改变改善，卵泡发育良好，卵巢组织PPARα、PPARγ的mRNA及蛋白表达水平上调（P<0.05）。结论 健脾化痰方能有效降低来曲唑联合高脂饲料诱导的PCOS-IR大鼠体质量，改善胰岛素抵抗和脂代谢紊乱，调节性激素分泌，保护PCOS-IR大鼠卵巢生殖功能，可能是通过激活PPARα、PPARγ来发挥作用。 |
| 关键词: 多囊卵巢综合征 健脾化痰方 来曲唑 高脂饲料 胰岛素抵抗 PPARα、PPARγ |
| DOI：10.3969/j.issn.1674-070X.2024.12.003 |
| 投稿时间：2024-06-17 |
| 基金项目:湖南省自然科学基金项目（2022JJ40317）;湖南中医药大学中药粉体与创新药物省部共建国家重点实验室培育基地开放基金项目（21PTKF1011）;国家级大学生创新创业训练计划项目（202210541064）。 |
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| Mechanism of Jianpi Huatan Formula in improving PCOS-IR rats by regulating PPAR signaling pathway |
| LIN Anying, YANG Luyu, YANG Zhengwang, YU Ximing |
| (Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;Maternal and Child Health Hospital in Guangzhou Huadu District, Guangzhou, Guangdong 510810, China;Integrated Traditional Chinese and Western Medicine Hospital in Jiangxi Province, Nanchang, Jiangxi 330012, China;The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China) |
| Abstract: |
| Objective To investigate the mechanism of action of Jianpi Huatan Formula (JPHTF) in improving polycystic ovary syndrome (PCOS) with insulin resistance (IR) in a rat model, based on the peroxisome proliferators-activated receptor (PPAR) signaling pathway. Methods Forty SD rats were randomized into a blank control group (n=10) and a model group (n=30). The mode group was induced with letrozole by gavage and fed with a high-fat diet for eight weeks. The successfully modeled rats were then randomly subdivided into a model control group, a metformin group, and a JPHTF group, with 10 rats in each group. The JPHTF and metformin groups were treated with JPHTF and metformin, respectively, for four consecutive weeks. HE staining was used to observe the histopathological changes in ovarian tissues; ELISA was performed to measure the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), testosterone (T), fasting blood glucose (FBG), fasting serum insulin (FINS), and adiponectin, and to calculate the homeostatic model assessment of insulin resistance (HMOR-IR); PCR and Western blot were used to examine the mRNA and protein expression levels of PPARα and PPARγ in ovarian tissues, respectively. Results Compared with the blank control group, the model control group showed significantly increased body weight, serum levels of LH and T, as well as LH/FSH ratio, decreased levels of E2 and FSH, evident ovarian polycystic changes, and dysregulation of glucose and lipid metabolism (P<0.01); compared with the model control group, the rats in the JPHTF group showed a slower body weight gain, improved serum, glucose, and lipid metabolism, and reduced T and LH levels (P<0.05). The group also demonstrated elevated FSH, E2, and adiponectin levels (P<0.05), alleviated ovarian polycystic changes, enhanced follicular development, and upregulated mRNA and protein expression levels of PPARα and PPARγ in ovarian tissues (P<0.05). Conclusion JPHTF can effectively reduce body weight, improve insulin resistance and lipid metabolism disorders, regulate sex hormone secretion, and protect ovarian reproductive function in PCOS-IR rats induced by letrozole combined with a high-fat diet. It may exert its effects through activating PPARα and PPARγ |
| Key words: polycystic ovary syndrome Jianpi Huatan Formula letrozole high-fat diet insulin resistance PPARα,PPARγ |
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