Novel mechanisms underlying anti-polycystic ovary like syndrome effects of electroacupuncture in rats: suppressing SREBP1 to mitigate insulin resistance, mitochondrial dysfunction and oxidative stress

被引:41
作者
Peng, Yan [1 ]
Yang, Xinming [2 ]
Luo, Xi [2 ]
Liu, Chunhong [3 ]
Cao, Xia [4 ]
Wang, Hongyan [5 ]
Guo, Liyuan [5 ]
机构
[1] Heilongjiang Univ Chinese Med, Affiliated Hosp 1, Dis Prevent Ctr, Harbin 150040, Peoples R China
[2] Heilongjiang Univ Chinese Med, Affiliated Hosp 1, Dept Obstet & Gynecol, Harbin 150040, Peoples R China
[3] Heilongjiang Univ Chinese Med, Coll Basic Med Sci, Harbin 150040, Peoples R China
[4] Heilongjiang Univ Chinese Med, Document Retrival Ctr, Harbin 150040, Peoples R China
[5] Harbin Med Univ, Dept Gynecol Oncol, Canc Hosp, Harbin 150081, Peoples R China
基金
中国国家自然科学基金;
关键词
Electroacupuncture; PCOS; SREBP1; AMPK; Insulin resistance; GENE-EXPRESSION; ACUPUNCTURE; WOMEN; DEHYDROEPIANDROSTERONE; CYSTOGENESIS; PREVENTION; LIVER;
D O I
10.1186/s40659-020-00317-z
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background Acupuncture, a therapy of traditional Chinese medicine, is confirmed to exert the therapeutic action on polycystic ovary syndrome (PCOS). However, the detailed therapeutic mechanisms of acupuncture in PCOS remain ambiguous. In this study, we further investigated whether electroacupuncture (EA) alleviated PCOS-like symptoms in rats via regulating a metabolic regulator, sterol regulatory element binding protein-1 (SREBP1). Methods The PCOS-like rat model was built by hypodermic injection with dehydroepiandrosterone (DHEA). The rats were subjected to EA intervention (ST29 and SP6 acupuncture points) for 5 weeks. Primary granulosa cells were isolated from control and PCOS-like rats for evaluating insulin resistance, mitochondrial dysfunction and oxidative stress in vitro. Results The expression of SREBP1 was increased in PCOS-like rats, which was suppressed by EA treatment. In addition, lentivirus-mediated overexpression of SREBP1 restrained EA treatment-induced improvement in pathological changes, serum hormone levels and insulin resistance in rats. In addition, overexpression of SREBP1 repressed insulin-stimulated phosphorylation of insulin receptor beta (IR) and AKT in primary granulosa cells. Moreover, upregulation of SREBP1 further exacerbated mitochondrial dysfunction and oxidative stress in granulosa cells isolated from PCOS-like rats. Mechanically, EA treatment suppressed SREBP1 expression through inducing the activation of AMP-activated protein kinase (AMPK) signaling pathway in PCOS-like rats. Conclusion EA intervention alleviated PCOS-like symptoms in rats via improving IR, mitochondrial dysfunction and oxidative stress through regulating SREBP1, a lipid metabolism regulator. Our findings illuminate the novel protective mechanisms of EA in the treatment of PCOS.
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页数:13
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