scholarly journals The Ameliorating Effects of Bushen Huatan Granules and Kunling Wan on Polycystic Ovary Syndrome Induced by Dehydroepiandrosterone in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Yang Xu ◽  
Chun-Shui Pan ◽  
Quan Li ◽  
Hao-Lin Zhang ◽  
Li Yan ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Polycystic Ovary Syndrome ◽  
Endoplasmic Reticulum Stress ◽  
Pregnancy Outcome ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Post Treatment ◽  
Caspase 9 ◽  
Ovary Syndrome ◽  
Insulin In Serum

AimTo investigate the effects of Bushen Huatan Granules (BHG) and Kunling Wan (KW), the two Chinese medicines, on the regulation of polycystic ovary syndrome (PCOS) and their underlying mechanisms.Materials and MethodsPCOS rat model was established by subcutaneous injection of dehydroepiandrosterone (DHEA) (6 mg/100 g/day) for 20 days, followed by treatment with BHG (0.75, 1.49, and 2.99 g/kg) or KW (0.46, 0.91, and 1.82 g/kg) by gavage for 4 weeks. Estrous cycle was detected by vaginal smears. Follicles development was assessed by histology. Levels of testosterone and insulin in serum were tested by ELISA. Apoptosis of Granulosa cells (GCs) was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining. Pathways associated with apoptosis were detected with western blot. Pregnancy outcome was also assessed. GCs were pre-treated with 10–5 M testosterone in vitro for 24 h, then incubated with serum from rats receiving BHG (1.49 g/kg) or KW (1.82 g/kg). The parameters concerning apoptosis, mitochondrial function and endoplasmic reticulum stress were assessed.ResultsPost-treatment with either BHG or KW ameliorated DHEA-induced irregular estrous cycles, follicles development abnormalities, increase of testosterone and insulin in serum, and the apoptosis of GCs. Post-treatment with BHG decreased the expression of cleaved caspase-9/caspase 9, release of cytochrome C from mitochondria, and mitochondria reactive oxygen species production, increased activities of complex I, II, IV of ovarian tissue. Post-treatment with KW decreased the levels of caspase-12, GRP78, C/EBP homologous protein, phosphorylation of IRE-I, x-box-binding protein 1s, as well as phosphorylation of proline-rich receptor-like protein kinase, phosphorylation of eukaryotic translation initiation factor 2α and ATF4 of ovarian tissue and GCs. Both BHG and KW ameliorated pregnancy outcome.ConclusionThis study demonstrated BHG or KW as a potential strategy for treatment of PCOS induced by DHEA, and suggested that the beneficial role of the two medicines were mediated by different pathway with the effect of BHG being correlated with the regulation of mitochondria, while the effect of KW being attributable to protection of endoplasmic reticulum stress.

Abnormal expression of uncoupling protein-2 correlates with CYP11A1 expression in polycystic ovary syndrome

2011 ◽  
Vol 23 (4) ◽  
pp. 520 ◽  
Author(s):  
Yun Liu ◽  
Hong Jiang ◽  
Ling-Yun He ◽  
Wu-Jian Huang ◽  
Xiao-Yu He ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Early Stage ◽  
Uncoupling Protein ◽  
Serum Insulin ◽  
Ovarian Tissue ◽  
Fasting Blood Glucose ◽  
Control Group ◽  
Ovary Syndrome ◽  
Protein Levels

Polycystic ovary syndrome (PCOS) may result from hypersensitivity to insulin, which is negatively regulated by uncoupling protein (UCP)-2. Because cholesterol side-chain cleavage enzyme (CYP11A1) is closely linked to PCOS, the expression of UCP-2 and CYP11A1 in ovarian tissues from PCOS patients was examined in the present study. Twelve PCOS patients with hyperandrogenaemia who underwent laparoscopic ovarian wedge resection and 12 age-matched control patients who underwent contralateral ovarian biopsy were enrolled in the study. UCP-2 expression in early stage (primordial, primary and secondary) and late stage (sinus and mature) follicles was examined using immunohistochemistry, whereas UCP-2 and CYP11A1 mRNA and protein levels in ovarian tissue were determined using quantitative reverse transcription–polymerase chain reaction and western blot analyses, respectively. UCP-2 expression increased significantly with follicular development in both control and PCOS tissue, with expression in early stage follicles from PCOS patients significantly greater than that in controls. In addition, both UCP-2 and CYP11A1mRNA and protein levels, mean fasting blood glucose concentrations and fasting serum insulin levels were significantly higher in PCOS patients compared with the control group. Finally, a significant correlation between UCP-2 and CYP11A1 expression was found in PCOS but not control patients. In conclusion, in PCOS patients, there was a correlation between UCP-2 and CYP11A1 expression, which was significantly higher than in the control group. These changes in UCP-2 and CYP11A1 expression may mediate follicle development in PCOS.

Impacts of Metformin on Local Ovarian Cell Tissue of Rats with Polycystic Ovary Syndrome and Intestinal Flora Under Aerobic Exercise

2021 ◽  
Vol 11 (12) ◽  
pp. 2381-2388
Author(s):  
Xiao Yan
Keyword(s):  
Growth Factor ◽  
Polycystic Ovary Syndrome ◽  
Aerobic Exercise ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Ovary Syndrome ◽  
Ovarian Cell ◽  
Expression Levels ◽  
Cell Tissue ◽  
Igf I

In order to explore the possible treatment mechanism of metformin on the local ovarian cell tissue of rats with polycystic ovary syndrome (PCOS), 35 female clean sterile rats were selected as the research objects in this study, and randomly divided a PCOS model group (PCOS MG) (25 rats) and a control group (CG) (10 rats). After the modelling was completed, 5 rats were randomly selected to evaluate the modelling effect. When the success rate was higher than 80%, the remaining model rats were divided into two groups randomly, namely the (PCOS MG) (10 rats) and the treatment group (TG) (10 rats). Hematoxylin-eosin (HE) staining was performed on ovarian tissue of the rat, and the ovarian tissue structure was observed under light microscope. Immunohistochemistry was used to detect the distribution and expression levels of tumour necrosis factor-α (TNF-α), insulin-like growth factor-I (IGF-I), and connective tissue growth factor (CTGF) on the ovaries of rats in each group. It was found by observing the vaginal smear under the microscope that the rats in the (PCOS MG) had lost the regular estrous cycle, suggesting that there was no ovulation. The expression levels of TNF-α and CTGF in rats in the (PCOS MG) were greatly higher than those in the CG (P < 0.05); compared with the (PCOS MG), the expression levels of TNF-α and CTGF in the TG were decreased observably (P < 0.05). IGF-I was mainly expressed in granulosa cells (GCs) and follicular membrane cells (FMCs) of the ovarian tissue. The expression level of IGF-I in ovarian GCs in rats in the (PCOS MG) was significantly higher than that in the CG (P < 0.05). The expression level of IGF-I in GCs in the TG was lower significantly than that in the (PCOS MG) (P < 0.05). By comparing with rats in the CG, the rats in the (PCOS MG) had obviously decreased Actinobacteria and Betaproteobacteria in the intestinal tract, and the proportion of Firmicutes in the intestine was significantly increased; the amount of butyric acid in the faeces of rats with aerobic exercise was obviously higher than that in the (PCOS MG), because exercise increased the proportion of intestinal butyric acid-producing bacteria. Conclusion: metformin combined with aerobic exercise can treat the PCOS by regulating serum hormone levels and the expression levels of TNF-α, IGF-I, and CTGF.

scholarly journals Autophagy is activated in the ovarian tissue of polycystic ovary syndrome

Reproduction ◽  
2018 ◽  
Vol 155 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Da Li ◽  
Yue You ◽  
Fang-Fang Bi ◽  
Tie-Ning Zhang ◽  
Jiao Jiao ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Potential Role ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Ovary Syndrome ◽  
Cellular Processes ◽  
Transmission Electron ◽  
Wide Range ◽  
Response To Stress

The importance of autophagy in polycystic ovary syndrome (PCOS)-related metabolic disorders is increasingly being recognized, but few studies have investigated the role of autophagy in PCOS. Here, transmission electron microscopy demonstrated that autophagy was enhanced in the ovarian tissue from both humans and rats with PCOS. Consistent with this, ovarian granulosa cells from PCOS rats showed increases in the autophagy marker protein light chain 3B (LC3B), whereas levels of the autophagy substrate SQSTM1/p62 were decreased. In addition, the ratio of LC3-II/LC3-I was markedly elevated in human PCOS ovarian tissue compared with normal ovarian tissue. Real-time PCR arrays indicated that 7 and 34 autophagy-related genes were down- and up-regulated in human PCOS , Signal-Net, and regression analysis suggested that there are a wide range of interactions among these 41 genes, and a potential network based on EGFR, ERBB2, FOXO1, MAPK1, NFKB1, IGF1, TP53 and MAPK9 may be responsible for autophagy activation in PCOS. Systematic functional analysis of 41 differential autophagy-related genes indicated that these genes are highly involved in specific cellular processes such as response to stress and stimulus, and are linked to four significant pathways, including the insulin, ERBB, mTOR signaling pathways and protein processing in the endoplasmic reticulum. This study provides evidence for a potential role of autophagy disorders in PCOS in which autophagy may be an important molecular event in the pathogenesis of PCOS.

scholarly journals Polycystic Ovary Syndrome, Insulin Resistance, and Obesity: Navigating the Pathophysiologic Labyrinth

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Joselyn Rojas ◽  
Mervin Chávez ◽  
Luis Olivar ◽  
Milagros Rojas ◽  
Jessenia Morillo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Ovary Syndrome ◽  
Main Culprit ◽  
Exact Etiology

Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine-metabolic disorder that implies various severe consequences to female health, including alarming rates of infertility. Although its exact etiology remains elusive, it is known to feature several hormonal disturbances, including hyperandrogenemia, insulin resistance (IR), and hyperinsulinemia. Insulin appears to disrupt all components of the hypothalamus-hypophysis-ovary axis, and ovarian tissue insulin resistance results in impaired metabolic signaling but intact mitogenic and steroidogenic activity, favoring hyperandrogenemia, which appears to be the main culprit of the clinical picture in PCOS. In turn, androgens may lead back to IR by increasing levels of free fatty acids and modifying muscle tissue composition and functionality, perpetuating this IR-hyperinsulinemia-hyperandrogenemia cycle. Nonobese women with PCOS showcase several differential features, with unique biochemical and hormonal profiles. Nevertheless, lean and obese patients have chronic inflammation mediating the long term cardiometabolic complications and comorbidities observed in women with PCOS, including dyslipidemia, metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease. Given these severe implications, it is important to thoroughly understand the pathophysiologic interconnections underlying PCOS, in order to provide superior therapeutic strategies and warrant improved quality of life to women with this syndrome.

Sign in / Sign up

Export Citation Format

Share Document