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

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.

2018 ◽  
Author(s):  
Ivica Lazurova ◽  
Jana Figurova ◽  
Zora Lazurova ◽  
Silvia Toporcerova ◽  
Miroslava Rabajdova ◽  
...  

2011 ◽  
Vol 23 (4) ◽  
pp. 520 ◽  
Author(s):  
Yun Liu ◽  
Hong Jiang ◽  
Ling-Yun He ◽  
Wu-Jian Huang ◽  
Xiao-Yu He ◽  
...  

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.


Reproduction ◽  
2018 ◽  
Vol 155 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Da Li ◽  
Yue You ◽  
Fang-Fang Bi ◽  
Tie-Ning Zhang ◽  
Jiao Jiao ◽  
...  

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.


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