Synergic effect of bee pollen and metformin on proliferation and apoptosis of granulosa cells: Rat model of polycystic ovary syndrome

2021 ◽  
Author(s):  
Leila Naseri ◽  
Mohammad Rasool Khazaei ◽  
Mozafar Khazaei
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cells ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Synergic Effect ◽  
Ovary Syndrome ◽  
Bee Pollen ◽  
Proliferation And Apoptosis

scholarly journals The LINC00477/miR-128 axis promotes the progression of polycystic ovary syndrome by regulating ovarian granulosa cell proliferation and apoptosis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Haijie Gao ◽  
Jinna Jiang ◽  
Yingying Shi ◽  
Jiying Chen ◽  
Lijian Zhao ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cells ◽  
Polycystic Ovary ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Serum Samples ◽  
Ovary Syndrome ◽  
Ovarian Granulosa Cell ◽  
Proliferation And Apoptosis ◽  
And Migration

Abstract Background Long noncoding RNAs (lncRNAs) participate in the pathogenesis of various human diseases. This study aims to investigate the roles of lncRNA LINC00477 in polycystic ovary syndrome (PCOS), especially the impacts of LINC00477 on the proliferation and migration of human granulosa cells and the related mechanisms. Methods qRT-PCR analysis was performed to examine the expression pattern of LINC00477 in serum samples of PCOS patients as well as PCOS animal models. The effect of LINC00477 on the viability and apoptosis of ovarian granulosa cells was detected by MTT and flow cytometry assays. The correlation between LINC00477 and miR-128 was verified by bioinformatics analysis and dual-luciferase reporter and RNA pull-down assays. Finally, rescue assays were performed to analyze the effects of the LINC00477-miR-128 axis on the biological behaviors of granulosa cells. Results LINC00477 was significantly upregulated in the serum of PCOS patients as well as PCOS mouse models. LINC00477 overexpression inhibited the proliferation and promoted the apoptosis of granulosa cells, whereas knockdown of LINC00477 yielded the opposite effects. Moreover, miR-128 mimics partially abrogated the effect of LINC00477 on granulosa cells. Conclusion LINC00477 may function as a ceRNA to inhibit proliferation and apoptosis of granulosa cells by modulating miR-128 expression.

scholarly journals Chemerin regulates autophagy to participate in polycystic ovary syndrome

2021 ◽  
Vol 49 (11) ◽  
pp. 030006052110583
Author(s):  
Xiaodong Luo ◽  
Yangyang Gong ◽  
Liuyun Cai ◽  
Lei Zhang ◽  
Xiaojing Dong
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cells ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Mammalian Target Of Rapamycin ◽  
Ectopic Expression ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Phosphoinositide 3 Kinase

Objective Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of reproductive age. Chemerin has recently been discovered as a novel adipokine associated with obesity and metabolic syndrome. Excessive autophagy activity and overexpression of autophagy-related genes in follicular granulosa cells are important mechanisms of PCOS. This study aimed to investigate the effect of chemerin on autophagy in PCOS. Methods A rat model of PCOS was established by subcutaneous injection of testosterone propionate under a high-fat diet. Expression levels of chemerin and its receptor CMKLR1 were determined by real-time polymerase chain reaction and western blot. Proliferation and apoptosis of human granulosa cells in vitro and expression of autophagy-related genes were examined using bafilomycin A1 (autophagy inhibitor) and Torin1 (autophagy inducer). Results Chemerin and CMKLR1 expression were significantly increased in the ovary in a rat model of PCOS. Ectopic expression of chemerin promoted the proliferation and inhibited the apoptosis of COV434 cells. Ectopic expression of chemerin also induced autophagy by inhibiting the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway. Conclusions Chemerin and CMKLR1 were overexpressed in PCOS rats. Chemerin promoted autophagy through inhibiting the PI3K/Akt/mTOR pathway, and may provide a potential target and biomarker of PCOS.

Dioscin Ameliorates Polycystic Ovary Syndrome by Inhibiting PI3K/Akt Pathway-Mediated Proliferation and Apoptosis of Ovarian Granulosa Cells

2020 ◽  
Vol 18 (4) ◽  
pp. 331-336
Author(s):  
Xinrong Li ◽  
Beili Lv ◽  
Haiyan Wang ◽  
Qiaohong Qian
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Western Blot ◽  
Granulosa Cells ◽  
Caspase 3 ◽  
Polycystic Ovary ◽  
Akt Pathway ◽  
Ovary Syndrome ◽  
Ovarian Granulosa Cells ◽  
Proliferation And Apoptosis ◽  
Induced Apoptosis

To understand the mechanism underlying Dioscin inhibition of polycystic ovary syndrome, we have examined its effects on ovarian granulosa cells from letrozole-treated rats. To this end, Western blot was utilized to determine changes in the levels of Bcl-2, cleaved caspase-3, caspase-3, and phosphatidylinositol 3-kinase (PI3K)/protein kinase B pathway after Dioscin treatment in letrozole-treated rats. Dioscin ameliorated polycystic ovary syndrome by reducing the serum level of testosterone and increasing progesterone levels. It also inhibited proliferation and induced apoptosis of ovarian granulosa cells in the rat model by decreasing the level of Bcl-2 and elevating cleaved caspase-3. Western blot analysis revealed that Dioscin suppressed the PI3K/Akt pathway by inhibiting p-AKT/AKT. SC79, a p-AKT/AKT activator, reversed the effects of Dioscin on the proliferation and apoptosis of ovarian granulosa cells. In conclusion, Dioscin might present a novel therapeutic opportunity for patients with polycystic ovary syndrome.

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