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Purpose: To investigate the regulatory influence of Prok1 on apoptotic and proliferative changes in PCOS, and the implication of Pi3k/Akt/nf-κ B signaling pathway in the process.
Methods: Ovarian granulosa cells from a rat model of PCOS were assigned to control and si-Prok1 groups, after cell culture. Then, control lentivirus and Prok1 siRNA lentivirus (50 μL each) were added to the cells to the groups, respectively. Cell cycle ratio and apoptosis in the two groups were determined using flow cytometry, while Pi3k/Akt signal route-linked protein levels were assayed by immunoblot method.
Results: The proportions of cells at G0/G1 and S phases of the cell cycle in si-Prok1 group were significantly lower than those in the control group, but G2/M phase cell population was significantly higher, relative to the control (p < 0.01). There was significant down-regulation of protein expressions of cyclin A2 and cycline1 in si-Prok1 group, relative to control group, but p21 protein level was significantly higher in si-Prok1 group (p < 0.05). There was a significantly higher apoptosis in si-Prok1 group. In the si-Prok1 cells, there were significant increases in protein levels of Bcl-2, cleaved caspase-9 and caspase-3, relative to control group, while protein expression levels of Bax, p-Pi3k and p-Akt in si-Prok1 group were significantly lower than the corresponding control values (p < 0.05).
Conclusion: si-Prok1 arrests cell cycle, induces apoptotic changes, and inhibits the proliferation of ovarian granulosa cells through a mechanism related to the regulation of Pi3k/Akt signaling pathway. Therefore, it might play a potential role in the treatment of polycystic ovary syndrome.