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  • Berberine regulates lipid m...
    Dai, JiaGe; Huang, XiaoMeng; Zhang, Chao; Luo, XiaoFei; Cao, SuYing; Wang, JunLi; Liu, Bing; Gao, JianMing

    Veterinary medicine and science, 20/May , Volume: 7, Issue: 3
    Journal Article

    Background The berberine (Ber) is an isoquinoline alkaloid compound extracted from Rhizoma coptidis and has the effect that reduces adipose. MicroRNA‐192 (miR‐192) is related to fat metabolism. However, the relevant mechanism of berberine on lipid metabolism during in vitro maturation (IVM) of porcine oocytes remains unclear. Objectives In this study, we investigated the molecular mechanism by which berberine promotes the IVM and lipid metabolism of porcine oocytes via miR‐192. Methods Ber was added to IVM medium of porcine oocytes. MiR‐192 agomir, miR‐192 antagomir and negative control fragment were microinjected into the cytoplasm of oocytes without Ber. Rates of oocyte IVM and embryonic development in each group were observed. The content of lipid droplets in IVM oocytes in each group was analyzed by Nile red staining. Expression levels of miR‐192 and FABP3, SREBF1 and PPARG, were detected by qPCR and western blotting. The target genes of miR‐192 were determined by luciferase reporter assays. Results and Conclusions We found that Ber significantly increased the rate of oocytes IVM and blastocyst development, and decreased the area and numbers of lipid droplets in IVM oocytes. Ber significantly increased the expression of miR‐192 in IVM oocytes, and significantly decreased the expression of SREBF1 and PPARG, which were target genes of miR‐192. This study indicates that Ber promotes lipid metabolism in porcine oocytes by activating the expression of miR‐192 and down‐regulating SREBF1 and PPARG, thus, improving IVM of porcine oocytes. This study investigated the molecular mechanism of Berberine (Ber) promoting the in vitro maturation (IVM) and lipid metabolism of porcine oocytes via miR‐192. The results suggest that Ber promotes lipid metabolism in IVM porcine oocytes and improves oocyte IVM by activating miR‐192 and downregulating SREBF1 and PPARG.