自噬
PTEN公司
多囊卵巢
张力素
免疫印迹
细胞凋亡
卵巢
下调和上调
化学
癌症研究
分子生物学
PI3K/AKT/mTOR通路
生物
内分泌学
基因
胰岛素抵抗
胰岛素
生物化学
作者
Peijuan Wu,Ying Zhu,Junjie Li,H. Chen,Hanwei Wu,Xiao Hu,He Zhu
标识
DOI:10.1080/09513590.2023.2210232
摘要
Objective To investigate the potential molecular mechanism of traditional Chinese medicine Guizhi Fuling Wan (GZFLW) inhibiting granulosa cells (GCs) autophagy in polycystic ovary syndrome (PCOS).Methods Control GCs and model GCs were cultured and treated with blank serum or GZFLW-containing serum. The levels of H19 and miR-29b-3p in GCs were detected using qRT-PCR, target genes of miR-29b-3p were identified using luciferase assay. The protein expressions of Phosphatase and tensin homolog (PTEN), Matrix Metalloproteinase (MMP)-2, and Bax were measured using western blot. The level of autophagy was detected via MDC staining, the degree of autophagosomes and autophagic polymers was observed using dual fluorescence-tagged mRFP-eGFP-LC3.Results GZFLW intervention reduced the expression of autophagy-related proteins PTEN, MMP-2 and Bax, by upregulating the expression of miR-29b-3p and downregulated the expression of H19 (p < .05 or p < .01). The number of autophagosomes and autophagy polymers was significantly decreased by GZFLW treatment. However, the inhibition of miR-29b-3p and overexpression of H19 induced a significant increase in the number of autophagosomes and autophagic polymers, which attenuated the inhibitory effect of GZFLW on autophagy (p < .05 or p < .01). In addition, inhibition of miR-29b-3p or overexpression of H19 can attenuate the effect of GZFLW on the expression of PTEN, MMP-2 and Bax proteins (p < .05 or p < .01).Conclusion Our study found that GZFLW inhibits autophagy in PCOS GCs via H19/miR-29b-3p pathway.
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