Quercetin ameliorates oxidative stress-induced apoptosis of granulosa cells in dairy cow follicular cysts by activating autophagy via the SIRT1/ROS/AMPK signaling pathway  

作　　者：Hongwei Duan Fang Wang Ke Wang Shuai Yang Rong Zhang Chen Xue Lihong Zhang Xiaofei Ma Xianghong Du Jian Kang Yong Zhang Xingxu Zhao Junjie Hu Longfei Xiao 

机构地区：[1]College of Veterinary Medicine,Gansu Agricultural University,Lanzhou 730070,Gansu,China [2]Gansu Key Laboratory of Animal Generational Physiology and Reproductive Regulation,Lanzhou 730070,Gansu,China [3]Gansu Institute of Animal Husbandry and Veterinary,Pingliang 744000,Gansu,China [4]School of Animal Science and Technology,Guangdong Polytechnic of Science and Trade,Guangzhou 510640,Guangdong,China [5]Animal Science and Technology College,Beijing University of Agriculture,Beijing 102206,China

出　　处：《Journal of Animal Science and Biotechnology》2024年第6期2351-2365,共15页畜牧与生物技术杂志(英文版)

基　　金：supported by the Science and Technology Department of Gansu Province(21JR7RA858);the National Natural Science Foundation of China(32160858);Gansu Youth Science and Technology Fund Program(21JR7RA843);the Beijing University of Agriculture Youth Science Innovation Ability Improvement Project(QJKC2022007);Research Project of Guangdong Vocational College of Science and Trade(GDKM2022-96)。

摘　　要：Background Follicular cysts contribute significantly to reproductive loss in high-yield dairy cows.This results from the death of follicular granulosa cells(GCs)caused by oxidative stress.Quercetin is known to have significant antioxidant and anti-apoptotic effects.However,the effect of quercetin on follicular cysts has yet been elucidated.Therefore,this study aimed to explore the anti-oxidant and anti-apoptosis effects and potential molecular mechanisms of quercetin in H_(2)O_(2)-induced primary cow GCs and 3-nitropropionic acid(3-NPA)-induced mouse model of oxidative stress and thus treat ovarian cysts in dairy cows.Results In this study,compared with estrus cows,cows with follicular cysts showed heightened levels of oxidative stress and increased follicular cell apoptosis,while autophagy levels were reduced.A model of oxidative stress was induced in vitro by H_(2)O_(2)and showed significant increases in apoptosis together with reduced autophagy.These effects were significantly ameliorated by quercetin.Effects similar to those of quercetin were observed after treatmeat of cells with the reactive oxygen species(RCS)inhibitor N-acetylcysteine(NAC).Further investigations using chloroquine(autophagy inhibito r)]rapamycin(autophagy activato r),selisistat(SIRT1 inhibito r),and compound C(AMPK inhibitor)showed that chloroquine counteracted the effects of quercetin on oxidative stress-induced apoptosis,while rapamycin had the same effect as quercetin.In addition,the SIRT1/AMPK pathway inhibitors antagonized quercetin-mediated mitigation of the effects of oxidative stress on increased apoptosis and reduced autophagy.Consistent with the results in vitro,in mouse ovarian oxidative stress model induced by 3-NPA,quercetin activated autophagy through the SIRT1/AMPK signaling pathway,while alleviating oxidative stress damage and inhibiting apoptosis in mouse ovaries.Conclusions These findings indicate that quercetin can inhibit apoptosis in GCs and restore ovarian function by activating autophagy through the SIRT1/ROS/AMPK si

关 键 词：Apoptosis AUTOPHAGY Follicular cyst Oxidative stress QUERCETIN 

分 类 号：S858.23[农业科学—临床兽医学]