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脂联素对氧化应激诱导的鹅卵巢颗粒细胞衰老的保护作用。

Protective effect of adiponectin on oxidative stress-induced ovarian granulosa cell senescence in geese.

作者信息

Zheng Yan, Qiu Yunqiao, Gao Ming, Wang Qianhui, Yu Lei, Cao Zhongzan, Luan Xinhong

机构信息

Key Laboratory of Livestock Infectious Diseases, Ministry of Education, and Key Laboratory of Ruminant Infectious Disease Prevention and Control (East), Ministry of Agriculture and Rural Affairs, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China.

Key Laboratory of Livestock Infectious Diseases, Ministry of Education, and Key Laboratory of Ruminant Infectious Disease Prevention and Control (East), Ministry of Agriculture and Rural Affairs, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China.

出版信息

Poult Sci. 2025 Jan;104(1):104529. doi: 10.1016/j.psj.2024.104529. Epub 2024 Nov 7.

Abstract

Geese are susceptible to oxidative stress during breeding, leading to senescence of granulosa cells (GCs) and reduced egg production. Adiponectin (ADPN) is a cytokine secreted by adipose tissue that functions to regulate metabolism and antioxidants. However, its role in the regulation of goose GCs is unclear. To investigate this, senescence in primary goose GCs was induced by D-gal and assessed via RT‒qPCR, senescence-associated β-galactosidase (SA-β-gal) staining, immunofluorescence, flow cytometry, and transcriptomics. The effect of ADPN on GC senescence was investigated by overexpressing and knocking down ADPN expression. The results showed that ADPN could alleviate oxidative stress and cell cycle arrest in GCs, reduce the expression of the senescence-associated secretory phenotype (SASP)-related genes IL-6 and IL-8, regulate the metabolic capacity of GCs, reduce the accumulation of SA-β-gal, maintain telomere length, and alleviate the senescence of GCs induced by D-gal. The RNA-seq results provided further evidence for the regulatory effect of ADPN on GC senescence. ADPN was shown to attenuate oxidative stress-induced GC senescence through the AGE (Advanced glycation end products)-RAGE (Receptor of advanced glycation end products) and NOD-like receptor pathways. These findings may contribute to the development of improved theoretical references for improving egg-laying performance and prolonging the service life of geese.

摘要

鹅在繁殖期间易受氧化应激影响,导致颗粒细胞(GCs)衰老并降低产蛋量。脂联素(ADPN)是一种由脂肪组织分泌的细胞因子,具有调节代谢和抗氧化的功能。然而,其在鹅颗粒细胞调节中的作用尚不清楚。为了研究这一点,用D-半乳糖诱导原代鹅颗粒细胞衰老,并通过RT-qPCR、衰老相关β-半乳糖苷酶(SA-β-gal)染色、免疫荧光、流式细胞术和转录组学进行评估。通过过表达和敲低ADPN表达来研究ADPN对颗粒细胞衰老的影响。结果表明,ADPN可以减轻颗粒细胞中的氧化应激和细胞周期阻滞,降低衰老相关分泌表型(SASP)相关基因IL-6和IL-8的表达,调节颗粒细胞的代谢能力,减少SA-β-gal的积累,维持端粒长度,并减轻D-半乳糖诱导的颗粒细胞衰老。RNA测序结果为ADPN对颗粒细胞衰老的调节作用提供了进一步的证据。结果表明,ADPN通过晚期糖基化终末产物(AGE)-晚期糖基化终末产物受体(RAGE)和NOD样受体途径减轻氧化应激诱导的颗粒细胞衰老。这些发现可能有助于为提高鹅的产蛋性能和延长鹅的使用寿命提供改进的理论参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae5e/11609555/6d23095a5aff/gr1.jpg

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