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Alterations in mitochondrial biogenesis and respiratory activity, inflammation of the senescence-associated secretory phenotype, and lipolysis in the perirenal fat and liver of rats following lifelong exercise and detraining
The FASEB Journal ( IF 4.4 ) Pub Date : 2021-08-30 , DOI: 10.1096/fj.202100868r
Lei Sun 1 , Fang-Hui Li 1 , Chong Han 1 , Zhuang-Zhi Wang 1 , Ke-Ke Gao 1 , Yi-Bo Qiao 1 , Song Ma 1 , Tian Xie 1 , Jing Wang 1
Affiliation  

The primary aims of this study were to determine the effects of lifelong exercise and detraining on age-related alterations in mitochondrial function, inflammation associated with senescence-associated secretory phenotype (SASP), and lipolysis in the perirenal fat and liver of rats. Female Sprague–Dawley rats were randomly assigned to four groups: young control (n = 12), old control (n = 12), detraining (n = 12), and lifelong exercise (n = 12). We then investigated mitochondrial function, SASP-associated inflammation, and lipolysis in the perirenal fat and liver using qRT-PCR and western blotting to assess the expression of AKT, hypoxia-inducible factor 1α (HIF-1α), nuclear factor-kappa B (NF-κB), c-jun kinase (JNK), and p38 mitogen-activated protein kinase (p38MAPK). In the tissues of both the perirenal fat and liver, lifelong exercise significantly improved mitochondrial function, SASP-associated inflammation, and lipolysis. Meanwhile, pathways associated with inflammatory regulation were inhibited, predominantly via the activation of phosphorylated-AKT (p-AKT) and suppression of HIF-1α in both tissues, and via JNK in the perirenal fat and p38MAPK in the liver. Furthermore, detraining activated NF-κB expression in both tissues and induced the upregulation of serum high-sensitivity C-reactive protein (hsCRP) levels. Collectively, lifelong exercise was found to exert beneficial effects by ameliorating age-related alterations in mitochondrial function, SASP-associated inflammation, and lipolysis in perirenal fat and liver tissues, potentially inhibiting inflammation via the JNK and p38 MAPK pathways, respectively, as well as the HIF-1α and AKT pathways in both tissues. In contrast, detraining induced high levels of circulating hsCRP by activating the NF-κB signaling pathway in both tissues.

中文翻译:

线粒体生物发生和呼吸活动的改变,衰老相关分泌表型的炎症,以及终生运动和停止训练后大鼠肾周脂肪和肝脏的脂肪分解

本研究的主要目的是确定终身锻炼和去训练对线粒体功能的年龄相关改变、与衰老相关分泌表型 (SASP) 相关的炎症以及大鼠肾周脂肪和肝脏脂肪分解的影响。雌性 Sprague-Dawley 大鼠被随机分配到四组:年轻对照组 ( n  = 12)、老年对照组 ( n  = 12)、停止训练 ( n  = 12) 和终身运动 ( n = 12)。然后,我们使用 qRT-PCR 和蛋白质印迹法研究了肾周脂肪和肝脏中的线粒体功能、SASP 相关炎症和脂解作用,以评估 AKT、缺氧诱导因子 1α (HIF-1α)、核因子-κB 的表达。 NF-κB)、c-jun 激酶 (JNK) 和 p38 丝裂原活化蛋白激酶 (p38MAPK)。在肾周脂肪和肝脏组织中,终身运动显着改善了线粒体功能、SASP 相关炎症和脂肪分解。同时,与炎症调节相关的通路受到抑制,主要是通过磷酸化 AKT (p-AKT) 的激活和两种组织中 HIF-1α 的抑制,以及通过肾周脂肪中的 JNK 和肝脏中的 p38MAPK。此外,去训练激活的 NF-κB 在两个组织中的表达并诱导血清高敏 C 反应蛋白 (hsCRP) 水平的上调。总的来说,终生锻炼被发现通过改善线粒体功能的年龄相关改变、SASP 相关炎症以及肾周脂肪和肝组织中的脂解来发挥有益作用,分别可能通过 JNK 和 p38 MAPK 途径抑制炎症,以及两种组织中的 HIF-1α 和 AKT 通路。相反,去训练通过激活两种组织中的 NF-κB 信号通路来诱导高水平的循环 hsCRP。和脂肪分解在肾周脂肪和肝组织中,可能分别通过 JNK 和 p38 MAPK 途径以及两种组织中的 HIF-1α 和 AKT 途径抑制炎症。相反,去训练通过激活两种组织中的 NF-κB 信号通路来诱导高水平的循环 hsCRP。和脂肪分解在肾周脂肪和肝组织中,可能分别通过 JNK 和 p38 MAPK 途径以及两种组织中的 HIF-1α 和 AKT 途径抑制炎症。相反,去训练通过激活两种组织中的 NF-κB 信号通路来诱导高水平的循环 hsCRP。
更新日期:2021-08-31
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