白细胞介素-6在抑制运动小鼠肝脏自噬标志物中的作用。
Role of interleukin-6 in inhibiting hepatic autophagy markers in exercised mice.
作者信息
Pinto Ana P, da Rocha Alisson L, Cabrera Elisa M B, Marafon Bruno B, Kohama Eike B, Rovina Rafael L, Simabuco Fernando M, Bueno Junior Carlos R, de Moura Leandro P, Pauli José R, Cintra Dennys E, Ropelle Eduardo R, da Silva Adelino S R
机构信息
Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Institute of Translational Nutrigenetics and Nutrigenomics, Department of Molecular Biology and Genomics, Health Sciences University Center, University of Guadalajara, Guadalajara, Mexico.
出版信息
Cytokine. 2020 Apr 4;130:155085. doi: 10.1016/j.cyto.2020.155085.
BACKGROUND
Based on the crosstalk of inflammation with apoptosis, autophagy, and endoplasmic reticulum (ER) stress, the main objective of this study was to explore the role of interleukin-6 (IL-6) on genes and proteins related to these phenomena in the livers of mice submitted to acute exhaustive exercise.
METHODS
Reverse transcription-quantitative polymerase chain reaction and immunoblotting technique were used to evaluate the livers of wild-type (WT) and IL-6 knockout (KO) mice at baseline (BL) and 3 h after the acute exhaustive physical exercise (EE).
RESULTS
Compared to the WT at baseline, the IL-6 KO had lower exhaustion velocity, mRNA levels of Mtor, Ulk1, Map1lc3b, and Mapk14, and protein contents of ATG5 and p-p70S6K/p70S6K. For the WT group, the EE decreased glycemia, mRNA levels of Casp3, Mtor, Ulk1, Foxo1a, Mapk14, and Ppargc1a, and protein contents of ATG5 and p-p70S6K/p70S6K, but increased mRNA levels of Sqstm1. For the IL-6 KO group, the EE decreased glycemia, mRNA levels of Casp3 and Foxo1a, and protein contents of pAkt/Akt and Mature/Pro IL-1beta, but increased mRNA levels of Sqstm1, and protein contents of p-AMPK/AMPK.
CONCLUSION
The inhibition of the hepatic autophagy markers induced by the acute EE was attenuated in IL-6 KO mice, highlighting a new function of this cytokine.
背景
基于炎症与细胞凋亡、自噬和内质网（ER）应激之间的相互作用，本研究的主要目的是探讨白细胞介素-6（IL-6）对急性力竭运动小鼠肝脏中与这些现象相关的基因和蛋白质的作用。
方法
采用逆转录定量聚合酶链反应和免疫印迹技术，对野生型（WT）和IL-6基因敲除（KO）小鼠在基线（BL）和急性力竭运动（EE）后3小时的肝脏进行评估。
结果
与基线时的WT相比，IL-6 KO小鼠的力竭速度、Mtor、Ulk1、Map1lc3b和Mapk14的mRNA水平以及ATG5和p-p70S6K/p70S6K的蛋白质含量较低。对于WT组，EE降低了血糖、Casp3、Mtor、Ulk1、Foxo1a、Mapk14和Ppargc1a的mRNA水平以及ATG5和p-p70S6K/p70S6K的蛋白质含量，但增加了Sqstm1的mRNA水平。对于IL-6 KO组，EE降低了血糖、Casp3和Foxo1a的mRNA水平以及pAkt/Akt和成熟/前体IL-1β的蛋白质含量，但增加了Sqstm1的mRNA水平以及p-AMPK/AMPK的蛋白质含量。
结论
IL-6基因敲除小鼠中急性力竭运动诱导的肝脏自噬标志物的抑制作用减弱，突出了这种细胞因子的新功能。
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