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Melatonin prevents lung injury by regulating apelin 13 to improve mitochondrial dysfunction
Lu Zhang,Fangli Liu,Xiaomin Su,Yue Li,Yining Wang,Ruonan Fang,Yingying Guo,Tongzhu Jin,Huitong Shan,Xiaoguang Zhao,Rui Yang,Hongli Shan,Haihai Liang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Pulmonary fibrosis is a progressive disease characterized by epithelial cell damage, fibroblast proliferation, excessive extracellular matrix (ECM) deposition, and lung tissue scarring. Melatonin, a hormone produced by the pineal gland, plays an important role in multiple physiological and pathological responses in organisms. However, the function of melatonin in the development of bleomycin-induced pulmonary injury is poorly understood. In the present study, we found that melatonin significantly decreased mortality and restored the function of the alveolar epithelium in bleomycin-treated mice. However, pulmonary function mainly depends on type II alveolar epithelial cells (AECIIs) and is linked to mitochondrial integrity. We also found that melatonin reduced the production of reactive oxygen species (ROS) and prevented apoptosis and senescence in AECIIs. Luzindole, a nonselective melatonin receptor antagonist, blocked the protective action of melatonin. Interestingly, we found that the expression of apelin 13 was significantly downregulated in vitro and in vivo and that this downregulation was reversed by melatonin. Furthermore, ML221, an apelin inhibitor, disrupted the beneficial effects of melatonin on alveolar epithelial cells. Taken together, these results suggest that melatonin alleviates lung injury through regulating apelin 13 to improve mitochondrial dysfunction in the process of bleomycin-induced pulmonary injury.
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Yaru Li,Shuchen Zhang,Ziwei Zhu,Ruonan Zhou,Pingyuan Xu,Lingyan Zhou,Yue Kan,Jiao Li,Juan Zhao,Penghua Fang,Xizhong Yu,Wenbin Shang 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4
Background: Ginsenoside Rb1 (GRb1) is capable of regulating lipid and glucose metabolism through itsaction on adipocytes. However, the beneficial role of GRb1-induced up-regulation of adiponectin in liversteatosis remains unelucidated. Thus, we tested whether GRb1 ameliorates liver steatosis and insulinresistance by promoting the expression of adiponectin. Methods: 3T3-L1 adipocytes and hepatocytes were used to investigate GRb1's action on adiponectinexpression and triglyceride (TG) accumulation. Wild type (WT) mice and adiponectin knockout (KO)mice fed high fat diet were treated with GRb1 for 2 weeks. Hepatic fat accumulation and function as wellas insulin sensitivity was measured. The activation of AMPK was also detected in the liver andhepatocytes. Results: GRb1 reversed the reduction of adiponectin secretion in adipocytes. The conditioned medium(CM) from adipocytes treated with GRb1 reduced TG accumulation in hepatocytes, which was partlyattenuated by the adiponectin antibody. In the KO mice, the GRb1-induced significant decrease of TGcontent, ALT and AST was blocked by the deletion of adiponectin. The elevations of GRb1-induced insulinsensitivity indicated by OGTT, ITT and HOMA-IR were also weakened in the KO mice. The CM treatmentsignificantly enhanced the phosphorylation of AMPK in hepatocytes, but not GRb1 treatment. Likewise,the phosphorylation of AMPK in liver of the WT mice was increased by GRb1, but not in the KO mice. Conclusions: The up-regulation of adiponectin by GRb1 contributes to the amelioration of liver steatosisand insulin resistance, which further elucidates a new mechanism underlying the beneficial effects ofGRb1 on obesity
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