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Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
Published on: February 9, 2014
miR-125b Attenuates Sepsis-Induced Hippocampal Mitochondrial Fission and Cognitive Impairment via the ROS/p53 Pathway
Xingshu Ren1, Yunan Mo1, Lanlan Zhong1
1Department of Critical Care Medicine, Hunan Provincial Clinical Research Center for Critical Care Medicine, National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, No. 87 Xiang-Ya Road, Changsha, 410008, Hunan Province, China.
Abstract:
Sepsis-associated encephalopathy (SAE) is a common complication of sepsis characterized by neuronal injury and cognitive impairment. However, its underlying mechanisms remain unclear. In this study, we investigated the role of miR-125b in sepsis-induced hippocampal injury. A cecal ligation and puncture (CLP) model was established in mice, and miR-125b was overexpressed in the hippocampus using lentiviral vectors. CLP-induced sepsis increased mitochondrial fission and neuronal apoptosis in the hippocampus, accompanied by p53 activation and reduced miR-125b expression. miR-125b overexpression suppressed mitochondrial fission markers, reduced neuronal apoptosis, and improved cognitive deficits. Mechanistically, miR-125b inhibited ROS accumulation and p53 activation, whereas p53 overexpression reversed these protective effects. Conversely, hippocampal knockdown of miR-125b with LV-anti-miR-125b aggravated mitochondrial fission and neuronal apoptosis, further supporting its protective role. These findings indicate that miR-125b protects against sepsis-induced hippocampal injury by regulating the ROS/p53 pathway.