title: Insulin alleviates the inflammatory response and oxidative stress injury in cerebral tissues in septic rats.
abstract: Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction that occurs secondary to infection in the body without overt central nervous system (CNS) infection. SAE is frequently encountered in critically ill patients in intensive care units and can be detected in up to 50-70% of septic patients. Previous studies have demonstrated that inflammatory cytokine release and oxidative stress injury are major pathophysiological mechanisms of SAE in critically ill patients. However, there are no effective strategies for the treatment of SAE. Insulin has important immunomodulatory effects and protective effects against oxidative stress injury in the peripheral organs of septic patients. However, very few studies of the possible effects of insulin in cerebral tissues of septic patients have been reported. Therefore, in this study, we aimed to explore whether insulin therapy can inhibit cytokine production (IL-1, IL-6, and TNF-a) and oxidative stress injury of the brain tissue in septic rats. We observed that the protein concentrations of IL-1, IL-6, and TNF-а, in addition to MDA and H2O2 were notably increased, inversely SOD, and GSH were sigificantly decreased in cortex, hippocampus, and hypothalamus of septic rats. Furthermore, the levels of S100 and NSE significantly increased. After 6 hours of insulin therapy, we found that the cytokine concentrations notably decreased and oxidative stress injuries in the cortex, hypothalamus, and hippocampus were alleviated in septic rats. In addition, the S100 and NSE levels significantly decreased. We concluded that insulin can inhibit the production of inflammatory cytokines and the oxidative stress response, thereby improving brain tissue damage.
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Qiyi
authors.initials: Q
authors.lastname: Chen
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Wenkui
authors.initials: W
authors.lastname: Yu
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Jiangliang
authors.initials: J
authors.lastname: Shi
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Juanhong
authors.initials: J
authors.lastname: Shen
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Gao
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Juanjuan
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Fengchan
authors.initials: F
authors.lastname: Xi
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Li
keywords: Inflammation; Neurologic injury; Oxidative stress; Sepsis; Sepsis-associated encephalopathy
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