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.
Highlights
Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction that occurs secondary to infection in the body in the absence of central nervous system (CNS) infection
Variation in the protein concentrations of the cytokines IL-1β, IL-6, and TNF-a in cerebral tissues The protein concentrations of the cytokines IL-1β, IL-6, and TNF-a in the cortex, hypothalamus, and hippocampus significantly increased after intraperitoneal injection of 10 mg/kg LPS
SOD and GSH activities were upregulated to different degrees in all brain regions; SOD upregulation was most obvious in the cortex and hypothalamus, whereas GSH upregulation was most significant in the cerebral cortex
Summary
Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction that occurs secondary to infection in the body in the absence of central nervous system (CNS) infection. Further studies have shown that the mechanisms underlying sepsis are related to cytokine generation and oxidative stress injury [3,5]. These effects can have several deleterious consequences, including nerve cell apoptosis and necrosis [6,7,8], neuronal bioenergetic failure and cerebral oxidative metabolism injury [9], axonal injury and brain tissue edema [10,11], neurotransmitter transporter inhibition [12], and destruction of the blood–brain barrier [7]. The inhibition of inflammation and oxidative stress can prevent brain tissue injury and ameliorate SAE
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