Abstract
Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1β, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-α expression levels; coenzyme Q10 also increased beclin 1 levels. Coenzyme Q10 might be a significant agent in the treatment of liver injury induced by sepsis.
Highlights
Sepsis is a lethal health issue worldwide, which has high incidence annually [1]
Recent advancements have reported the intimate interaction between cecal ligation and puncture- (CLP-) induced septic organ failure and cell dysfunction owing to autophagy and pyroptosis [5,6,7]
The CLP group exhibited a marked increase in the ALT, AST, and alkaline phosphatase (ALP) levels; these levels were decreased in the Coenzyme Q10 (CoQ10)+CLP group
Summary
Sepsis is a lethal health issue worldwide, which has high incidence annually [1]. It is an organ dysfunction that is induced by a dysregulated host reaction to pathogen infection [2]. Recent advancements have reported the intimate interaction between cecal ligation and puncture- (CLP-) induced septic organ failure and cell dysfunction owing to autophagy and pyroptosis [5,6,7]. Pyroptosis can be described as certain programmed cell death, and the inflammatory cytokines release its characterization Previous studies have reported that CoQ10 can prevent the start and diffusion of lipid peroxidation, scavenge free radicals, and decrease proinflammatory cytokine production [21, 22] The deficiency of CoQ10 induced by mitochondrial failure in sepsis may play role in hypoxia, oxidative organ damage, hypoperfusion, and leading to death. The current work aims at investigating the effects of CoQ10 on autophagy, pyroptosis, and inflammatory injuries and the histopathological and biochemical alterations in the septic liver injury induced by CLP
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