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Article Publish Status: FREE
Abstract Title:

Inhibition of oxidative stress and NLRP3 inflammasome by Saikosaponin-d alleviates acute liver injury in carbon tetrachloride-induced hepatitis in mice.

Abstract Source:

Int J Immunopathol Pharmacol. 2020 Jan-Dec;34:2058738420950593. PMID: 32816567

Abstract Author(s):

Yirong Chen, Renye Que, Liubing Lin, Yanting Shen, Jinkai Liu, Yong Li

Article Affiliation:

Yirong Chen

Abstract:

NLRP3 inflammasome activation results in severe liver inflammation and injury. Saikosaponin-d (SSd) possesses anti-inflammatory and hepatoprotective effects. This study aimed to determine the protective effects of SSd on carbon tetrachloride (CCl)-induced acute liver injury in mice, and whetherxidative stress and NLRP3 inflammasome activation participate in the process.The CClmice model and controls were induced. The mice were treated with SSd at 1, 1.5, or 2.0 mg/kg in a total volume of 100 µl/25 g of body weight. Liver injury was assessed by histopathology. Oxidative stress was determined using mitochondrial superoxide production (MSP), malondialdehyde (MDA) content, and superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT)activities. NLRP3, ASC, and Caspase 1 were determined by real-time PCR and western blot. IL-1β and IL-18 levels were determined by ELISA.Significantly elevated oxidative stress was induced in the liver by CCl, as demonstrated by histopathology and increases of MDA and MSP levels and decreases of SOD, GPx, and CAT activities (all < 0.01). SSd significantly decreased the MDA and MSP levels and increased the activities of SOD, GPx, and CAT (all < 0.05). The mRNA expression of NLRP3, ASC, and Caspase 1, and the protein expression of Caspase 1-p10, NLRP3, ASC, IL-1β, and IL-18 were significantly increased after CClinduction (all < 0.01). These changes were reversed by SSd (all < 0.05).Suppression of the oxidative stress and NLRP3 inflammasome activation were involved in SSd-alleviated acute liver injury in CCl-induced hepatitis.

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