Baluchnejadmojarad, Tourandokht, Roghani, Mehrdad. (1401). Licochalcone A attenuates oxidative stress and inflammation in carbon tetrachloride-instigated acute hepatotoxicity in the mouse. , 10(2), 18-23. doi: 10.22070/jbcp.2023.17270.1165
Tourandokht Baluchnejadmojarad; Mehrdad Roghani. "Licochalcone A attenuates oxidative stress and inflammation in carbon tetrachloride-instigated acute hepatotoxicity in the mouse". , 10, 2, 1401, 18-23. doi: 10.22070/jbcp.2023.17270.1165
Baluchnejadmojarad, Tourandokht, Roghani, Mehrdad. (1401). 'Licochalcone A attenuates oxidative stress and inflammation in carbon tetrachloride-instigated acute hepatotoxicity in the mouse', , 10(2), pp. 18-23. doi: 10.22070/jbcp.2023.17270.1165
Baluchnejadmojarad, Tourandokht, Roghani, Mehrdad. Licochalcone A attenuates oxidative stress and inflammation in carbon tetrachloride-instigated acute hepatotoxicity in the mouse. , 1401; 10(2): 18-23. doi: 10.22070/jbcp.2023.17270.1165

Licochalcone A attenuates oxidative stress and inflammation in carbon tetrachloride-instigated acute hepatotoxicity in the mouse

Journal of Basic and Clinical Pathophysiology
دوره 10، شماره 2، اسفند 2022، صفحه 18-23    اصل مقاله (476.84 K)
نوع مقاله: Research Paper
شناسه دیجیتال (DOI): 10.22070/jbcp.2023.17270.1165
نویسندگان
Tourandokht Baluchnejadmojarad* 1؛ Mehrdad Roghani2
1Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
2Neurophysiology Research Center, Shahed University, Tehran, Iran
چکیده
Background and Objective: Liver disorders are associated with high rate of morbidity and mortality. Carbon tetrachloride (CCL4)-instigated model of ALI is a valid model for exploring liver damage. Licochalcone A is a bioflavonoid which is primarily isolated from roots of Glycyrrhiza species. In this study, the effect of this flavonoid in CCl4 mouse model of acute liver injury (ALI) was assessed.
Materials and Methods: For induction of ALI, CCl4 (10 ml/kg body weight, 0.175% in olive oil) was intraperitoneally injected and licochalcone A was orally administered at doses of 10 or 50 mg/kg. Functional markers of liver dysfunction were determined in addition to hepatic analysis of oxidative stress and inflammatory factors.
Results: Licochalcone A pretreatment at a dose of 50 mg/kg significantly and notably decreased level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and myeloperoxidase (MPO) and significantly improved total antioxidant capacity (TAC) and superoxide dismutase (SOD) activity and with no significant effect on interleukin-1β (IL-1β). In addition, these beneficial effects were not obtained for licochalcone A at a dose of 10 mg/kg in CCL4-injured group.
Conclusion: These findings show beneficial property of licochalcone A following CCL4-induced liver injury that is exerted via its regulation of oxidative and inflammatory processes and upregulating antioxidant power.
کلیدواژه‌ها
Acute liver injury؛ Hepatotoxicity؛ Carbon tetrachloride؛ Licochalcone A؛ Oxidative stress؛ Inflammation
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