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Abstract Title:

Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress.

Abstract Source:

Int J Mol Sci. 2020 Mar 17 ;21(6). Epub 2020 Mar 17. PMID: 32192079

Abstract Author(s):

Suvesh Munakarmi, Lokendra Chand, Hyun Beak Shin, Kyu Yun Jang, Yeon Jun Jeong

Article Affiliation:

Suvesh Munakarmi

Abstract:

3,3'-Diindolylmethane (DIM), a metabolic product of indole-3-carbinol extracted from cruciferous vegetables exhibits anti-inflammatory and anti-cancer properties. Earlier, the product has been demonstrated to possess anti-fibrotic properties; however, its protective effects on liver injury have not been clearly elucidated. In this study, we postulated the effects and molecular mechanisms of action of DIM on carbon tetrachloride (CCl)-induced liver injury in mice. Acute liver injury was induced by a single intraperitoneal administration of CCl(1 ml/kg) into mice. DIM was injected via subcutaneous route for three days at various doses (2.5, 5 and 10 mg/kg) before CClinjection. Mice were sacrificed and serum was collected for quantification of serum transaminases. The liver was collected and weighed. Treatment with DIM significantly reduced serum transaminases levels (AST and ALT), tumor necrosis factor-α (TNF-α) and reactive oxygen species (ROS). CCl- induced apoptosis was inhibited by DIM treatment by the reduction in the levels of cleaved caspase-3 and Bcl2 associated X protein (Bax). DIM treated mice significantly restored Cytochrome P450 2E1, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression in CCltreated mice. In addition, DIM downregulated overexpression of hepatic nuclear factor kappa B (NF-κB) and inhibited CClmediated apoptosis. Our results suggest that the protective effects of DIM against CCl- induced liver injury are due to the inhibition of ROS, reduction of pro-inflammatory mediators and apoptosis.

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