p‐Coumaric acid pronounced protective effect against potassium bromate‐induced hepatic damage in Swiss albino mice

Abstract

AbstractPotassium bromate (KBrO3) is a common dietary additive, pharmaceutical ingredient, and significant by‐product of water disinfection. p‐coumaric acid (PCA) is a naturally occurring nutritional polyphenolic molecule with anti‐inflammatory and antioxidant activities. The goal of the current investigation was to examine the protective effects of p‐coumaric acid against the liver damage caused by KBrO3. The five groups of animals‐control, KBrO3 (100 mg/kg bw), treatment with KBrO3 along with Silymarin (100 mg/kg bw), KBrO3, followed by PCA (100 mg/bw, and 200 mg/kg bw) were randomly assigned to the animals. Mice were slaughtered, and blood and liver tissues were taken for assessment of the serum biochemical analysis for markers of liver function (alanine transaminase, aspartate transaminase, alkaline phosphatase, albumin, and protein), lipid markers and antioxidant markers (TBARS), glutathione peroxidase [GSH‐Px], glutathione (GSH), and markers of hepatic oxidative stress (CAT), (SOD), as well as histological H&E stain, immunohistochemical stain iNOS, and COX‐2 as markers of inflammatory cytokines. PCA protects against acute liver failure by preventing the augmentation of blood biochemical markers and lipid profiles. In mice liver tissues, KBrO3 increases lipid indicators and depletes antioxidants, leading to an increase in JNK, ERK, and p38 phosphorylation. Additionally, PCA inhibited the production of pro‐inflammatory cytokines and reduced the histological alterations in KBrO3‐induced hepatotoxicity. Notably, PCA effectively mitigated KBrO3‐induced hepatic damage by obstructing the TNF‐α/NF‐kB‐mediated inflammatory process signaling system. Additionally, in KBrO3‐induced mice, PCA increased the intensities of hepatic glutathione (GSH), SOD, GSH‐Px, catalase, and GSH activities. Collectively, we demonstrate the molecular evidence that PCA eliminated cellular inflammatory conditions, mitochondrial oxidative stress, and the TNF‐α/NF‐κB signaling process, thereby preventing KBrO3‐induced hepatocyte damage.