Study of the protective effect of carvacrol on acetic acid-induced colitis in rats; its oxidative stress and inflammation-modulating role

Inflammatory bowel disease is a chronic inflammatory disease whose prevalence is rising worldwide. The treatment-related challenges of this disease have expanded the research on other compounds with suitable therapeutic properties. Carvacrol monoterpene phenolic compound, with a wide range of therapeutic properties, can be an appropriate choice. This study aims to investigate the protective effect of carvacrol on acetic acid-induced colitis in mice, further emphasizing the modulating role of oxidative stress and inflammation.  This experimental study was conducted on 60 mice divided into six groups. Colitis was induced by intrarectal injection of acetic acid. Five groups of mice received carvacrol at doses of 12.5, 25, 50, and 100 mg/kg and normal saline (1 ml/kg). One group was considered normal (without colitis) and received normal saline (1 ml/kg). The severity of colitis complications was assessed through histopathological examination of colon tissue samples. Furthermore, the malondialdehyde (MDA) level, total antioxidant capacity (TAC), and gene expression of inflammatory markers were investigated in the colon samples. Data analysis was done by PRISM version 8 using one-way ANOVA and Tukey’s test.  The results showed that the induction of colitis caused significant damage to the intestinal mucosal layers, and the administration of carvacrol reduced the severity of this damage. Interestingly, the TAC of all groups that received carvacrol was higher than that of the group that received normal saline (P < 0.05). The administration of carvacrol decreased the MDA level (P < 0.05). In addition, the gene expression of interleukin-1beta (IL-1β), Toll-like receptor 4 (TLR4), and tumor necrosis factor-alpha (TNF-α) reduced after carvacrol administration (P < 0.05).  Carvacrol exerted a protective effect on the acetic acid-induced colitis in mice, probably via inhibiting the inflammatory cascade and modulating oxidative stress.