OBJECTIVE: Due to the high side effects of commonly used drugs and according to the pharmacological properties reported for coumaric acid (CA), this study was designed to determine the impact of CA on acetic acid-induced colitis in rats, considering its possible anti-inflammatory, antioxidant, and anti-apoptotic properties. MATERIALS AND METHODS: Forty-eight male Wistar rats were divided into 6 equal groups (n = 8). Colitis was induced by acetic acid intrarectally. CA in three different doses (50, 100, and 150 mg/kg) was administrated for 5 days. Finally, the macroscopic and histopathological changes in the colon tissue were examined. The expression of inflammatory and apoptotic genes, including NF-κB, TNF-α, INOS, IL-1β, IL-6, TLR4, Caspase-3, Caspase-8, Bax, Bcl-2 was assessed. In addition, changes in the levels of catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), nitrite, and total antioxidant capacity (TAC) were measured in the colon tissue. RESULTS: Colitis led to a decrease in TAC and the activity levels of CAT and SOD and an increase in the expression of inflammatory and apoptotic genes, MDA, and nitrite levels in the colon. Colitis was also associated with edema and severe damage to the epithelium, infiltration of inflammatory cells, and the presence of ulcers and necrosis in the colon tissue. CA significantly improved the inflammation, oxidative stress, apoptosis, and histopathological indices caused by acetic acid-induced colitis on the colon. CONCLUSION: It is concluded that CA probably exerts its positive effects in the management of colitis, through its anti-inflammatory, antioxidant, and anti-apoptotic properties.
OBJECTIVE: Due to the high side effects of commonly used drugs and according to the pharmacological properties reported for coumaric acid (CA), this study was designed to determine the impact of CA on acetic acid-induced colitis in rats, considering its possible anti-inflammatory, antioxidant, and anti-apoptotic properties. MATERIALS AND METHODS: Forty-eight male Wistar rats were divided into 6 equal groups (n = 8). Colitis was induced by acetic acid intrarectally. CA in three different doses (50, 100, and 150 mg/kg) was administrated for 5 days. Finally, the macroscopic and histopathological changes in the colon tissue were examined. The expression of inflammatory and apoptotic genes, including NF-κB, TNF-α, INOS, IL-1β, IL-6, TLR4, Caspase-3, Caspase-8, Bax, Bcl-2 was assessed. In addition, changes in the levels of catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), nitrite, and total antioxidant capacity (TAC) were measured in the colon tissue. RESULTS: Colitis led to a decrease in TAC and the activity levels of CAT and SOD and an increase in the expression of inflammatory and apoptotic genes, MDA, and nitrite levels in the colon. Colitis was also associated with edema and severe damage to the epithelium, infiltration of inflammatory cells, and the presence of ulcers and necrosis in the colon tissue. CA significantly improved the inflammation, oxidative stress, apoptosis, and histopathological indices caused by acetic acid-induced colitis on the colon. CONCLUSION: It is concluded that CA probably exerts its positive effects in the management of colitis, through its anti-inflammatory, antioxidant, and anti-apoptotic properties.