Quinic acid ameliorates ulcerative colitis in rats, through the inhibition of two TLR4‐NF‐κB and NF‐κB‐INOS‐NO signaling pathways

Abstract

ObjectiveIn this study, the therapeutic effect of quinic acid (QA), which has anti‐inflammatory activity, was investigated on acetic acid‐induced colitis in male Wistar rats.MethodsUlcerative colitis (UC) was induced in rats by acetic acid intrarectally, and the protective effects of QA in 10, 30, 60, and 100 mg/kg doses were investigated. Rats were treated for 5 days and their colon tissues were dissected out at the end. Macroscopic and histopathological examinations were performed in colon tissues. Also, the expression of inflammatory and apoptotic genes, including TLR4, IL‐1β, INOS, IL‐6, TNF‐α, NF‐κB, Caspase‐3, Caspase‐8, Bax, and Bcl‐2, was measured. Biochemistry indices, such as malondialdehyde (MDA) and nitrite oxide (NO) content, in addition to, total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT), and enzymes activities were also assessed.ResultsColitis increased the levels of MDA and NO, and enhanced the inflammatory and apoptotic gene expressions, while reducing the SOD and CAT enzymes activity, and TAC levels in the colitis rats. Also, results showed that colitis was associated with the infiltration of inflammatory cells, epithelium damage, and edema in colon tissue. QA significantly ameliorated histopathological indices, oxidative stress, inflammation, and apoptosis in colitis rats.ConclusionQA ameliorated UC through the inhibition of two TLR4‐NF‐κB and NF‐κB‐INOS‐NO signaling pathways, which results in the reduction of colitis complications, including oxidative stress, inflammation, apoptosis and histopathological injuries in rats. Therefore it can be concluded, that QA exerts its therapeutic effects through antiapoptotic, antioxidant, and anti‐inflammatory properties.

Neuroimmune response and oxidative stress in the prefrontal cortex mediate seizure susceptibility in experimental colitis in male mice

“…They have determined that the expression of these mediators increased in the colon tissue. [ 61,65 ] The role of neuroinflammatory response in seizure pathogenesis has been reported previously. [ 66 ] It has been determined that expression of NLRP3 and TLR4 as well as downstream cytokines like TNF‐α, IL‐1β increased in the brain following seizure attack.…”