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Thymol reduces acetic acid-induced inflammatory response through inhibition of NF-kB signaling pathway in rat colon tissue

Aim The aim of the present study was to evaluate the anti-inflammatory effect of thymol in acetic acid-induced rat colitis through inhibiting the NF-κB signaling pathway. Methods Colitis was induced by intra-rectal administration of 2 mL of diluted acetic acid (4%) solution using a flexible plastic...

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Bibliographic Details
Published in:Inflammopharmacology 2019-12, Vol.27 (6), p.1275-1283
Main Authors: Chamanara, Mohsen, Abdollahi, Alireza, Rezayat, Seyed Mahdi, Ghazi-Khansari, Mamoud, Dehpour, Ahmadreza, Nassireslami, Ehsan, Rashidian, Amir
Format: Article
Language:English
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Summary:Aim The aim of the present study was to evaluate the anti-inflammatory effect of thymol in acetic acid-induced rat colitis through inhibiting the NF-κB signaling pathway. Methods Colitis was induced by intra-rectal administration of 2 mL of diluted acetic acid (4%) solution using a flexible plastic rubber catheter in Wistar rats. Colitis was induced on the first day and all treatments were applied 5 days after the induction of colitis. Thymol was dissolved in 0.2% tween 80 in saline and administered orally at doses of 10, 30, and 100 mg/kg per day. Macroscopic and histopathologic investigations were done. The expression of myeloperoxidase (MPO) and tumor necrosis factor-α (TNF-α) was determined by immunohistochemistry (IHC) assay. The protein expression level of pNF-κB p65 was measured by the Western blot technique. Results Treatment with thymol reduced mucosal and histological damages compared to the acetic acid group. Our results showed that thymol markedly inhibited the production of MPO and TNF-α in the colon tissue of the acetic acid-induced group. In addition, thymol decreased acetic acid-induced up-regulation of pNFκB p65 protein. Conclusions: The results of our study suggest that thymol exerts an anti-inflammatory effect in acetic acid-induced rat colitis by inhibiting the NF-κB signaling pathway and downregulating TNF-α and MPO expressions.
ISSN:0925-4692
1568-5608
DOI:10.1007/s10787-019-00583-8