α-Terpineol Mitigates Dextran Sulfate Sodium-Induced Colitis in Rats by Attenuating Inflammation and Apoptosis

结肠炎 化学 药理学 炎症 髓过氧化物酶 细胞凋亡 一氧化氮 免疫染色 免疫学 生物化学 医学 免疫组织化学 有机化学
作者
Rehan Khan,Chandrashekhar Jori,Md. Meraj Ansari,Anas Ahmad,Ahmed Nadeem,Nahid Siddiqui,Sarwat Sultana
出处
期刊:ACS omega [American Chemical Society]
卷期号:8 (32): 29794-29802 被引量:11
标识
DOI:10.1021/acsomega.3c04317
摘要

Ulcerative colitis (UC) is one of the major inflammatory disorders of the gastrointestinal tract. α-Terpineol (αTL) is naturally present in several plants, and it belongs to the monoterpenes category. αTL possesses various pharmacological properties such as antioxidant, antibacterial, antifungal, anticancer, and antiulcer activities. Importantly, αTL has been reported to possess potent anti-inflammatory effects also. In this study, we hypothesize that αTL may have protective effects against dextran sodium sulfate (DSS)-induced colitis in Wistar rats. Animals were randomly allocated to 3 groups of 6 rats each. In group III, αTL was administered at a dose of 50 mg/kg b. wt. orally from days 1 to 14, while in groups II and III, 4% DSS in drinking water was given to rats ad libitum from the 7th to 14th days. After 24 h of the last dose of αTL, all animals were euthanized. αTL administration reduced the DSS-induced colonic disease activity index, tissue damage, and goblet cell disintegration. αTL suppressed the orchestration of mast cells in the inflamed colon, enhanced the immunostaining of NF-kB-p65, COX-2, iNOS, p53, caspase-9, and cleaved caspase-3, and suppressed the immunostaining of connexin-43, survivin, and Bcl-2. The activities of caspases-9 and -3 were reduced significantly by αTL pretreatment, as also confirmed by calorimetric assays. Moreover, αTL significantly attenuated the nitric oxide level and myeloperoxidase activity. Histological results further support the fact that αTL reduced DSS-induced colonic damage and reduced inflammatory cell infiltration. Overall, our findings suggest that αTL has strong protective effects against DSS-induced colitis by mitigating inflammatory and apoptotic responses.
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