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KMID : 1200820210210030463
Oriental Pharmacy and Experimental Medicine
2021 Volume.21 No. 3 p.463 ~ p.474
Blumea lacera DC., accelerates the healing of acetic acid induced ulcerative colitis in rats by regulating oxidative stress and colonic inflammation: in-vivo and in silico molecular docking experiments
Adhikari Ashish

Basnet Santosh
Vijayakumar Sacchidanana
Suhas Doddamavattur Shivalingaiah
Puneeth Tumbadi Adinarayanashetty
Thippeswamy Boreddy Shivanandappa
Chandramohan Vivek
Veerapur Veeresh Prabhakar
Abstract
To expound the protective outcome of standardised hydroalcoholic extract of Blumea lacera (EEBL) in acetic acid-induced ulcerative colitis (UC). Further, in silico computational experiments were performed to identify the inhibitory activity of bioactive constituents of EEBL against inflammatory targets. Rats were pre-treated with EEBL (100 and 200 mg/kg) for 7 days and on eighth day, UC was induced by intrarectal instillation of 2 ml of 4% v/v acetic acid and treatment continues till 11th day. Colonic injury was examined by clinical activity score and mucosal inflammation was assessed by colon wet weight, macroscopic scoring and histopathological examination. In addition, colonic contractility studies and biochemical analysis were carried out. Further, bioactive compounds from title plant were subjected to drug likeness prediction and molecular docking studies against myeloid differentiation factor-2 (MD-2), nuclear factor-kappa B (NF-¥êB), tumor necrosis factor alpha (TNF-alpha) and soluble epoxide hydrolase (sEH). Pre-treatment with both the doses of EEBL significantly ameliorated the acetic acid-induced colonic injury and these results were parallels with biochemical and histopathology examinations. Out of fifteen selected bioactive compounds, 5-hydroxy-3methyl-3,6,7,4-tetramethoxy flavones, lachnophyllic acid and d-fenchone exhibited better drug likeness property with higher docking score. The observed protective outcome might be recognized due to the synergistic effect of identified bioactive compounds by inhibition of key targets of inflammation.
KEYWORD
Inflammatory bowel disease, Lipinski¡¯s rule of five, Myeloid differentiation factor-2, Nuclear factor-kappa B, Tumor necrosis factor alpha, Soluble epoxide hydrolase
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