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ORIGINAL ARTICLE
Year : 2016  |  Volume : 12  |  Issue : 47  |  Page : 225-234

Protective effect of baicalin against experimental colitis via suppression of oxidant stress and apoptosis


1 Department of Gastroenterology, Shenzhen genetic engineering Animal Center, Jinan University of Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, China
2 Department of Internal Medicine-Neurology, Shenzhen genetic engineering Animal Center, Jinan University of Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, China
3 Department of General Surgery, Shenzhen Children's Hospital, Shenzhen 518026, Guangdong Province, China

Correspondence Address:
Jian-yao Wang
Department of Gastroenterology, Shenzhen Children's Hospital, Shenzhen 518026, Guangdong Province
China
Li-sheng Wang
Department of Gastroenterology, Shenzhen Municipal People's Hospital, Jinan University of Medical Sciences, 1017 East Gate Road, Shenzhen 518020, Guangdong Province
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1296.186342

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Background: Baicalin is a bioactive ingredient extracted from the root of Scutellariae radix, which is used to treat ulcerative colitis (UC). Objective: We investigated the activity of baicalin on lipopolysaccharide-stimulated RAW264.7 cells and 2,4,6-trinitrobenzene sulfonic acid-induced rats, including the attenuation of oxidant stress and apoptosis. Materials and Methods: The severity of colitis was assessed by disease activity index. The activities of catalase (CAT), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), and the content of malondialdehyde (MDA) were determined by their corresponding kits. The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) was performed to study whether experimental colitis was associated with intestinal epithelial cell (IEC) apoptosis and the effect of baicalin on IEC apoptosis. Western blot analysis and immunocytochemistry assay were applied to determine the protein expressions. The reactive oxygen species (ROS) level in the colon of UC rats treated with baicalin was determined by ROS assay kit. Results: Baicalin remarkably upregulated the activities of CAT, GSH-PX, and SOD and decreased the content of MDA in a dose-dependent manner in vitro and in vivo. The TUNEL-positive cells in rats treated baicalin were remarkably reduced. Both Western blot analysis and immunocytochemistry assay indicated that baicalin significantly decreased the expressions of transforming growth factor beta-1, Bax protein and upregulated the expression of Bcl-2 protein. In addition, the expressions of total and cleaved caspase-3, total and cleaved caspase-9 protein, Fas, and FasL in vitro were downregulated by the treatment with baicalin. Baicalin of different doses reduced the generation of ROS in UC rats. Conclusion: Taken together, these evidences provide scientific basics for the application of baicalin in the treatment of UC and suggest that baicalin exerts its effect via suppression of oxidant stress and apoptosis. SUMMARY
  • Baicalin remarkably upregulated the activities of catalase, glutathione peroxidase, and superoxide dismutase and decreased the content of MDA, both in vivo and in vitro
  • The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling-positive cells in rats treated baicalin remarkably reduced in a concentration-dependent manner
  • Western blot analysis and immunocytochemistry assay indicated that baicalin significantly decreased the expressions of transforming growth factor beta-1, Bax protein, and upregulated the expression of Bcl-2 protein
  • The expressions of total and cleaved caspase-3, total and cleaved caspase-9 protein, Fas, and FasL in vitro were downregulated by the treatment with baicalin.
Abbreviations used: UC: Ulcerative colitis, LPS: Lipopolysaccharide, TNBS: 2,4,6-trinitrobenzene sulfonic acid, DAI: Disease activity index, CAT: Catalase, GSH-PX: Glutathione peroxidase, SOD: Superoxide dismutase, MDA: Malondialdehyde, TUNEL: Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling, ROS: Reactive oxygen species, IEC: Intestinal epithelial cell, SD: Sprague-Dawley, HE: H and E, DNTB: 5,5'-dithiobis-2-nitrobenzoic acid, TBA: Thiobarbituric acid, TBARS: Thiobarbituric acid-reactive substances, S.D: Standard deviation, and PBS: Phosphate-buffered saline.


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