سامانه مدیریت نشریات علمی دانشگاه علوم پزشکی مشهد

He, Miao, Yu, Wan-xin, Shen, Yongmei, Zhang, Jing-na, Ni, Lian-li, Li, Yue, Liu, Heng, Zhao, Yu, Zhao, Hairong, Zhang, Chenggui. (1402). Kangfuxin alleviates ulcerative colitis in rats by inhibiting NF-κB p65 activation and regulating T lymphocyte subsets. , 26(8), 882-890. doi: 10.22038/ijbms.2023.68771.14990
Miao He; Wan-xin Yu; Yongmei Shen; Jing-na Zhang; Lian-li Ni; Yue Li; Heng Liu; Yu Zhao; Hairong Zhao; Chenggui Zhang. "Kangfuxin alleviates ulcerative colitis in rats by inhibiting NF-κB p65 activation and regulating T lymphocyte subsets". , 26, 8, 1402, 882-890. doi: 10.22038/ijbms.2023.68771.14990
He, Miao, Yu, Wan-xin, Shen, Yongmei, Zhang, Jing-na, Ni, Lian-li, Li, Yue, Liu, Heng, Zhao, Yu, Zhao, Hairong, Zhang, Chenggui. (1402). 'Kangfuxin alleviates ulcerative colitis in rats by inhibiting NF-κB p65 activation and regulating T lymphocyte subsets', , 26(8), pp. 882-890. doi: 10.22038/ijbms.2023.68771.14990
He, Miao, Yu, Wan-xin, Shen, Yongmei, Zhang, Jing-na, Ni, Lian-li, Li, Yue, Liu, Heng, Zhao, Yu, Zhao, Hairong, Zhang, Chenggui. Kangfuxin alleviates ulcerative colitis in rats by inhibiting NF-κB p65 activation and regulating T lymphocyte subsets. , 1402; 26(8): 882-890. doi: 10.22038/ijbms.2023.68771.14990

Kangfuxin alleviates ulcerative colitis in rats by inhibiting NF-κB p65 activation and regulating T lymphocyte subsets

Iranian Journal of Basic Medical Sciences
مقاله 4، دوره 26، شماره 8، آبان 2023، صفحه 882-890    اصل مقاله (728.96 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2023.68771.14990
نویسندگان
Miao He1، 2، 3؛ Wan-xin Yu1؛ Yongmei Shen4؛ Jing-na Zhang5؛ Lian-li Ni1، 6؛ Yue Li1؛ Heng Liu1، 2؛ Yu Zhao1، 2؛ Hairong Zhao* 1، 2؛ Chenggui Zhang* 1، 2
1Yunnan Provincial Key Laboratory of Entomological Biopharmaceutical R&D, College of Pharmacy, Dali University, Dali, China
2Yunnan Provincial 2011 Collaborative Innovation Center for Entomoceutics, Dali, Yunnan, China
3School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China
4Good Doctor Pharmaceutical Group, Chengduo, Sichuang, China
5Yunnan Provincial Key Laboratory of Entomological Biopharmaceutical R&D, College of Pharmacy, Dali University, Dali, China
6Cancer and Anticancer Drug Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China
چکیده
Objective(s): Ulcerative colitis (UC) remains an enduring, idiopathic inflammatory bowel disease marked by persistent mucosal inflammation initiating from the rectum and extending in a proximal direction. An ethanol extract of Periplaneta americana L., namely Kangfuxin (KFX), has a significant historical presence in Traditional Chinese Medicine and has been broadly utilized in clinical practice for the treatment of injury. Here, we aimed to determine the effect of KFX on 2,4,6-trinitro’benzene sulfonic acid (TNBS)-induced UC in Sprague-Dawley rats.
Materials and Methods: We established the UC model by TNBS/ethanol method. Then, the rats were subject to KFX (50, 100, 200 mg/kg/day) for 2 weeks by intragastric gavage. The body weight, disease activity index (DAI), colonic mucosal injury index (CMDI), and histopathological score were evaluated. The colonic tissue interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), IL-10, transforming growth factor-1 (TGF-β1), and epidermal growth factor (EGF) were determined by Elisa. To study T-lymphocyte subsets, flow cytometry was performed. In addition, the expression level of NF-κB p65 was evaluated by immunohistochemistry and western blot analysis.
Results: Compared with the TNBS-triggered colitis rats, the treatment of rats with KFX significantly increased the body weight, and decreased DAI, CMDI, and histopathological score. Also, KFX elicited a reduction in the secretion of colonic pro-inflammatory cytokines, namely IL-1β, IL-6, and TNF-α, concomitant with up-regulation of IL-10, TGF-β1, and EGF levels. Upon KFX treatment, the CD3+CD4+/CD3+CD8+ ratio in the spleen decreased, while the CD3+CD8+ subset and the CD3+CD4+CD25+/CD3+CD4+ ratio demonstrated an increase. In addition, the expression of NF-κB p65 in the colon was decreased.
Conclusion: KFX effectively suppresses TNBS-induced colitis by inhibiting the activation of NF-κB p65 and regulating the ratio of CD4+/CD8+.
کلیدواژه‌ها
Inflammation mediators؛ Inflammatory bowel disease؛ Kangfuxin؛ T lymphocyte subsets؛ Ulcerative colitis
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