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. 2023;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

Miao He  1   2   3   4 , Wan-Xin Yu  1   4 , Yongmei Shen  5 , Jing-Na Zhang  1 , Lian-Li Ni  1   6 , Yue Li  1 , Heng Liu  1   2 , Yu Zhao  1   2 , Hai-Rong Zhao  1   2 , Cheng-Gui Zhang  1   2
Affiliations

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

Miao He et al. Iran J Basic Med Sci. 2023.

Abstract

Objectives: 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+.

Keywords: Inflammation mediators; Inflammatory bowel disease; Kangfuxin; T lymphocyte subsets; Ulcerative colitis.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
Content determination of the main chemical compounds in KFX
Figure 2
Figure 2
Effect of KFX on disease activity index (DAI) and immune organ index in rats with TNBS-induced colitis
Figure 3
Figure 3
Effect of KFX on colon length, length-width ratio of the colon, and colon mucosal damage index (CMDI) in rat with TNBS-induced colitis
Figure 4.
Figure 4.
Effects of KFX on colonic IL1-β, IL-6, TNF-α, IL-10, EGF, and TGF-β1 in rats with TNBS-induced colitis
Figure 5
Figure 5
Effects of KFX on colon histology in rats with TNBS-induced colitis
Figure 6
Figure 6
KFX inhibits NF-κB p65 protein expression in the colon
Figure 7
Figure 7
Effects of KFX on T cell subtypes in the spleen in rats with TNBS-induced colitis
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