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Archive > Volume 9 Issue 4 > 2017,9(4):344-352. DOI:10.1016/S1674-6384(17)60114-X Prev Next

Original articles

Amelioration of Tripterygium wilfordii Polycoride on TNBS/Ethanol-induced Ulcerative Colitis via Inhibiting Lipid Peroxidation and Its Downstream Inflammatory Meditors

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    Abstract:
    Objective To study the protective effect of Tripterygium wilfordii polycoride (TWP) against TNBS/ethanol-induced ulcerative colitis (UC) rat model. Methods TNBS and ethanol enema were adopted to build TNBS/ethanol-induced UC rat model. Ninety male Wistar rats were divided into six groups: normal, model, low-, medium-, high-dose TWP and azathioprine (AZA) groups, each for 15 rats. All rats were administered by corresponding medicine for 14 d. After 14 d, corresponding colon tissues underwent general and microscopic evaluation. Blood samples were taken from heart and serum was separated by centrifugation. MDA, SOD, GSH, IL-1β and TNF-α levels in serum were tested by ELISA. Colonic samples underwent RT-PCR and Western blotting analysis. Results DAI, general and microscopic evaluation all showed that TWP could promote colonic mucosa healing and such effect was equal to AZA. ELISA results about lipid peroxidation indicated that TWP could decrease MDA level and increase SOD and GSH levels in a dose-dependent manner. TWP with high dose could strongly decrease the MDA level and increase the SOD and GSH levels (P ＜ 0.01). ELISA results about inflammatory cytokines indicated that TWP could inhibit the expression of IL-1β and TNF-α in a dose-dependent manner. Western blotting analysis and RT-PCR all indicated that no matter in mRNA level or protein level, TWP could inhibit the expression of NF-κB, TNF-α, IL-1β, and IFN-γ in a dose-dependent manner. The inhibitory effect of AZA towards NF-κB was slightly weaker than TWP with high dose (P ＞ 0.05), whereas slightly stronger towards terminal inflammatory cytokines (P ＞ 0.05). Conclusion TWP could significantly lower the infiltration of inflammatory cells under microscope, eventually led to mucosa healing, the mechanism of which was to inhibit lipid peroxidation, then further inhibit NF-κB activation, eventually lower the expression of inflammatory meditors locally and systemically.

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    Project Supported:
    National Natural Science Foundation of China Granted Project (No. 81273903 and No. 81673798)

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