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作 者:迟宏罡[1,2] 邹颖[3] 戴世学[4] 郑学宝[2]
机构地区:[1]南方医科大学中医药学院2010级博士研究生,广州510515 [2]广东医学院中医教研室,广东湛江524023 [3]广东医学院中美联合肿瘤研究所,广东东莞523808 [4]南方医院急诊科,广州510515
出 处:《中国实验方剂学杂志》2013年第1期211-215,共5页Chinese Journal of Experimental Traditional Medical Formulae
基 金:国家自然科学基金面上项目(81173240)
摘 要:目的:观察黄芩汤对2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎大鼠白细胞介素23(IL-23)/白细胞介素17(IL-17)通路的影响。方法:将32只大鼠随机分为正常对照组、TNBS结肠炎组、TNBS+黄芩汤治疗组(1.2 g·kg-1)、TNBS+美沙拉嗪治疗组(10 mL·kg-1,ig),每组8只。除正常对照组外,其余各组均应用2,4,6-三硝基苯磺酸(TNBS)灌肠法建立结肠炎模型,造模完成后,各组分别按设计剂量连续给药1周。用酶联免疫吸附法(ELISA)分析大鼠血清中白细胞介素17(IL-17)、白细胞介素23(IL-23)的水平,用real-time PCR方法检测大鼠结肠组织中IL-17,IL-17R,IL-23,IL-23R,RORγt的mRNA水平。结果:黄芩汤治疗能有效降低TNBS诱导的结肠炎大鼠血清中IL-17(262.75±17.19 ng·L-1和IL-23(56.75±6.20)ng·L-1的蛋白水平,降低结肠组织中IL-17(2.606±0.8),IL-17R(5.33±1.10),IL-23(2.16±0.19),IL-23R(3.34±0.70),RORγt(0.74±0.17)的mRNA水平。结论:黄芩汤能有效的调节TNBS诱导的结肠炎大鼠IL-23/IL-17通路,这可能是其治疗结肠炎的免疫机制之一。Objective: To evaluate the effects of Huangqin Tang on the IL-23/IL-17 pathway in 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) -induced colitis model. Method: SD rats were distributed into four group, containing TNBS-induced colitis, Huangqin Tang (1.2 g · kg^-1 ) or mesalazine treatment group (10 mL · kg^-1, ig), negative control with no treatment and the last one was normal sham rats. Except for control group, experimental colitis was induced by rectal instillation of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) into rats. Drugs were given intragastrically for one week in each group continuously according to respectively-designed doses. The protein expressions of IL-17 and IL-23 in serum were determined by ELISA. The mRNA expressions of IL-17, IL-23, IL-17R, IL-23R and RORγt were determined by Real-time PCR. Result: Huangqin Tang markedly attenuated TNBS-induced colitis and effectively inhibited the protein expressions of IL-17 (262.75 ± 17.19) ng · L^-1 and IL-23 (56.75 ±6.20) ng· L^-1. Furthermore, mRNA levels of IL-17 (2. 606 ±0. 8), IL-17R (5.33 ±1.10), IL-23 (2.16 ±0.19), IL-23R (3.34 ±0.70), RORγ/t (0.74 ±0.17) showed a marked reduction after Huangqin Tang teatment. Conclusion: Taken together, our findings demonstrate that Huangqin Tang can exerte therapeutic effects on TNBS-induced colitis, mediate probably by the IL-23/IL-17 pathway.1.10), IL-23 (2.16 ±0.19), IL-23R (3.34 ±0.70), RORγt (0.74 ±0.17) showed a marked reduction after Huangqin Tang teatment. Conclusion: Taken together, our findings demonstrate that Huangqin Tang can exerte therapeutic effects on TNBS-induced colitis, mediate probably by the IL-23/IL-17 pathway.
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