首页|姜黄素对TNBS诱导的大鼠结肠炎IL-36α和IL-36γ表达的影响

姜黄素对TNBS诱导的大鼠结肠炎IL-36α和IL-36γ表达的影响

The effect of curcumin on the expression of IL-36α and IL-36γ in TNBS induced colitis in rats

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目的 研究姜黄素对三硝基苯磺酸(TNBS)诱导大鼠结肠炎IL-36α和IL-36γ表达的影响.方法实验于2022 年5 月在广西医科大学医学实验动物中心进行.选取40 只雄性 SD大鼠随机分为正常对照组、模型组、姜黄素组、柳氮磺吡啶组,每组10 只.模型组、姜黄素组、柳氮磺吡啶组大鼠分别以TNBS 乙醇溶液灌肠制备大鼠结肠炎模型,正常对照组予等体积 0.9%氯化钠溶液灌肠.姜黄素组、柳氮磺吡啶组自造模第 2 天起分别予姜黄素及柳氮磺吡啶溶液100 mg·kg-1·d-1灌胃,正常对照组、模型组每日予等体积的0.9%氯化钠溶液灌胃;给药7d后处死,采集血清及结肠黏膜,比较各组大鼠体质量、疾病活动指数(DAI)、肠黏膜损伤指数(CMDI);ELISA法检测大鼠血清IL-36α、IL-36γ水平,免疫组化方法测定肠黏膜组织IL-36α和IL-36γ蛋白表达.结果 与正常对照组比较,模型组DAI、CMDI评分均升高,差异有统计学意义(P均<0.01),血清IL-36α、IL-36γ水平均升高(P<0.01);与模型组比较,姜黄素组和柳氮磺吡啶组DAI、CMDI评分及血清 IL-36α、IL-36γ水平均降低,且姜黄素组低于柳氮磺吡啶组,差异有统计学意义(F =3.531、3.842、24.503、36.435,P均<0.001).与正常对照组比较,模型组结肠组织IL-36α、IL-36γ蛋白表达水平升高(P<0.05);与模型组比较,姜黄素组和柳氮磺吡啶组结肠黏膜IL-36α、IL-36γ蛋白表达水平降低,且姜黄素组低于柳氮磺吡啶组,差异有统计学意义(F =3.461、3.524,P均<0.001).结论 姜黄素能够明显抑制实验性大鼠结肠炎血清及结肠黏膜IL-36α、IL-36γ的表达.
Objective To investigate the effect of curcumin on the expression of IL-36α and IL-36γ in colitis in-duced by trinitrobenzenesulfonic acid(TNBS)in rats.Methods The experiment was conducted in May 2022 at the Medical Experimental Animal Center of Guangxi Medical University.Forty male SD rats were randomly divided into a normal control group,a model group,a curcumin group,and a sulfasalazine group,with 10 rats in each group.The model group,curcumin group,and sulfasalazine group of rats were prepared with TNBS ethanol solution enema to create rat colitis models,while the normal control group was given an equal volume of 0.9%sodium chloride solution enema.The curcumin group and sul-fasalazine group were orally administered with curcumin and sulfasalazine solutions of 100 mg·kg-1·d-1 from the second day of modeling.The normal control group and model group were orally administered with an equal volume of 0.9%sodium chloride solution daily;After 7 days of administration,the rats were euthanized and serum and colon mucosa were collected.The body weight,disease activity index(DAI),and intestinal mucosal injury index(CMDI)of each group of rats were com-pared;ELISA method was used to detect the serum levels of IL-36α and IL-36γ in rats,and immunohistochemical method was used to measure the protein expression of IL-36α and IL-36γ in intestinal mucosal tissue.Results Compared with the normal control group,the DAI and CMDI scores of the model group increased significantly(P<0.01);The levels of serum IL-36α and IL-37 both increased(P<0.01);Compared with the model group,the DAI,CMDI scores,and serum IL-36αand IL-36γ levels in both the curcumin group and the sulfasalazine group decreased,and the curcumin group was lower than the sulfasalazine group,with statistically significant differences(F=3.531,3.842,24.503,36.435,P<0.001);Compared with the normal control group,the protein expression levels of IL-36 and IL-37 in the model group increased(P<0.05);Compared with the model group,the protein expression levels of IL-36α and IL-36γ in the colon mucosa of the curcumin group and the sulfasalazine group decreased,and the curcumin group was lower than the sulfasalazine group,with statistical signifi-cance(F=3.461,3.524,P<0.001).Conclusion Curcumin can significantly inhibit the expression of IL-36α and IL-36γ in se-rum and colon mucosa of experimental colitis rats.

Inflammatory bowel diseaseCurcuminInterleukin-36αInterleukin-36γRats

梁昌显、吕晓丹、范俊华、李世权、詹灵凌、吕小平

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530021 南宁,广西医科大学第一附属医院消化内科

530021 南宁,广西医科大学第一附属医院检验科

炎性肠病 姜黄素 白介素-36α 白介素-36γ 大鼠

国家自然科学基金资助项目广西医疗卫生适宜技术开发与推广应用项目广西壮族自治区卫生健康委员会自筹基金广西医科大学青年科学基金

81860104S2018049Z20200398GXMUYSF201913

2024

疑难病杂志
中国医师协会

疑难病杂志

CSTPCD
影响因子:1.171
ISSN:1671-6450
年,卷(期):2024.23(2)
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