摘要
目的:研究体外培育牛黄(Calculus Bovis Sativus,CBS)在慢性溃疡性结肠炎(ulcerative colitis,UC)中的抗凋亡机制。方法:将28只雄性C57BL/6小鼠采用随机数表法分为4组,分别为:正常对照组,模型对照组,CBS低剂量组和CBS高剂量组。给予2%葡聚糖硫酸钠(dextran sulfate sodium,DSS)溶液分3个周期诱导慢性溃疡性结肠炎模型。CBS低剂量组和CBS高剂量组在造模期间的最后7 d分别给予50,150 mg·kg^(-1)·d^(-1)CBS灌胃处理。计算小鼠生存率,观察结肠组织形态学改变,苏木素-伊红染色、糖原染色评价小鼠结肠损伤情况,TUNEL检测结肠细胞凋亡情况,Western Blot检测细胞凋亡相关蛋白Caspase3、Bcl-2、Bax表达水平。结果:与正常对照组相比,模型对照组小鼠生存率明显下降,结肠组织损伤严重,结肠细胞凋亡率显著增加;Caspase3、Bax蛋白表达量增加而Bcl-2表达减少,Bax/Bcl-2比值升高。经CBS处理后,小鼠生存率提高,结肠组织损伤得到缓解,结肠细胞凋亡率明显下降;Caspase3、Bax蛋白表达水平下调而Bcl-2表达上调,Bax/Bcl-2比值也有所降低。结论:CBS能够通过抑制结肠细胞的凋亡对DSS诱导的慢性UC产生疗效,其抗凋亡机制可能是对细胞凋亡相关蛋白Caspase3、Bcl-2、Bax表达的调控作用。
OBJECTIVE To study the anti-apoptosis mechanism of Calculus Bovis Sativus（ CBS） on chronic ulcerative colitis（UC） in mice. METHODS Twenty eight male C57 BL/6 mice were randomly divided into four groups： control group,model group,CBS 50 group,CBS 150 group. The chronic UC model was induced by 2% dextran sulfate sodium（ DSS） solution for three cycles of totally 35 days. For the last 7 days of modeling,mice were orally given CBS（50 or 150 mg·kg^-1·d^-1）. The survival rates of mice were calculated,and the morphology of colon tissues was analyzed. Hematoxylin and eosin（ HE） and periodic acid-Schiff（ PAS） staining were applied to evaluate the damage of colons,Td T-mediated d UTP nick end labeling（ TUNEL） assays were performed to test the apoptosis of colonic cells,and the levels of apoptosis-associated proteins,Caspase3,Bcl-2 and Bax,were determined by Western blot.RESULTS In model group,the survival rates significantly decreased,colon tissues damaged greatly,and the apoptosis rates of colonic cells markedly increased compared with the control group. At the same time,the protein contents of Caspase3 and Bax increased,Bcl-2 declined and Bax/Bcl-2 value also increased in mice exposed to DSS. However,administration of CBS improved the survival rates and inflammatory colon tissues,inhibited the apoptosis of colonic cells,and down-regulated the expressions of Caspase3 and Bax while up-regulated Bcl-2 expressions,and decreased the value of Bax/Bcl-2. CONCLUSION CBS can attenuate DSS-induced chronic UC via inhibiting the apoptosis of colonic cells,and the anti-apoptotic mechanism may be the regulation of CBS on apoptosis-associated proteins Caspase3,Bcl-2 and Bax.
作者
张思
刘雅楠
雷凯
李娟
向东
杨金玉
任秀华
刘东
ZHANG Si;LIU Ya-nan;LEI Kai;LI Juan;XIANG Dong;YANG Jin-yu;REN Xiu hua;Liu Dong(Department of Pharmacy,Tongji Hospital Affiliated to Tongji Medical College,Huazhong University of Science and Technology,Hubei Wuhan 430030,China)
出处
《中国医院药学杂志》
CAS
北大核心
2018年第15期1572-1577,共6页
Chinese Journal of Hospital Pharmacy
基金
国家自然科学基金资助项目(编号:81573788
81503225)
关键词
体外培育牛黄
慢性溃疡性结肠炎
细胞凋亡
：Calculus Boris Sativus （CBS）
ulcerative colitis （UC）
cell apoptosis
