摘要
目的观察黄芪多糖(APS)对梗阻性黄疸(OJ)大鼠肠损害的影响,并探讨其可能机制。方法48只雄性Wistar大鼠随机分为干预组、模型组、对照组各16只,干预组、模型组大鼠均制备OJ模型,对照组不制备模型(仅分离胆总管)。造模24 h之后,干预组大鼠灌胃给予APS生理盐水溶液(100 mg/kg),对照组及模型组灌胃给予同量生理盐水,2次/d。各组大鼠在制模14天时取血,采用ELISA法检测血清二胺氧化酶(DAO)及肠型脂肪酸结合蛋白(I-FABP);取血后处死大鼠,取小肠组织,采用Western blotting法检测组织增殖细胞核抗原(PCNA)蛋白,光学显微镜下观察组织腺窝深度、绒毛高度,末端脱氧核苷酸转移酶dUTP镍端标记法(TUNEL)计数组织上皮细胞凋亡数,ELISA法检测组织TNF-α、IL-1β、IL-1Ra、IL-10,免疫荧光染色法检测组织TLR4、NF-κB P65阳性细胞数,Western blotting法检测组织TLR4、NF-κB P65蛋白。结果模型组大鼠小肠组织出现明显病理损害,血清DAO、I-FABP水平及组织TNF-α、IL-1β表达均于对照组,组织IL-1Ra、IL-10低于对照组(P均<0.05)。干预组小肠组织病理损害减轻,血清DAO、I-FABP水平及组织TNF-α、IL-1β表达低于模型组,组织IL-1Ra、IL-10高于模型组(P均<0.05)。结论APS对OJ大鼠肠损害有治疗作用,其可保护大鼠肠黏膜屏障及抗小肠上皮细胞凋亡,机制可能是通过TLR4/NF-κB P65通路维持抗炎与促炎平衡。
Objective To observe the effect of Astragalus polysaccharide(APS)on intestinal damage in obstructive jaundice(OJ)rats and to explore its possible mechanism.Methods Forty-eight Wistar rats were randomly divided into the intervention group,model group,and control group,with 16 rats in each.The OJ models were prepared in the intervention group and model group,and in the control group,only the common bile ducts of rats were isolated.At 24 h after modeling,the rats in the intervention group were orally administered APS normal saline solution(100 mg/kg),and the control group and the model group with the same amount of normal saline,twice a day.Blood was taken from rats in each group at 14 days after modeling,and the serum diamine oxidase(DAO)and intestinal fatty acid binding protein(I-FABP)were detected by ELISA.After the blood was taken,the rats were sacrificed,and the small intestine tissues were taken.The proliferating cell nuclear antigen(PCNA)protein was detected by Western blotting.The depth of glandular fossa and the height of villi were observed under an optical microscope.The terminal deoxynucleotidyl transferase dUTP nickel terminal labeling method(TUNEL)was used to count the number of apoptotic cells.IL-1β,IL-1Ra,IL-10,TLR4 and NF-κB P65 positive cells were detected by immunofluorescence staining,and TLR4 and NF-κB P65 proteins were detected by Western blotting.Results Significant pathological damage occurred in the small intestine of rats in the model group.The levels of serum DAO,I-FABP,and TNF-αand IL-1βexpression in the tissues were higher,while the tissue IL-1Ra,IL-10 levels were lower in the model group than in the control group(all P<0.05).The pathological damage of small intestine tissues became less in the intervention group;the levels of serum DAO,I-FABP,and TNF-αand IL-1βexpression in the tissues were lower,but the levels of IL-1Ra and IL-10 in the tissues were higher in the intervention group than in the model group(all P<0.05).Conclusions APS has a therapeutic effect on intestinal damage
作者
黄忠义
陈飞
张贯启
邬善敏
HUANG Zhongyi;CHEN Fei;ZHANG Guanqi;WU Shanmin(People′s Hospital of Wuhan University,Wuhan 430000,China)
出处
《山东医药》
CAS
2020年第12期32-36,共5页
Shandong Medical Journal
