摘要
目的:探讨白芨多糖对胃溃疡(GU)模型大鼠胃组织TLR-4、NF-κB p65基因蛋白及其介导的细胞因子IL-17、IL-23表达水平的影响。方法:将60只SPF级Wistar大鼠随机分为空白组(Control,n=10)和模型组(Model,n=50)。模型组大鼠采用乙酸直接烧灼法复制GU模型。将GU模型大鼠按随机数字表法分为模型组、阳性对照组(Rh)和白芨多糖大(Bsp-h)、中(Bsp-m)、小剂量组(Bsp-l),共5组,每组10只。空白组和GU模型组大鼠给予10 ml/(kg·d)蒸馏水灌胃,白芨多糖大、中、小剂量组分别予0.5 g/(kg·d)、0.25 g/(kg·d)、0.125 g/(kg·d)白芨多糖药剂灌胃,阳性对照组给予0.3 g/(kg·d)雷尼替丁药剂灌胃,治疗15 d。采用ELISA法检测各组大鼠胃溃疡病灶组织细胞因子IL-17、IL-23含量,RT-PCR法检测胃溃疡病灶组织IL-17、IL-23、TLR-4及NF-κB p65基因表达水平,WB法检测胃溃疡病灶组织TLR-4及NF-κB p65蛋白表达水平。结果:与空白组比较,GU大鼠病理切片见胃底腺结构紊乱,胃黏膜上皮细胞脱落;胃组织细胞因子IL-17、IL-23含量及基因表达显著升高,TLR-4及NF-κB p65基因及蛋白表达水平显著升高,差异具有统计学意义(P<0.01);与GU模型组比较,白芨多糖大剂量组大鼠病理切片见胃黏膜出现较多腺体,炎症细胞浸润,坏死层明显减少;白芨多糖大、中、小剂量组IL-17、IL-23含量及基因表达均降低,以白芨多糖大剂量组降低显著。TLR-4及NF-κB p65基因及蛋白表达水平均降低,以白芨多糖大、中剂量组降低显著,差异具有统计学意义(P<0.05或P<0.01)。结论:白芨多糖可通过下调TLR-4及NF-κB p65基因和蛋白表达水平,抑制细胞因子IL-17、IL-23异常分泌而发挥保护胃黏膜的作用。
Objective:To investigate the effect of Bletilla striata polysaccharide on expression of TLR-4,NF-κB p65 gene protein and its mediated cytokines IL-17 and IL-23 in gastric tissue of rats with gastric ulcer(GU).Methods:Sixty SPF Wistar rats were randomly divided into blank group and model group.The GU model was replicated by direct acetic acid cauterization in model group.The GU model rats were randomly divided into five groups:model group,positive control group and large,medium and small dose group of Bletilla striata polysaccharide,with 10 rats in each group.Rats in blank group and GU model group were given 10 ml/(kg·d)distilled water by gavage,rats in large,medium and small dose groups were given 0.5 g/(kg·d),0.25 g/(kg·d),0.125 g/(kg·d)Bletilla striata polysaccharide by gavage,while rats in positive control group were given 0.3 g/(kg·d)ranitidine by gavage for 15 days.The levels of cytokines IL-17 and IL-23 in gastric ulcer tissues were detected by ELISA,IL-23,TLR-4 and NF-κB p65 gene expression by RT-PCR,and TLR-4 and NF-κB p65 protein expression by WB.Results:Compared with the blank group,pathological sections of GU rats showed structural disorder of gastric fundus gland and exfoliation of gastric mucosal epithelial cells;the contents and gene expression of cytokines IL-17 and IL-23 in gastric tissue were significantly increased,and the levels of TLR-4 and NF-κB p65 gene and protein expression were significantly increased(P<0.01);compared with GU model group,pathological sections of rats in high dose group of Bletilla striata polysaccharide showed more glands in gastric mucosa,infiltration of inflammatory cells and decrease of necrotic layer;the contents of IL-17 and IL-23 and gene expression in large,medium and small dose groups of Bletilla striata polysaccharide were all decreased.The levels of TLR-4 and NF-κB p65 gene and protein expression in large dose group of Bletilla striata polysaccharide were significantly lower than those in large and medium dose group of Bletilla striata polysaccharide(P<0.05 or P<0.01).Conclusion:Bletilla striata polysaccharide can protect gastric mucosa by down-regulating the levels of TLR-4 and NF-κB p65 gene and protein and inhibiting the abnormal secretion of cytokines IL-17 and IL-23.
作者
巩子汉
段永强(指导)
成映霞
虎峻瑞
王强
付晓艳
白敏
GONG Zi-Han;DUAN Yong-Qiang;CHENG Ying-Xia;HU Jun-Rui;WANG Qiang;FU Xiao-Yan;BAI Min(Gansu University of Chinese Medicine,Lanzhou 730000,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2020年第7期821-825,836,共6页
Chinese Journal of Immunology
基金
甘肃省教育厅高等学校科研项目(2018A-044)
甘肃中医药大学研究生创新基金项目(CX2019-40)资助。
