摘要
目的探究黄芪多糖(APS)对甲型流感病毒(IAV)性肺炎大鼠肺组织NOD样受体蛋白3(NLRP3)信号通路的影响。方法将40只大鼠随机分为对照组、模型组、黄芪多糖低剂量组(APS-L组,50 mg/kg)和黄芪多糖高剂量组(APS-H组,100 mg/kg),每组10只。除对照组外,其余各组大鼠采用甲型流感病毒H1N1滴鼻法建立病毒性肺炎模型。感染24 h后,APS-L组和APS-H组灌胃给予相应剂量的APS,对照组和模型组灌胃等量生理盐水,1次/d,持续5 d。给药结束后,观察大鼠一般状态,并计算大鼠肺指数。ELISA法检测肺匀浆中IL-1β、IL-18含量。HE染色观察肺组织病理学变化。qRT-PCR检测肺组织NLRP3 mRNA、IL-1βmRNA水平。Western blot检测肺组织NLRP3、cleaved Caspase-1蛋白表达。结果与对照组相比,模型组大鼠一般状态较差,肺组织出现明显病变,肺泡结构破坏,肺指数、肺组织IL-18、IL-1β、NLRP3 mRNA和蛋白、cleaved Caspase-1 P10、cleaved Caspase-1 P20蛋白表达显著增加(P<0.05)。与模型组相比,APS-L组和APS-H组大鼠一般状态和肺部的病理损伤明显改善,肺指数、肺组织IL-18、IL-1β、NLRP3 mRNA和蛋白、cleaved Caspase-1 P10、cleaved Caspase-1 P20蛋白表达明显降低(P<0.05),且APS-H组上述指标的变化均优于APS-L组,差异有统计学意义(P<0.05)。结论APS可能通过抑制NLRP3炎症小体的活化,进而降低IL-1β、IL-18水平,减轻流感病毒感染引起的肺部炎性损伤。
Objective To explore the effect of astragalus polysaccharide(APS)on the NOD-like receptor protein 3(NLRP3)signaling pathway in lung tissue of rats with influenza A virus(IAV)pneumonia.Methods Forty rats were randomly divided into control group,model group,astragalus polysaccharide low-dose group(APS-L group,50 mg/kg),astragalus polysaccharide high-dose group(APS-H group,100 mg/kg),with ten rats in each group.Except control group,the rats in the other groups were intranasally dripped with influenza A virus H1N1 to establish the model of viral pneumonia.The rats in APS-L group and APS-H group were given corresponding doses of APS by gavage at 24 h after infection,and the rats in control group and model group were given the same amount of normal saline by gavage once a day for 5 d.After administration,the general state of the rat was observed,and the rat lung index was calculated.ELISA method was used to detect the contents of IL-1βand IL-18 in lung homogenate.HE staining was used to observe the pathological changes of lung tissue.QRT-PCR was used to detect the levels of NLRP3 mRNA and IL-1βmRNA in lung tissue.Western blot was used to detect the expression of NLRP3 and cleaved Caspase-1 proteins in lung tissue.Results Compared with control group,the rats were in poorer general conditions in model group,with obvious lung tissue lesions and alveolar structure destruction,and the lung index,the contents of IL-18 and IL-1β,the expression levels of NLRP3 mRNA and protein,and cleaved Caspase-1 P10,cleaved Caspase-1 P20 protein were increased significantly in lung tissue(P<0.05).Compared with model group,the general state of the rats and the pathological damage of the lungs in APS-L group and APS-H group were significantly improved,and the lung index,the contents of IL-18 and IL-1β,the expression levels of NLRP3 mRNA and protein,and cleaved Caspase-1 P10,cleaved Caspase-1 P20 protein were decreased significantly(P<0.05),and the changes of the above indexes in APS-H group were better than those in APS-L group(P<0.05).Conclusion APS may inhibit the activation of NLRP3 inflammasomes,thereby reducing the levels of IL-1βand IL-18,and alleviating the lung inflammatory damage caused by influenza virus infection.
作者
沈钦华
李素娟
董苏一
SHEN Qinhua;LI Sujuan;DONG Suyi(Department of Pharmacy,People’s Hospital of Dongxihu District,Wuhan 430040,China)
出处
《山西医科大学学报》
CAS
2021年第9期1154-1159,共6页
Journal of Shanxi Medical University
基金
武汉市医学科研项目(WZ20Y03)。
