大黄素可通过抑制NLRP3炎性小体活化减轻哮喘小鼠的炎症反应

目的探讨大黄素对哮喘小鼠炎症反应及对肺组织中NOD样受体蛋白结构域相关蛋白3(NODlike receptor pyrin domain containing 3,NLRP3)、凋亡相关微粒蛋白(apoptosis-associated speck-like protein containing CARD,ASC)和胱冬肽-1(caspase-1)表达的影响。方法36只BALB/c雌性小鼠随机分为对照组、哮喘组和大黄素组。以卵蛋白为致敏原制备哮喘小鼠模型。收集肺泡灌洗液(BALF)进行细胞计数和分类计数,ELISA方法检测BALF中肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)与白介素-4(IL-4)水平。HE染色观察小鼠肺组织病理学改变。Western-blot检测各组小鼠肺组织中NLRP3、ASC和caspase-1的表达。结果大黄素能减少BALF中炎性细胞总数和嗜酸性粒细胞,降低BALF中TNF-α、IL-1β与IL-4含量,减轻肺组织炎性反应。Western-blot结果显示,哮喘组小鼠肺组织NLRP3、ASC和caspase-1的蛋白表达显著高于对照组(P<0.01);与哮喘组比较,大黄素组小鼠肺组织NLRP3、ASC和caspase-1的蛋白表达显著降低(P<0.01)。结论大黄素可通过抑制NLRP3炎性小体活化减轻哮喘小鼠的炎症反应。

Emodin can reduce the inflammatory response of asthmatic mice by inhibiting the activation of NLRP3 inflammatory bodies

Objective To investigate the effects of emodin on the inflammatory response of asthmatic mice and the expression of nod like receptor protein domain containing 3(NLRP3),apoptosis associated speck like protein containing card(ASC)and caspase-1 in lung tissue.Methods 36 BALB/C female mice were randomly divided into control group,asthma group and emodin group.The asthmatic mice model was made with ovalbumin as the allergen.BALF was collected for cell count and classification count.The levels of Tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-4(IL-4)in BALF were measured by ELISA.HE staining was used to observe the lung histopathological changes.Western blot was used to detect the expression of NLRP3,ASC and caspase-1.Results Emodin can reduce the total number of inflammatory cells and eosinophils in BALF,the content of TNF-α,IL-1βand IL-4 in BALF,and the inflammatory response of lung tissue.Western blot showed that the expression of NLRP3,ASC and caspase-1 in lung tissue of asthmatic group was higher significantly than that of control group(P<0.01);compared with asthmatic group,the expression of NLRP3,ASC and caspase-1 in lung tissue of emodin group was significantly lower(P<0.01).Conclusion Emodin can reduce the inflammatory response of asthmatic mice by inhibiting the activation of NLRP3 inflammatory bodies.