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目的:探讨大黄素对脂多糖(LPS)诱导小鼠巨噬细胞炎性反应的保护机制。方法:分离C57BL/6小鼠腹腔巨噬细胞进行培养,MTT法筛选大黄素浓度。LPS诱导小鼠巨噬细胞,分为空白组、LPS组、LPS+大黄素组,采用实时荧光定量PCR检测各组细胞核苷酸结合寡聚化结构域受体(NLRP3)、半胱氨酸蛋白水解酶-1(Caspase-1)、白介素-1β(IL-1β)的m RNA表达水平。结果:LPS处理后NLRP3、IL-1β的m RNA表达量高于空白组,而Caspase-1的m RNA表达量低于空白组(P<0.01);大黄素干预后,NLRP3、IL-1β的m RNA表达量低于LPS组,而Caspase-1 m RNA表达量高于LPS组(P<0.01,P<0.05)。结论:大黄素对LPS诱导NLRP3/IL-1β炎性小体信号通路的激活具有保护作用。
Objective: To investigate the protective mechanism of emodin on lipopolysaccharide (LPS) -induced macrophage inflammatory reaction in mice. Methods: C57BL / 6 mouse peritoneal macrophages were isolated and cultured, and the emodin concentration was screened by MTT method. LPS-induced macrophages were divided into blank group, LPS group and LPS + emodin group. Real-time fluorescent quantitative PCR was used to detect the expression of nucleotide-binding oligomerization domain receptor (NLRP3), cysteine proteolysis The mRNA expression levels of Caspase-1, IL-1β were measured. Results: The mRNA expression of NLRP3 and IL-1β in LPS group was higher than that in blank group, while the mRNA expression of Caspase-1 was lower than that in blank group (P <0.01). After emodin intervention, the expression of NLRP3 and IL- The expression of m RNA was lower in LPS group than in LPS group (P <0.01, P <0.05). Conclusion: Emodin has a protective effect on the activation of NLRP3 / IL-1β inflammasome signaling pathway induced by LPS.