首页|甘青青兰多糖对脂多糖诱导小鼠脓毒症心肌损伤的保护作用

甘青青兰多糖对脂多糖诱导小鼠脓毒症心肌损伤的保护作用

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目的 研究甘青青兰多糖保护脂多糖诱导小鼠脓毒症心肌损伤的作用机制.方法 建立H9c2心肌细胞炎症模型,采用RT-qPCR评价甘青青兰多糖对NOD样受体热蛋白结构域相关蛋白3(NLRP3)、白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、IL-10的mRNA表达的影响.采用脂多糖建立小鼠脓毒症心肌损伤模型,通过小动物超声成像系统评价小鼠心脏的功能;ELSIA法检测小鼠血清中炎症因子的水平;用试剂盒检测血清中心肌酶的水平.结果甘青青兰多糖可通过调节小鼠心肌组织及血液中NLRP3、IL-1β、TNF-α、IL-10以及心肌酶的表达来改善小鼠的心脏功能.结论 甘青青兰多糖对脂多糖诱导小鼠脓毒症心肌损伤具有保护作用,其机制可能是通过抑制NLRP3小体活化,进而抑制炎症因子的释放,改善心肌组织的炎症水平.
Protective effects of Dracocephalum tanguticum polysaccharide on myocardial injury induced by lipopolysaccharide in septic mice
OBJECTIVE To explore the protective mechanism of Dracocephalum tanguticum polysaccharide(DTP)on lipopolysaccharide induced myocardial injury in mice with sepsis.METHODS The H9c2 cardiomyocyte inflammation model was established,and RT-qPCR was used to evaluate the effect of DTP on the mRNA expressions of NLRP3,IL-1β,IL-6 and IL-10.A mice model of septic myocardial injury was establish using lipopolysaccharide,and the cardiac function of the mice was evaluated by small animal ultrasound imaging system.The serum levels of inflammatory factors of mice were detected by ELSIA,and the levels of myocardial enzymes were detected by kit assays.RESULTS DTP improved the cardiac function of mice by regulating the expression of NLRP3,IL-1β,TNF-α and IL-10 in myocardial tissues and blood,as well as the expression of myocardial enzymes.CONCLUSION DTP exerts a protective effect on myocardial injury induced by lipopolysaccharide in septic mice,and its mechanism may be attributed to the inhibition of NLRP3 activation,the suppression of inflammatory factors release,and the improvement of myocardial inflammation.

Dracocephalum tanguticum Maxim.PolysaccharideNLRP3Myocardial injuryCardiac enzymesSepsisMyocardial cells

次旦南卓、米玛、侯豹、邱丽颖

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西藏藏医药大学,西藏拉萨 850000

江南大学,江苏无锡 214122

甘青青兰 多糖 NOD样受体热蛋白结构域相关蛋白3 心肌损伤 心肌酶 脓毒症 心肌细胞

中医学(藏医)博士点建设及中药学(藏药)博士点培育科研资助计划(2022)藏医药规划内涵建设项目(十四五)西藏藏医药大学校级科研项目

BSDJS-22-212023ZYYGH042022ZRYB11

2024

10.13375/j.cnki.wcjps.2024.03.008

华西药学杂志
四川大学,四川省药学会

华西药学杂志

CSTPCD北大核心
影响因子：0.624
ISSN：1006-0103
年,卷(期)：2024.39(3)