汉防己甲素对缺氧缺糖损伤BV2细胞炎症反应的影响  

Effects of tetrandrine on inflammation caused by hypoxic and hypoglycemic in BV2 cells

作　　者：吴飞飞[1,2] 郭明 WU Fei-fei;GUO Ming(Department of Cardiology,Zhejiang Xiaoshan Hospital,Hangzhou 311200,Zhejiang Province,China;School of Medicine,Hangzhou Normal University,Hangzhou 311123,Zhejiang Province,China)

机构地区：[1]浙江萧山医院心血管内科,浙江杭州311200 [2]杭州师范大学医学院,浙江杭州311123

出　　处：《中国临床药理学杂志》2020年第10期1350-1352,共3页The Chinese Journal of Clinical Pharmacology

摘　　要：目的研究汉防己甲素(Tetrandrine,Tet)对缺氧缺糖诱导的BV2细胞炎症反应的机制。方法将BV2细胞随机分为对照组、模型组和低、中、高剂量实验组。对照组正常培养,模型组糖氧剥夺(OGD)1 h再灌注24 h;低、中、高剂量实验组分别以0.1,1,10μmol·L^-1预孵育30 min并OGD/再灌注持续孵育。用细胞计数(CCK-8)法检测细胞存活率,以乳酸脱氢酶(LDH)法检测细胞损伤,以免疫荧光法观察NLRP3表达变化,以酶联免疫吸附(ELISA)试剂盒检测白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)表达。结果与对照组比较,模型组对BV2细胞有明显损伤,细胞活性下降了23.45%,且LDH释放增加36%;与模型组比较,低剂量实验组有改善细胞活性趋势,而中、高剂量实验组可显著改善细胞活性(P<0.05),LDH释放减少(P<0.05)。OGD诱导BV2细胞NLRP3/IL-1β/IL-18炎症通路表达增加,实验组明显抑制NLRP3炎症小体表达。结论汉防己甲素能改善OGD诱导的BV2细胞损伤,部分是通过抑制NLRP3炎症通路起作用的。Objective To investigate the mechanism of tetrandrine(Tet)on inflammatory reaction induced by hypoxia and sugar deficiency in BV2 cells.Methods BV2 cells were randomly divided into control group,model group and low,medium,high dose experimental groups.Control cells were cultured normally,model cells were treated by oxygen glucose deprivation(OGD)for 1 h and recovery for 24 h.Low,medium,high dose experimental groups were pre-incubated for 30 min with 0.1,1,10μmol·L^-1Tet and persistently incubated with OGD/reperfusion.Cell count kit(CCK-8)assay was used to observe the cell survival rate.The levels of lactic dehydrogenase(LDH)was used to measure cell injury.The changes of NLRP3 expression were detected by immunofluorescence.The levels of interleukin-1β(IL-1β)and interleukin-18(IL-18)were measured by enzyme linked immunosorbent assay(ELISA)Kit.Results Compared with control group,model group had significant cell damage,cell activity decreased by 23.45%,and the release of LDH increased by 36%.Compared with model group,low dose experimental group had a tendency to improve cell viability,medium and high dose experimental groups could significantly increase cell viability(P<0.05)and reduce the release of LDH(P<0.05).The expression of inflammatory pathway of NLRP3/IL-1β/IL-18 was increased induced by OGD in BV2 cells.Experimental groups treatment could greatly reduce the expression of NLRP3/IL-1β/IL-18.Conclusion Tet could improve BV2 cell injury induced by OGD partly through inhibition of NLRP3 inflammatory signaling pathways.

关 键 词：汉防己甲素 缺糖缺氧损伤 BV2细胞 NLRP3炎症小体 

分 类 号：R28[医药卫生—中药学]