文献类型：期刊文献

中文题名：藁本内酯衍生物抑制大鼠软骨细胞凋亡和炎症的作用及机制

英文题名：The Effect and Mechanism of Ligustilide Cycloprolactam on Inhibiting Apoptosis and Inflammation of Rat Chondrocytes

作者：陈欣[1,2];汪欣月[3];李元贞[2];齐鑫[1];席芳琴[2];李宁[1,2];柳军玺[4];谢兴文[1,2];刘建军[1]

第一作者：陈欣

机构：[1]甘肃中医药大学附属医院,兰州730000;[2]甘肃中医药大学,兰州730020;[3]北京中医药大学,北京100105;[4]中国科学院兰州化学物理研究所,兰州730000

第一机构：甘肃中医药大学第二附属医院

年份：2023

卷号：45

期号：5

起止页码：770

中文期刊名：中国细胞生物学学报

外文期刊名：Chinese Journal of Cell Biology

收录：CSTPCD;;CSCD:【CSCD_E2023_2024】；PubMed;

基金：甘肃省青年科技基金(批准号:20JR10RA345);兰州市城关区科技计划(批准号:2020-2-2-7);甘肃中医药大学附属医院院内创新基金(批准号:gzfy-2019-12);甘肃省科技计划(批准号:20JR5RA129);兰州市科技发展指导性计划(批准号:2020-ZD-65)资助的课题。

语种：中文

中文关键词：软骨细胞;藁本内酯衍生物;白细胞介素-1β;凋亡;炎症反应

外文关键词：chondrocytes;LIGc(ligusticum cycloprolactam);IL-1β(interleukin-1β);apoptosis;inflammatory response

摘要：该研究探究藁本内酯衍生物(LIGc)对IL-1β(10 ng/mL)诱导大鼠软骨细胞凋亡和炎症的作用及机制。将大鼠软骨细胞分为Control组、IL-1β组及LIGc高、中、低剂量组。除Control组外,其余组均采用IL-1β诱导建立软骨细胞炎症模型, LIGc高、中、低剂量组分别加入0.4、0.2、0.1μmol/mL的LIGc干预24 h。CCK-8检测LIGc对大鼠软骨细胞活性的影响;Hoechst 33258染色观察大鼠软骨细胞凋亡情况;Western blot检测细胞中Bcl-2、Caspase-3、TLR4、NF-κB p65蛋白表达情况;RTq PCR检测COX-2、HMGB1 mRNA的表达水平。研究发现不同浓度LIGc对大鼠软骨细胞的存活率无显著影响;与Control组相比, IL-1β组细胞凋亡水平明显升高;Caspase-3蛋白表达水平显著升高(P<0.01), Bcl-2蛋白表达水平显著降低(P<0.01)。COX-2、HMGB1 mRNA表达水平均显著升高(P<0.01);TLR4、NF-κB p65蛋白表达水平显著升高(P<0.01)。LIGc干预使得细胞活力显著升高并抑制细胞凋亡, Caspase-3蛋白表达水平显著降低(P<0.01), LIGc中、高剂量组Bcl-2蛋白表达水平显著升高(P<0.01);COX-2、HMGB1基因表达水平均显著降低(P<0.01)。TLR4、NF-κB p65蛋白表达水平显著降低(P<0.01)。因此,LIGc能够抑制IL-1β所致的软骨细胞凋亡和炎症反应,其作用机制可能与抑制TLR4/NF-κB通路相关。
This study investigated the effect and mechanism of LIGc(ligustilide cycloprolactam)on apoptosis and inflammation of rat chondrocytes induced by IL-1β(10 ng/mL).Rat chondrocytes were divided into Control group,IL-1βgroup and LIGc high-dose,medium-dose and low-dose groups.Chondrocyte inflammation model was established by IL-1βinduction in other groups except Control group.LIGc high-dose,medium-dose and low-dose groups were treated with 0.4,0.2 and 0.1μmol/mL LIGc for 24 h respectively.The effect of LIGc on the activity of rat chondrocytes was detected by CCK-8.The apoptosis of rat chondrocytes was observed by Hoechst 33258 staining.The protein expressions of Bcl-2,Caspase-3,TLR4 and NF-κB p65 were detected by Western blot.The expression levels of COX-2 and HMGB1 mRNA were detected by RT-qPCR.It was found that different concentrations of LIGc had no significant effect on the survival rate of rat chondrocytes.Compared with the Control group,the apoptosis of IL-1βgroup was significantly increased.The expression level of Caspase-3 protein was significantly increased(P<0.01),and the expression level of Bcl-2 protein was significantly decreased(P<0.01).The expression levels of COX-2 and HMGB1 genes were significantly increased(P<0.01);the expression levels of TLR4 and NF-κB p65 protein were significantly increased(P<0.01).After LIGc intervention,cell viability was significantly increased,cell apoptosis was inhibited,and the expression level of Caspase-3 protein was significantly decreased(P<0.01),the expression level of Bcl-2 protein LIGc(0.4,0.2μmol/mL)was significantly increased(P<0.01);the expression levels of COX-2 and HMGB1 genes were significantly decreased(P<0.01).The expression levels of TLR4 and NF-κB p65 protein were significantly decreased(P<0.01).Therefore,LIGc can inhibit the apoptosis and inflammatory response of chondrocytes induced by IL-1β,and its mechanism may be related to the inhibition of TLR4/NF-κB pathway.