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目的观察吡格列酮(Pioglitazone)对趋化素诱导成骨细胞代谢过程的影响,探讨吡格列酮改善成骨细胞凋亡的信号转导机制。方法将成骨细胞随机分组,选取适宜浓度的趋化素(Chemerin)进行诱导后,加入吡格列酮,观察成骨细胞活力变化。ELISA法检测细胞趋化蛋白1(MCP-1)、E选择素(E-selection)的影响,采用Western blot法检测成骨细胞黏附分子1(ICAM-1)、需肌醇跨膜激酶/核酸内切酶1(inositol-requiring transmembrane kinase/endonuclease 1,IRE1)、葡萄糖调节蛋白78(Glucose-regulated protein 78,GRP78)的表达变化,探究内质网应激反应在此过程中作用。结果 MTT法检测提示加入Pioglitazone后对成骨细胞活力未见明显影响;与对照组相比,成骨细胞ICAM-1、MCP-1、E-selection、IRE1、GRP78、在Chemerin组的指标较高(P<0.05),而Pioglitazone呈浓度依赖性地抑制Chemerin所诱导的上述效应,差异具有统计学意义(P<0.05),当吡格列酮浓度为20μmol/L时效果最显著。结论内质网应激可能参与趋化素诱导成骨细胞代谢中的细胞凋亡过程,吡格列酮可抑制趋化素的作用,对成骨细胞具有保护功能,其机制可能与抑制内质网应激反应相关。
Objective To observe the effect of Pioglitazone on chemokine-induced osteoblast metabolism and to explore the signal transduction mechanism of pioglitazone on osteoblast apoptosis. Methods Osteoblasts were randomly divided into groups. Chemerin was used to induce osteoblasts. Pioglitazone was added to observe the changes of osteoblast viability. The expression of MCP-1 and E-selectin was detected by ELISA. Western blot was used to detect the expression of ICAM-1, Inositol-requiring transmembrane kinase / endonuclease 1 (IRE1) and glucose-regulated protein 78 (GRP78) in human umbilical vein endothelial cells, and to explore the role of endoplasmic reticulum stress in this process. Results MTT assay showed that the addition of Pioglitazone had no significant effect on the viability of osteoblasts. Compared with the control group, ICAM-1, MCP-1, E-selection, IRE1, GRP78 and Chemerin were higher (P <0.05). However, Pioglitazone inhibited the above-mentioned effects induced by Chemerin in a concentration-dependent manner with statistical significance (P <0.05). When pioglitazone concentration was 20μmol / L, the effect was the most significant. Conclusion Endoplasmic reticulum stress may be involved in the process of chemotaxis-induced apoptosis in osteoblasts. Pioglitazone may inhibit the chemokines and protect osteoblasts. The mechanism may be related to inhibition of endoplasmic reticulum stress Response related.