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| 艾塞那肽通过p38MAPK通路对成骨细胞促增殖和抗凋亡的作用研究 |
| Study on the Effects of Exenatide on Proliferation and Anti-apoptosis of Osteoblasts via p38MAPK Pathway |
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| DOI：10.3969/j.issn.1006-7108.2020.06.016 |
| 中文关键词: 骨质疏松 成骨细胞 艾塞那肽 p38MAPK通路 |
| 英文关键词:osteoporosis osteoblasts exenatide p38MAPK pathway |
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| 中文摘要: |
| 目的 探讨艾塞那肽通过p38MAPK通路对成骨细胞促增殖和抗凋亡的作用机制。方法 将小鼠成骨细胞 MC3T3-E1 Subclone 14分为对照组、艾塞那肽组、棕榈酸钠组、棕榈酸钠组+艾塞那肽组，分别使用相应试剂培养48 h。通过CCK-8和流式细胞术检测细胞活力与凋亡。通过Western blot检测细胞中P38MAPK、Cyclin D1、Caspase-3的蛋白水平。结果 艾塞那肽对正常细胞活力无显著影响（P>0.05），棕榈酸钠组的细胞活力显著低于对照组（P<0.01），艾塞那肽+棕榈酸钠组的细胞活力显著高于棕榈酸钠组（P<0.01）；艾塞那肽对正常细胞凋亡无显著影响（P>0.05），棕榈酸钠组的细胞凋亡率显著高于对照组（P<0.01），艾塞那肽+棕榈酸钠组的细胞凋亡率显著低于棕榈酸钠组（P<0.01）；艾塞那肽对正常细胞中 P38MAPK、Cyclin D1和Caspase-3蛋白水平无明显影响（P>0.05），棕榈酸钠组的P38MAPK和Caspase-3显著高于对照组而Cyclin D1显著低于对照组（P<0.01），艾塞那肽+棕榈酸钠组的P38MAPK和Caspase-3显著低于棕榈酸钠组而Cyclin D1显著高于棕榈酸钠组（P<0.01）。结论 艾塞那肽可以通过p38MAPK通路，减少Caspase-3蛋白并上调Cyclin D1蛋白的表达，抑制高脂环境下成骨细胞的凋亡并提高细胞活力。 |
| 英文摘要: |
| Objective To explore the mechanism of action of exenatide on proliferation and anti-apoptosis of osteoblasts through p38MAPK pathway.Methods Mouse osteoblast MC3T3-E1 Subclone 14 was divided into control group, exenatide group, sodium palmitate group, sodium palmitate group and exenatide group, and cultured for 48 h with corresponding reagents. Cell viability and apoptosis were detected by CCK-8 and flow cytometry. Western blot was used to detect the protein levels of P38MAPK, Cyclin D1 and Caspase-3 in cells.Results Exenatide had no significant effect on normal cell viability (P>0.05).The cell viability of the sodium palmitate group was significantly lower than that of the control group (P<0.01).The cell viability of the exenatide + palmitate group was significantly higher than that of the sodium palmitate group (P<0.01).Exenatide had no significant effect on normal cell apoptosis (P>0.05).The apoptosis rate of the sodium palmitate group was significantly higher than that of the control group (P<0.01).The apoptosis rate of the exenatide + palmitate group was significantly lower than that of the sodium palmitate group (P<0.01).Exenatide had no significant effect on normal cells (P>0.05).P38MAPK and Caspase-3 in the sodium palmitate group were significantly higher than those in the control group, and Cyclin D1 was significantly lower than the control group (P<0.01).P38MAPK and Caspase-3 in the exenatide + palmitate group were significantly lower than those in the sodium palmitate group and Cyclin D1 was significantly higher than the sodium palmitate group (P<0.01).Conclusion Exenatide can reduce Caspase-3 protein and up-regulate the expression of Cyclin D1 protein through p38MAPK pathway, inhibit osteoblast apoptosis and increase cell viability in high-fat environment. |
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