التفاصيل البيبلوغرافية
| العنوان: |
长链非编码 RNA H19 抑制地塞米松致成骨细胞凋亡的作用. (Chinese) |
| العنوان البديل: |
Effects of long non-coding RNA H19 on apoptosis of osteoblasts induced by dexamethasone. (English) |
| المؤلفون: |
杨慧霞, 白志刚, 迟宏扬, 马天龙, 马胜超, 姜怡邓 |
| المصدر: |
Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 10/8/2023, Vol. 27 Issue 28, p4513-4518, 6p |
| مصطلحات موضوعية: |
LINCRNA, FEMUR head, PROTEIN expression, CELLULAR signal transduction, FLOW cytometry, IDIOPATHIC femoral necrosis |
| الملخص (بالإنجليزية): |
BACKGROUND: The pathogenesis of steroid-induced osteonecrosis of femoral head is still unclear, which is closely related to osteoblast apoptosis. OBJECTIVE: To investigate the role of long non-coding RNA H19 (lncRNA H19) in dexamethasone-induced osteoblast apoptosis. METHODS: Mouse osteoblasts (MC3T3-E1) were cultured and divided into control group (no treatment) and dexamethasone group (treated with 1 μmol/L dexamethasone for 24 hours). Western blot was used to detect the protein expression levels of Bax, Bcl-2, and p-ERK1/2/ERK1/2. Flow cytometry and cell viability staining were used to detected cell apoptosis. qRT-PCR was performed to detect the expression of lncRNA H19. lncRNA H19 negative control plasmid (ad-NC) and lncRNA H19 overexpression plasmid (ad-lncRNA H19) were transfected into MC3T3-E1 cells, followed by 24 hours of dexamethasone intervention. Cell apoptosis of MC3T3-E1 was detected using cell viability staining, western blot assay, and flow cytometry. MC3T3-E1 cells were treated with MAPK-ERK pathway inhibitor (PD98059) for 24 hours and western blot was used to detect the protein expression levels of Bax and Bcl-2. RESULTS AND CONCLUSION: Compared with the control group, the apoptotic rate of MC3T3-E1 cells was increased in the dexamethasone group (P < 0.01), while the expression of lncRNA H19 was decreased (P < 0.01) and the MAPK/ERK signaling pathway was inhibited. Up-regulation of lncRNA H19 in MC3T3-E1 cells reduced the apoptosis of cells (P < 0.01) and activated the MAPK/ERK signaling pathway. MC3T3-E1 cells treated with dexamethasone+ad-lncRNA H19+PD98059 showed an increase in the expression of Bax (P < 0.01) and a decrease in the expression of Bcl-2 (P < 0.01) compared with the cells treated with dexamethasone+ad-lncRNA H19. These findings indicate that overexpression of lncRNA H19 can inhibit dexamethasone-induced apoptosis in MC3T3-E1 cells by activating the MAPK-ERK signaling pathway. [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): |
背景: 激素性股骨头坏死的发病机制尚不清楚, 成骨细胞凋亡与其关系密切. 目的: 探讨长链非编码RNA H19(long Non-Coding RNA H19, lncRNA H19)在地塞米松促进成骨细胞凋亡中的作用. 方法: 培养小鼠成骨细胞MC3T3-E1, 分为对照组(不处理)和地塞米松组(1 μmol/L 地塞米松处理24 h), 采用Western blot检测各组细胞Bax、 Bcl-2和细胞外调节蛋白激酶(p-ERK1/2/ERK1/2)蛋白的表达, 流式细胞术和细胞活力染色检测细胞凋亡情况, qRT-PCR检测lncRNA H19的表 达. 转染lncRNA H19阴性对照(ad-NC)和lncRNA H19过表达质粒(ad-lncRNA H19)并给予地塞米松干预24 h后, 采用细胞活力染色、Western blot和流式细胞术检测MC3T3-E1细胞凋亡情况; 使用MAPK-ERK通路抑制剂PD98059处理MC3T3-E1细胞24 h, Western blot检测各组细胞Bax 和Bcl-2蛋白的表达. 结果与结论: ①与对照组相比, 地塞米松组MC3T3-E1细胞凋亡率升高, lncRNA H19相对表达降低(P < 0.01), MAPK/ERK信号通路被抑制; ②上调MC3T3-E1细胞lncRNA H19后, 细胞凋亡率降低(P < 0.01), MAPK/ERK信号通路被激活; ③与地塞米松+ad-lncRNA H19组相比, 地塞米 松+ad-lncRNA H19+PD98059组细胞Bax蛋白表达增加(P < 0.01), Bcl-2蛋白表达降低(P < 0.01); ④提示过表达lncRNA H19通过激活MAPK-ERK信 号通路抑制地塞米松诱导的MC3T3-E1细胞凋亡. [ABSTRACT FROM AUTHOR] |
|
Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
