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| LncRNA SNHG1下调miR-195-5p改善软骨细胞凋亡和炎症微环境 |
| LncRNA SNHG1 down-regulates miR-195-5p to improve chondrocyte apoptosis and inflammation microenvironment |
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| DOI：10.3969/j.issn.1006.7108.2022.04.001 |
| 中文关键词: 骨关节炎 SNHG1 miR-195-5p 凋亡 炎症微环境 |
| 英文关键词:osteoarthritis SNHG1 miR-195-5p apoptosis inflammatory microenvironment |
| 基金项目:黑龙江省医药卫生科研课题（20210202050004） |
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| 中文摘要: |
| 目的 探讨长链非编码RNA小核仁RNA宿主基因1（LncRNA SNHG1）和miR-195-5p在OA凋亡和炎症微环境中的作用及相关性。方法 先检测OA患者与大鼠模型软骨组织和正常软骨组织中SNHG1和miR-195-5p的表达情况。再对体外软骨细胞进行培养，转染，建立OA细胞模型。建立大鼠OA模型，将大鼠分为对照组（n=10）、模型组（n=10）、模型组+SNHG 1干预（SNHG 1，n=10）、模型组+inhibitor干预（inhibitor，n=10）。最后收集软骨组织进行一系列细胞功能实验，研究SNHG1、miR-195-5p对OA软骨细胞凋亡、炎症、增殖的影响，并与体外实验比较。研究SNHG1和miR-195-5p的关系。注射SNHG1过表达质粒、miR-195-5p抑制剂探究对OA大鼠模型的体内影响。结果 在OA组织中SNHG1的表达下调，而miR-195-5p的表达上调（P<0.001）。调高SNHG1或敲低miR-195-5p的表达可降低OA细胞凋亡率，改善炎性微环境，恢复细胞增殖能力（P<0.05）。得出SNHG1可充当miR-195-5p的分子海绵。SNHG1促进剂、miR-195-5p抑制剂能够减弱OA大鼠模型的凋亡与炎症反应。结论 通过调节SNHG1-miR-195-5p轴，调高SNHG1或敲低miR-195-5p有利于改善软骨细胞的凋亡与炎症微环境，为OA进展机理提供了新见解。 |
| 英文摘要: |
| Objective To investigate the role and correlation of long non-coding RNA micronucleolar RNA host gene 1 and miR-195-5p in apoptosis and inflammatory microenvironment of OA. Methods Firstly, the expression of SNHG1 and Mir-195-5p in OA patients, rat model cartilage tissues and normal cartilage tissues were detected. Then chondrocytes were cultured and transfected to establish OA cell model. OA model of rats was established, and rats were divided into control group (n=10) model group (n=10) model group +SNHG 1 intervention (SNHG 1, n=10) model group + intervention (inhibitor, n=10). Finally, cartilage tissues were collected for a series of cell function experiments to study the effect of SNHG1 Mir-195-5p on the apoptosis and inflammatory proliferation of OA chondrocytes, and compared with in vitro experiments. The relationship between SNHG1 and Mir-195-5p was studied. The in vivo effect of snHG1-overexpressed plasmid Mir-195-5p inhibitor on OA model was investigated. Results We found that the SNHG1 expression was down-regulated and the miR-195-5p expression was up-regulated in OA tissue（P<0.001）. Upregulation of SNHG1 or knockdown of Mir-195-5p could reduce OA cell apoptosis rate, improve inflammatory microenvironment and restore cell proliferation ability (P<0.05). Besides, we clarified that SNHG1 could act as a molecular sponge for miR-195-5p. Finally, we found that SNHG1 promoter and miR-195-5p inhibitor could reduce apoptosis and inflammatory reaction in OA rat models. Conclusion Adjusting the SNHG1-miR-195-5p axis, increasing SNHG1 or knocking down miR-195-5p is beneficial to improving the apoptosis and inflammatory microenvironment of chondrocytes and provides new insights for the mechanism of OA progression. |
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