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作者	单位	E-mail
董玉杰	武汉科技大学医学院湖北武汉 430080	dyj19900918@yeah.net
王晓景	武汉科技大学附属普仁医院心血管内科湖北武汉 430080
阮国然	武汉科技大学附属普仁医院心血管内科湖北武汉 430080
任浩进	武汉科技大学附属普仁医院心血管内科湖北武汉 430080
陈诗阳	武汉科技大学医学院湖北武汉 430080
黄海东	武汉科技大学附属普仁医院风湿免疫科湖北武汉 430080
张美春	武汉科技大学附属普仁医院心血管内科湖北武汉 430080

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中文摘要:

摘要目的：探讨下调miR-223表达对脓毒症心肌病（SCM）小鼠心肌的保护作用及其机制。方法：按随机数字表法将27只8-10 周龄SPF级雄性C57BL/6小鼠分配至SCM模型（0 h，6 h，12 h，18 h，24 h）时相组、Normal组、SCM组、miR-223 antagomir NC组、miR-223 antagomir组，每组3只。腹腔注射脂多糖（lipopolysaccharide, LPS）15 mg/kg构建SCM小鼠模型。miR-223 antagomir NC组与miR-223 antagomir组分别于建模前连续3天鼠尾静脉注射miR-223 antagomir NC、miR-223 antagomir预处理。采用反转录-聚合酶链反应（RT-PCR）研究SCM模型各个时相组小鼠心肌组织miR-223的表达情况。采用苏木素伊红（HE）染色法观察Normal组、SCM组、miR-223 antagomir NC组和miR-223 antagomir组小鼠心肌病理形态变化。采用酶联免疫吸附实验（ELISA）测定Normal组、SCM组、miR-223 antagomir NC组和miR-223 antagomir组小鼠血清cTnI、BNP、CK-MB、IL-6、IL-1β、TNF-α的含量并进行相关性分析。结果：SCM模型时相组小鼠随刺激时间延长，心肌组织miR-223表达水平逐渐升高。与Normal组比较，SCM组、miR-223 antagomir NC组、miR-223 antagomir组小鼠心肌组织出现不同程度损伤；血清心肌损伤标记物cTnI、BNP、CK-MB及炎性因子IL-6、IL-1β、TNF-α的表达水平均上升，差异具有统计学意义（P<0.05）；与SCM组比较，miR-223 antagomir NC组各项指标相差不大，差异均无统计学意义（P>0.05）；miR-223 antagomir组小鼠心肌组织病理损伤程度有所减轻，心肌损伤标记物cTnI、BNP、CK-MB及炎性因子IL-6、IL-1β、TNF-α水平下降，差异具有统计学意义（P<0.05）。相关性分析结果显示小鼠miR-223表达与心肌损伤标记物cTnI、BNP、CK-MB及炎性因子IL-6、IL-1β、TNF-α的表达呈正相关。结论：下调miR-223表达可通过减轻炎症反应对SCM小鼠心肌产生保护作用。

英文摘要:

ABSTRACT Objective: Investigating the protective effect and mechanisms of downregulating miR-223 expression on the myocardium of mice with septic cardiomyopathy (SCM). Methods: Using a random number table, 27 male SPF C57BL/6 mice aged 8-10 weeks were allocated into different groups: SCM model groups at different time points (0 h, 6 h, 12 h, 18 h, 24 h), Normal group, SCM group, miR-223 antagomir NC group, and miR-223 antagomir group, with 3 mice in each group. The SCM mouse model was established by intraperitoneal injection of lipopolysaccharide (LPS) at a dose of 15 mg/kg. The miR-223 antagomir NC group and miR-223 antagomir group received consecutive tail vein injections of miR-223 antagomir NC and miR-223 antagomir, respectively, for 3 days before modeling. Reverse transcription-polymerase chain reaction (RT-PCR) was used to study the expression of miR-223 in the myocardial tissue of mice in different time point groups of the SCM model. Hematoxylin-eosin (HE) staining was performed to observe the myocardial pathological changes in the Normal group, SCM group, miR-223 antagomir NC group, and miR-223 antagomir group. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of cTnI, BNP, CK-MB, IL-6, IL-1β, and TNF-α in mouse serum in the Normal group, SCM group, miR-223 antagomir NC group, and miR-223 antagomir group, and correlation analysis was conducted. Results: In the SCM model groups at different time points, the expression level of miR-223 in the myocardial tissue gradually increased with the extension of stimulation time. Compared to the Normal group, mice in the SCM group, miR-223 antagomir NC group, and miR-223 antagomir group exhibited varying degrees of myocardial damage. The expression levels of cardiac injury markers cTnI, BNP, CK-MB, and inflammatory factors IL-6, IL-1β, and TNF-α in serum were elevated, and the differences were statistically significant (P<0.05). When compared to the SCM group, there were no significant differences in various indicators between the miR-223 antagomir NC group (P>0.05). In the miR-223 antagomir group, the degree of pathological damage in the myocardial tissue was reduced, and the levels of cardiac injury markers cTnI, BNP, CK-MB, and inflammatory factors IL-6, IL-1β, and TNF-α decreased, with statistically significant differences (P<0.05). The results of correlation analysis showed that the expression of miR-223 in mice was positively correlated with the expression of cardiac injury markers cTnI, BNP, CK-MB, and inflammatory factors IL-6, IL-1β, and TNF-α. Conclusion: Downregulation of miR-223 expression can provide protection to the myocardium of SCM mice by alleviating the inflammatory response.

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