目的 探讨非编码长链 RNA ANRIL（lncRNA-ANRIL）通过调控miR‐181b 介导磷酸酶及张力蛋白同源物基因（PTEN）对冠状动脉粥样硬化性心脏病（冠心病）心肌损伤影响的机制。方法 纳入2023年10月—2024年6月广州市第一人民医院30例确诊为冠心病的患者为观察组, 另选择同期本院体检中心30名健康者为对照组,检测两组研究者血压指标、血脂指标以及血清 lncRNA-ANRIL、miR-181b、PTEN水平, 并比较检测结果。结果 两组的性别、年龄、BMI、吸烟、高血压一般资料对比差异无统计学意义（P>0.05）; 观察组收缩压、舒张压水平以及总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平均高于对照组,而高密度脂蛋白胆固醇则低于对照组（P<0.05）; 观察组血清 lncRNA ANRIL Exon 1-2、lncRNA ANRIL Exon 17-18相对表达水平以及PTEN水平低于对照组（t=12.623、7.741、8.231, P=0.001）, 而miR-181b水平则高于对照组（t=37.250, P=0.001）。结论 相较于正常人群, 冠心病患者血清lncRNA-ANRIL和PTEN水平明显降低,而miR-181b水平升高,提示lncRNA-ANRIL可通过调控miR-181b来调节PTEN的表达, 从而影响冠心病心肌损伤的过程。

Objective To explore the mechanism of competitive binding of non coding long stranded RNA ANRIL（lncRNA-ANRIL）to miR-181b to mediate phosphatase and tensin homolog gene（PTEN）on myocardial injury in coronary heart disease．Methods Thirty patients diagnosed with coronary heart disease in our hospital from October 2023 to June 2024 were included as the observation group,and another 30 individuals from physical examination center during the same period were selected as the control group．Blood pressure indicators,blood lipid indicators, and serum levels of lncRNA-ANRIL, miR-181b, and PTEN were measured in the two groups of patients, and the test results were compared．Results There was no significant difference between the two groups in terms of gender, age, BMI, smoking and hypertension（P>0.05）．The levels of systolic blood pressure（SBP）, diastolic blood pressure（DBP）, total cholesterol（TC）, triglycerides（TG）, and low-density lipoprotein cholesterol（LDL-C） in the observation group were higher than those in the control group,while high-density lipoprotein cholesterol（HDL-C） was lower than that in the control group（P<0.05）．The relative expression levels of lncRNA-ANRIL Exon 1-2, Exon 17-18, and PTEN levels in the observation group were lower than those in the control group（t=12.623, 7.741, 8.231, P=0.001）, while the level of miR-181b was higher than that in the control group（t=37.250, P=0.001）．Conclusions Compared with healthy individuals, serum levels of lncRNA-ANRIL and PTEN are significantly reduced in patients with coronary heart disease, while miR-181b levels are elevated, indicating that lncRNA ANRIL can regulate PTEN expression by miR-181b, thereby affecting the process of myocardial injury in coronary heart disease．

目的 探究超声-微泡介导的miR-128通过调节PTEN对乳腺癌细胞阿霉素耐药的影响。方法 qPCR检测miR-128在乳腺癌细胞系中的表达,并利用结合微泡的miR-128质粒(质粒+超声+SF6微泡)转染细胞,探究超声-微泡介导的miR-128对乳腺癌细胞阿霉素耐药的影响。CCK8实验检测乳腺癌细胞的活性;qPCR检测过表达miR-128后对PTEN的影响和对乳腺癌细胞阿霉素耐药的影响。结果 miR-128在阿霉素耐药乳腺癌细胞中低表达;过表达miR-128能够增加乳腺癌细胞对阿霉素的敏感性,超声-微泡介导的miR-128进一步增强了乳腺癌细胞对阿霉素的敏感性;miR-128通过调节PTEN从而促进乳腺癌细胞对阿霉素耐药。结论 miR-128过表达可以增强乳腺癌对阿霉素的敏感性,超声-微泡介导的miR-128进一步增强了乳腺癌细胞对阿霉素的敏感性,本研究为乳腺癌阿霉素耐药的治疗提供了新的分子靶标和治疗途径。

Objective To explore the effect of ultrasound-microbubble mediated miR-128 on doxorubicin resistance in breast cancer cells by regulating PTEN. Methods Quantitatine PCR (qPCR) was used to detect the expression of miR-128 in breast cancer cell lines, and the ultrasound-microbubble combined miR-128 plasmid(plasmid+ultrasound+SF6 microbubbles) was used to transfect the cells to explore the effects of ultrasound-microbubble mediated miR-128 on doxorubicin resistance in cancer cells. The CCK8 experiment was used to detect the activity of breast cancer cells; qPCR was used to detect the effect of overexpression of miR-128 on PTEN and the effect on doxorubicin resistance of breast cancer cells. Results miR-128 was under-expressed in doxorubicin-resistant breast cancer cells; overexpression of miR-128 increased the sensitivity of breast cancer cells to doxorubicin,ultrasound-microbubble mediated miR-128 further enhanced breast cancer cells sensitivity to doxorubicin; miR-128 promote resistance to doxorubicin in breast cancer cells by regulating PTEN. Conclusion Overexpression of miR-128 could enhance the sensitivity of breast cancer to doxorubicin. Ultrasound-microbubble mediated miR-128 further enhanced the sensitivity. This study provided a treatment for doxorubicin resistance in breast cancer with new molecular targets and therapeutic approaches.