Abstract

The possibility of micro ribonucleic acid-29b (miR-29b) regulating blood pressure and cardiac function in the rat model of hypertension was investigated. Sixty rat models of hypertension were established and randomly divided into the lentivirus group (n=20), the negative lentivirus group (n=20) and the control group (n=20). Rats in the lentivirus group were injected with the recombinant lentivirus, and those in the negative lentivirus and control groups were injected with the negative control virus and infection enhancement solution, respectively. The systolic pressure of rats was monitored using the tail-cuff method, and changes in the cardiac function of rats were evaluated via high-frequency ultrasound. At 3 weeks after virus infection, rats were weighed and sacrificed, the heart was taken and the left ventricular mass index was calculated. Moreover, the expression of miR-29b in myocardial tissues was detected via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The systolic pressure in the lentivirus group was significantly decreased compared with those in the negative lentivirus and control groups (P<0.05). In the lentivirus group, the systolic pressure was significantly reduced after virus transfection (P<0.05), and there were also statistically significant differences in ultrasonic measurement indexes (LVPWT, IVST, LVEDD and LVESD) (P<0.05). LVPWT was remarkably decreased at 5 weeks and 6 weeks compared with that in the previous week, and it was lower than those in the other two groups (all P<0.05). After virus transfection, IVST in the lentivirus group showed a decreasing trend, which was obviously lower than those in the other two groups (P<0.05). After virus transfection, LVEDD in the lentivirus group increased gradually, and was higher than that in the other two groups. The expression of miR-29b was upregulated in the lentivirus group compared with those in the other two groups (P<0.05). The overexpression of miR-29b can reduce the blood pressure and significantly improve the cardiac function of hypertension rats.

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