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| Effects of LncRNA KCNQ1OT1 on Myocardial Injury in Diabetic Cardiomyopathy Rats by Adjusting miR-324-5p |
| HUANG Liu, WEI Huiqing, YAN Jie, et al |
| The Second Hospital of Hebei Medical University, Hebei Shijiazhuang 050004, China |
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Abstract Objective: To explore the effect of long non-coding RNA (LncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) on myocardial damage in diabetic cardiomyopathy (DCM) rats by adjusting microRNA-324-5p (miR-324-5p). Methods: A DCM rat model was established by feeding high glucose and high-fat diet combined with intraperitoneal injection of streptozotocin (STZ). The rats were stochastically divided into DCM group, sh-NC group, sh-KCNQ1OT1 group, sh-KCNQ1OT1+antiagomir-NC group, and sh-KCNQ1OT1+miR-324-5p antiagomir group, each had 12 rats. Another 12 healthy rats were designated as control group and fed with regular food. The blood glucose meter was used to detect the fasting blood glucose (FBG) in each group. Echocardiography was used to detect cardiac function parameters in each group. ELISA was performed to detect the BNP and cTnⅠ in serum. HE staining was performed to observe the pathological changes of myocardial tissue. TUNEL staining was used to detect the apoptosis status of myocardial tissue cells. QRT-PCR was performed to detect the LncRNA KCNQ1OT1 and miR-324-5p in the myocardial tissues. In addition, dual luciferase reporter gene assay was used to detect the targeting relationship between LncRNA KCNQ1OT1 and miR-324-5p. Results: The DCM group had conspicuously lower LVFS, LVEF, LVSP, and miR-324-5p, and conspicuously higher LVSD, FBG, BNP, cTnⅠ, cell apoptosis rate, and LncRNA KCNQ1OT1 than control group (P<0.05). The sh-KCNQ1OT1 group had conspicuously higher LVFS, LVEF, LVSP, and miR-324-5p, and conspicuously lower LVSD, FBG, BNP, cTnⅠ, cell apoptosis rate, and LncRNA KCNQ1OT1 than the DCM and sh-NC groups (P<0.05). The sh-KCNQ1OT1+miR-324-5p antiagomir group had conspicuously lower LVFS, LVEF, LVSP, and miR-324-5p, and conspicuously higher LVSD, FBG, BNP, cTnⅠ, cell apoptosis rate, and LncRNA KCNQ1OT1 than the sh-KCNQ1OT1 group and sh-KCNQ1OT1+antiagomir-NC (P<0.05). And the dual luciferase reporter gene experiment confirmed that LncRNA KCNQ1OT1 could target the inhibition of miR-324-5p (P<0.05). Conclusion: Interference with LncRNA KCNQ1OT1 can target upregulation of miR-324-5p to improve myocardial damage in DCM rats.
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