الملخص
Objective:To explore the basic biological characteristics of lncRNA B230352I09 and its role in the process of myocardial injury.Methods:We analyzed the biological characteristics of lncRNA B230352I09 on the UCSC website and predicted the possible binding protein of lncRNA B230352I09 by the catRAPID. Real-time fluorescence quantitative (RT) PCR method was applied to detect the expression of lncRNA B230352I09 in heart tissues at different time points (0, 1, 3, 7d) within 7 days after birth, the organs distribution and expression of lncRNA B230352I09 in neonatal mouse and the expression pattern of lncRNA B230352I09 in the heart of mice with myocardial injury. In addition, we constructed hypoxia model by culturing primary cardiomyocytes to detect the effect of lncRNA 230352I09 overexpression on hypoxic cardiomyocyte apoptosis by Hoechst staining kit, the effect of lncRNA B230352I09 overexpression on ROS content of hypoxic cardiomyocyte by DCFDA probe and changes in mitochondrial membrane potential of hypoxic cardiomyocytes by JC-1 Fluorescent probes.Results:Full-length of mouse B230352I09 was 663bp, located in the chr7:123031415-123066439 forward strand. RBBP6 gene was adjacent to B230352I09, which may be the target of lncRNA B230352I09 by catrapid prediction analysis. With the development of the heart, the expression level of lncRNA B230352I09 showed a gradual downward trend. The main expression organs of lncRNA B230352I09 in 1-day-old mice were heart, brain, kidney and liver. In heart tissue, lncRNA B230352I09 expression in non-cardiomyocytes was significantly less than in cardiomyocytes [ (1.0± 0.03) vs. (9.2± 3.29), P=0.013]. After myocardial injury, the expression level of lncRNA B230352I09 showed an increasing trend compared with the normal developing mice, but there was no statistical significance. Hoechst staining showed that lncRNA B230352I09 could inhibit the apoptosis of hypoxic cardiomyocytes. Detecting the content of ROS in cardiomyocytes showed that compared with the hypoxia group, the generation of ROS was significantly reduced in the lncRNA B230352I09 overexpression group ([(3.8±0.71) vs. (1.65±0.56), P=0.015]). JC-1 fluorescent probe was used to detect the mitochondrial membrane potential, and the results showed that the mitochondrial membrane potential of cardiomyocytes in the lncRNA B230352I09 overexpression group was significantly higher than that in the hypoxia group. Conclusions:In heart tissue, lncRNA B230352I09 was mainly expressed in cardiomyocytes. LncRNA B230352I09 has a protective effect in the process of myocardial injury in mice, mainly by inhibiting apoptosis of cardiomyocytes, reducing ROS production, and protecting mitochondrial membrane potential of cardiomyocytes.
الملخص
There is a high degree of information asymmetry in medical services.Public hospitals are characteristic of the nature of multi-layer principal-agent relationships.Asymmetric information can lead to inconsistent value goals between the principal and the agent,giving birth to the government regulation capture as a result.Such capture ranks a fundamental cause for diluted public welfare nature of public hospitals.To offset such capture at public hospitals calls for reconstruction of government regulation system within the framework of public hospital corporate governance at an institution level.It is also necessary to eliminate the information asymmetry and its negative results,bringing public hospitals back on track to public welfare.