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A high-glucose environment is involved in the progression of diabetes mellitus (DM). This study aims to explore the regulatory effects of quercetin (QUE) on autophagy and apoptosis after myocardial injury in rats with DM. The type 2 DM rat models were constructed using low-dose streptozotocin (STZ) treatment combined with a high-carbohydrate (HC) diet in vivo. Compared with the control group, the body weight was decreased, whereas blood pressure, blood glucose, and the LVW/BW ratio were increased in the diabetic group. The results showed that the myocardial fibers were disordered in the diabetic group. Moreover, we found that the myocardial collagen fibers, PAS-positive cells, and apoptosis were increased, whereas the mitochondrial structure was destroyed and autophagic vacuoles were significantly reduced in the diabetic group compared with the control group. The expression levels of autophagy-related proteins LC3 and Beclin1 were decreased, whereas the expression levels of P62, Caspae-3, and Bax/Bcl-2 were increased in the diabetic group in vitro and in vivo. Moreover, QUE treatment alleviated the cellular oxidative stress reaction under high-glucose environments. The results of immunoprecipitation (IP) showed that the autophagy protein Beclin1 was bound to Bcl-2, and the binding capacity increased in the HG group, whereas it decreased after QUE treatment, suggesting that QUE inhibited the binding capacity between Beclin1 and Bcl-2, thus leading to the preservation of Beclin1-induced autophagy. In addition, the blood pressure, blood glucose, and cardiac function of rats were improved following QUE treatment. In conclusion, QUE suppressed diabetic myocardial injury and ameliorated cardiac function by regulating myocardial autophagy and inhibition of apoptosis in diabetes through the AMPK/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To investigate the expression of serum transforming growth factor β2(TGF-β2) and galectin-2 (Galectin-2) in patients with atrial fibrillation and its clinical significance. Methods: A total of 150 inpatients in the Department of Cardiology of the First Affiliated Hospital of Bengbu Medical College from January 2019 to June 2019 were selected, including 84 patients in the paroxysmal atrial fibrillation group, 66 patients in the persistent atrial fibrillation group, and 120 patients with sinus rhythm excluding atrial fibrillation who were hospitalized during the same period were selected as the control group. Blood routine, biochemical routine and cardiac ultrasonic morphological examination were improved after admission. In addition, the serum levels of TGF-β2 and Galectin-2 in each group were detected by Elisa and Western Blot, and the differences and clinical significance of TGF-β2 and Galectin-2 in different groups were statistically analyzed. The correlation between TGF-β2, Galectin-2 and left atrial end-diastolic diameter (LAD) was further determined by Pearson correlation analysis. By means of binary logistics regression analysis, the factors affecting atrial fibrillation were obtained. Results: Compared with the control group, age and LAD in atrial fibrillation group were significantly increased (P<0.05). The serum concentrations of TGF-β2 and galectin-2 in persistent af group were significantly increased compared with those in paroxysmal af group and control group (P<0.05), while those in control group were significantly decreased compared with paroxysmal AF group (P<0.05). Pearson correlation analysis showed that TGF-β2 and Galectin-2 concentrations were significantly positively correlated with LAD size in the experimental group (P<0.05). Binary logistic regression analysis showed that TGF-β2, galectin-2 and LAD were risk factors for atrial fibrillation (P<0.05). Conclusion: TGF-β2 and Galectin-2 are closely related to the occurrence and development of atrial fibrillation. Both TGF-β2 and Galectin-2 were positively correlated with LAD. The three have a synergistic effect on the occurrence and progression of atrial inflammatory fibrosis in patients with ATRIAL fibrillation, jointly promoting mechanical and electrical remodeling of atrial, and can be used as risk factors to evaluate the occurrence and progression of atrial fibrillation. [ABSTRACT FROM AUTHOR]

The coronavirus disease 2019(COVID-19) caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) is spreading around the world,while the specific drugs targeting SARS-CoV-2 are still under development.On the basis of the biological characteristics of SARS-CoV-2 and the key protein(spike protein) for viral replication,this paper introduces the research progress in the action sites of related drugs,providing information for clinical application and ideas for development of anti-SARS-CoV-2 drugs.