In the state of acute myocardial ischemia, miRNA expression can regulate related genes and proteins, reduce myocardial cell damage, and thus play a protective role in the myocardium. However, the specific mechanism still needs to be further explored. Recent studies have found that the opening of the mitoKATP channel can regulate mitochondrial autophagy, and the initiation of miRNA-DNA methylation plays a regulatory role in inducing cell autophagy. The applicant research team previously found that Qishen Yiqi Dropping Pills could significantly improve myocardial ischemia by mediating MitokATP channels to regulate mitochondrial autophagy., and animal experiments have confirmed that miR-155 plays a significant role in the aspect of autophagy regulates, inflammatory reaction and Vascular smooth muscle cell migration. Therefore, the applicant innovatively proposed that Qishen Yiqi Dropping Pills can regulate miRNA155-DNA methylation to mediate the opening of mitoKATP, thereby regulating mitochondrial autophagy and improving myocardial ischemia. In this paper, the association between mitochondrial autophagy and oxidative stress injury after myocardial ischemia was described, and the possible mechanism of Qisen Yiqi dropping pills regulating mitochondrial autophagy by regulating miRNA155-DNA methylation to mediate MitokATP to improve myocardial ischemia reperfusion injury was discussed, so as to provide theoretical ideas for related research.

Objective: To investigate the effects of Qishen Yiqi dropping pills serum on KATP channel opening and PI3K/AKT signaling pathway of hypoxic/reoxygenated H9C2 cardiocytes. Methods: H9C2 cardiocytes cultured in vitro were randomly divided into five groups, A: H9C2 cell group B: H9C2 cells +H2O2 model group C:H9C2 cells +H2O2 model + Qishen Yiqi group D:H9C2 cells +H2O2 model + Qishen Yiqi +wort group E:H9C2 cells +H2O2 model + Qishenyiqi +5-HD group, the drug intervention is according to the corresponding conditions. CCK-8 method was used to detect the cell activity of each group; Western blot was used to detect the expression of AKT and P-Akt proteins in myocardial cells in each group. The current was recorded by the standard patch clamp whole cell recording method, and the current was collected and analyzed by Pclamp6.0 software. Results: CCK-8 test results showed that compared with group A, the activity of myocardial cells in group B was significantly decreased, and the difference was statistically significant (P<0.01); compared with group B, the difference in group C was statistically significant (P<0.01); compared with C, cardiomyocyte activity in D and E group were significantly decreased, and the difference was statistically significant (P<0.05); WB results showed that compared with A, p-Akt protein expression in B, C, D and E groups were significantly decreased, and the difference was statistically significant (P< 0.01); compared with group B, p-Akt protein expression in C, D and E group were significantly increased, and the difference was statistically significant (P< 0.01),but there was no significant difference in AKT expression among groups (P>0.05); The results of whole cell patch clamp experiment showed that the outward current of B was significantly increased compared with that of A, and the difference between groups was statistically significant (P<0.01); compared with group B, cardiomyocytes in group C further increased the outward current, and the difference between groups was statistically significant (P<0.01); compared with C, the current of D and E group were significantly decreased, with statistical significance between groups (P<0.01). Conclusion: QishenYiqi dropping pills can protect cardiomyocytes by activating p-Akt protein expression and KATP channel opening in H9C2 cardiomyocytes.

目的 探讨扶阳强心方对慢性心力衰竭(CHF)大鼠心肌纤维化及转化生长因子(TGF)-β1/Smad信号通路表达的影响.方法 将40只大鼠随机分为模型组(M组)、西药组(X组)、扶阳强心方灌胃组(Z组)、假手术对照组(K组),每组10只.除K组外,其他3组采用腹主动脉缩窄法制作CHF大鼠模型.造模成功后,Z组、X组分别给予扶阳强心方中药、卡托普利混悬液灌胃,M组与K组给予生理盐水10 mL/kg灌胃.灌胃8周后,观察4组心肌细胞形态,并检测4组大鼠心肌收缩功能,血浆脑利钠肽(BNP)、肌酸激酶水平,心肌组织TGF-β1、Smad3和Smad7蛋白的相对表达水平.结果 病理学结果显示,Z组和X组大鼠的部分心肌纤维呈波浪状,心肌细胞肿胀较M组减轻.灌胃后,与M组相比,其他3组的左心室收缩末期内径、左心室舒张末期内径均减小而左心室射血分数(LVEF)升高,血浆BNP和肌酸激酶水平降低,TGF-β1蛋白相对表达水平降低而Smad7蛋白相对表达水平升高(均P<0.05);Z组的LVEF高于X组(P<0.05),而两组间其他指标差异均无统计学意义(均P>0.05).结论 扶阳强心方可抑制CHF大鼠的心肌纤维化,并可改善心肌收缩功能,其作用机制可能与调节TGF-β1/Smad信号通路的表达有关.

Objective: To study the correlation between plasma lipopolysaccharide and coronary atherosclerotic heart disease risk factors and plaque stability. Methods: 136 patients with unstable angina pectoris who underwent coronary angiography and intravascular ultrasound were selected from the First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine. According to the results of IVUS, they were divided into stable plaques (stable plaques, SP) group of 72 patients With 64 cases in the Unstable plaques (UP) group, venous blood was drawn from the two groups of patients for blood lipid and lipopolysaccharide index detection, and the general baseline data of the two groups were recorded; the structural characteristics of the intravascular ultrasound plaques in the two groups were analyzed. To study the influencing factors of unstable plaques, the correlation between lipopolysaccharide and plaque structural characteristics, and the diagnostic efficacy of unstable plaques. Results: The expression levels of cholesterol, low-density lipoprotein, and LPS in the UP group were higher than those in the SP group (P<0.05), and the high-density lipoprotein expression levels were lower than those in the SP group (P=0.035); and the intravascular ultrasound structure of the plaque was UP The lipid pool area, the ratio of lipid pool to plaque area, the plaque eccentricity index, and the maximum plaque thickness of the group were higher than those of the SP group (P<0.05), and the minimum plaque thickness was smaller than that of the SP group and the difference was statistically significant (P<0.05); LPS was positively correlated with cholesterol, low-density lipoprotein, lipid pool area, ratio of lipid pool to plaque area, plaque eccentricity index, and maximum plaque thickness by Pearson correlation test (P<0.05) , Is negatively correlated with high-density lipoprotein (P=0.021); LPS is a risk factor for coronary plaque stability, and HDL is a protective factor for coronary plaque stability by binary logistic regression test. The difference is statistically significant Scientific significance (P=0.049, P=0.002); LPS diagnosis of coronary atherosclerotic plaque stability ROC area under the curve (AUC) is 0.889, 95％ CI is (0.805, 0.974), the best diagnosis point is 57.485 mg /L, the sensitivity is 80.60％, and the specificity is 73.70％. Conclusion: Plasma lipopolysaccharide is a risk factor of unstable plaque, which has certain diagnostic value for coronary artery plaque, and can be used as a quantitative diagnostic index of plaque vulnerability.