IntroductionThe renin-angiotensin system is associated with blood pressure regulation, inflammation, oxidative stress and insulin resistance. It can decrease intracellular oxidative stress. Stimulation with H2O2 leads to increased oxidative stress and activation of the AKT/mTOR pathway. However, the role of renin-angiotensin system inhibitors in oxidative stress-induced endothelial cell dysfunction and H2O2-induced AKT activation remains unclear.Material and methodsHuman coronary artery endothelial cells (HCAECs) were used. The cells were treated with H2O2, captopril, the AKT inhibitor MK-2206, and the AKT activator SC79, either separately, or in combination. p53 and ICAM-1 expression, and p-eNOS, p-Akt and mTOR activation were measured by Western blot. Cell viability was assessed by MTT assay. Levels of reactive oxygen species (ROS) were assayed by flow cytometry. Proliferation was monitored by BrdU labeling, while cell migration and invasion were determined by wound healing and Transwell assays, respectively.ResultsThe renin-angiotensin system inhibitor captopril reversed H2O2-induced oxidative stress and apoptosis in HCAECs. Co-treatment with captopril and the AKT inhibitor MK-2206 reduced the H2O2-induced P53 and ICAM-1 protein expression (p < 0.05). The proliferation, migration and invasion of HCAECs were significantly enhanced by co-treatment with captopril and MK-2206 (p < 0.05).ConclusionsThe study revealed the protective effect of captopril against H2O2-induced endothelial cell dysfunction through the AKT/mTOR pathway, and its enhancement of cell survival. These findings provide new insights into the protective effects of captopril and novel therapeutic approaches to treatment of cardiovascular disease.
Combining microcrystal electron diffraction (MicroED) and a cloud-based and artificial intelligence implemented crystal structure prediction (CSP) platform to support selection of a stable solid form of remdesivir in quick time.
Objective: This study investigated the clinical efficacy and value of fractional flow reserve (FFR) in guiding the treatment of borderline coronary lesions.Methods: Forty-three patients with borderline coronary lesions, as demonstrated by coronary angiography, and who had FFR measurements were selected. The patients were grouped according to FFR values. All patients were evaluated 6 months after surgery to record major adverse cardiac events (MACE [sudden cardiac death, non-fatal myocardial infarction, or revascularization]) and recurrence of angina pectoris.Results: After the 6-month follow-up, no sudden cardiac deaths or myocardial infarctions occurred in either group, and there were no statistically significant differences (P>0.05). Intergroup comparisons showed that in the groups with a FFR<0.75, the recurrence rate of angina pectoris in the PCI group was significantly lower than the drug therapy group (0.08% vs. 0.27%, P<0.05). In contrast, the recurrence rate of angina pectoris in the PCI group among the groups with a FFR<0.75 revealed no statistical significance when compared to the groups with a FFR≥0.75 (0.08% vs. 0.05%, P>0.05). The recurrence rate of angina pectoris in the simple drug therapy group among the groups with a FFR<0.75 was higher than the same groups with a FFR≥0.75 (0.27% vs. 0.05%, P<0.05). Conclusion:When coronary intervention is used to treat borderline lesions, guiding interventional therapy with measurement of FFR does not increase the incidence of adverse cardiovascular events in the short term and can better guide PCI therapy.
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