Effect of Tegretol on Oxidative Stress, Serum Inflammatory Factors, and Left Ventricular Function in AMI Patients after Emergency PCI.

To investigate the effects of tegretol on oxidative stress, serum inflammatory factors, and left ventricular function in patients with acute myocardial infarction (AMI) after emergency percutaneous coronary intervention (PCI), 70 AMI patients who received PCI in the emergency department of our hospital from January 2021 to December 2021 were collected. The patients in the control group were treated with aspirin, clopidogrel, and heparin sodium during the perioperative period, and the patients in the study group were treated with tegretol. The levels of oxidative stress, serum inflammatory factors, and left ventricular function index were compared between the two groups. The patients in the control group were treated with TT ((12.00 ± 2.05) s), APTT ((35.50 ± 4.19) s), PT ((16.60 ± 1.58) s), TT ((15.90 ± 2.14) s) APTT ((30.40 ± 3.80) s), and PT ((14.30 ± 1.45) s)) and were comparable (P > 0.05), and the difference was statistically significant (t = 8.210, 4.600, 7.010, P < 0.001). There was no comparable difference in the level of oxidative stress index before treatment (P > 0.05). After treatment, there was significant difference in MDA ((14.53 ± 2.14) mmol/L), SOD ((120.45 ± 8.17) U/L), MDA ((11.15 ± 2.02) mmol/L), and SOD ((129.86 ± 8.55) U/L) in the control group (t = 7.320, 5.099, P < 0.001). The levels of inflammatory factors in patients before treatment were not comparable (P > 0.05). After treatment, there were levels of IL-6 ((3.20 ± 1.05) ng/L), CRP ((4.80 ± 1.16) mg/L), MPO ((196.78 ± 21.51) mg/L) and TNF-α ((3.96 ± 0.80) pmol/L), IL-6 ((1.95 ± 0.80) ng/L), CRP ((3.10 ± 1.02) mg/L), MPO ((163.60 ± 21.10) mg/L), and TNF-α in a study group level ((3.05 ± 0.70) pmol/L), with statistically significant difference (t = 5.187, 6.028, 6.031, 4.689,P < 0.001). Before treatment, there was no comparable difference in the level of left ventricular function index (P > 0.05). After treatment, there was significant difference in LVEF ((46.10 ± 2.39) %) and LVDD ((52.06 ± 1.07) mm), LVEF ((56.85 ± 2.33) %), and LVDD ((48.75 ± 1.02) mm) in the control group (t = 17.640, 21.540, P < 0.001). Tegretol as an adjunctive therapy for emergency PCI patients with acute myocardial infarction can effectively improve postoperative coagulation function, reduce oxidative stress and inflammatory reaction, and improve cardiac function indicators. It has a positive clinical value.

Celastrol mitigates high glucose-induced inflammation and apoptosis in rat H9c2 cardiomyocytes via miR-345-5p/growth arrest-specific 6.

BACKGROUND: Celastrol (Cel) has been corroborated as an anti-inflammatory and anti-apoptotic agent in multiple cell damage models. However, the protective effect of Cel in high glucose (HG)-induced cardiomyocyte injury is still unclear. The present study aimed to determine whether Cel can mitigate HG-stimulated cardiomyocyte injury via regulating the miR-345-5p/growth arrest-specific 6 (Gas6) signaling pathway. METHODS: Cardiomyocytes were exposed to normal glucose (NG; 5 mmol/l) or HG (30 mmol/l) and then administered with Cel. Cell counting kit-8 and flow cytometry assays were used to detect cell proliferative activity and apoptosis. mRNA and protein expression were analyzed using a quantitative reverse transcriptase-polymerase chain reaction and western blotting, respectively. A bioinformatics algorithm and a luciferase reporter gene assay were used to determine whether Gas6 is a direct target of miR-345-5p. RESULTS: The present study confirmed the inhibitory effects of Cel in HG-induced inflammation in cardiomyocytes. Moreover, Cel exhibited the ability to antagonize HG-induced cardiomyocyte apoptosis and suppress the elevated Bax/Bcl-2 ratio elicited by HG stimulation. Intriguingly, Cel treatment revoked the HG-triggered repression of Gas6 protein expression, and Gas6 loss-of-function accelerated HG-induced cardiomyocyte apoptosis. HG-triggered up-regulation of miR-345-5p expression was depressed following Cel treatment. Importantly, we validated that Gas6 is a direct target of miR-345-5p. Transfection with miR-345-5p inhibitors restrained HG-induced release of pro-inflammatory cytokines and cell apoptosis. CONCLUSIONS: The findings of the present study demonstrate that Cel administration antagonized HG-induced cardiomyocyte apoptosis and inflammation through up-regulating Gas6 expression by restraining miR-345-5p.