Reversal of lipopolysaccharide-induced cardiomyocyte apoptosis via α7nAChR by dexmedetomidine.

This study aims to analyze the reversal of lipopolysaccharide (LPS)-induced cardiomyocyte apoptosis via α7nAChR by dexmedetomidine (Dex), so as to provide references for clinical treatment of myocardial disorders in the future. First, the research team divided cardiomyocytes (H9C2) were divided into a control group (normal culture), an LPS group (LPS-induced injury model), and an experimental group (pretreated with Dex before LPS induction). Subsequently, lactate dehydrogenase (LDH) and cell activity were detected, and the research team found that the LDH content of the control, experimental and LPS groups were in ascending order (P<0.05). The cell viability decreased and apoptosis increased in the LPS group, with cells mainly concentrating in the G2-M phase; the viability increased and apoptosis decreased in the experimental group, with blocked G1-G0 phase (P<0.05). This demonstrates that Dex can reverse LPS-induced apoptosis in cardiomyocytes. Subsequently, the research group also detected the expression of α7nAChR and NF-κB/AKT pathway, and it was seen that the expression of α7nAChR in the LPS group was higher than that in the control group, with activated NF-κB/AKT pathway; the α7nAChR expression in the experimental group was further elevated, but the NF-κB/AKT pathway was inhibited (P<0.05). The effects of Dex on cardiomyocytes were seen to be related to the α7nAChR and NF-κB/AKT pathways.

LncRNA FOXD3-AS1 aggravates myocardial ischemia/reperfusion injury by inactivating the Redd1/AKT/GSK3ß/Nrf2 signaling pathway via the miR-128/TXNIP axis.

Long noncoding RNA forkhead box D3-antisense RNA 1 (FOXD3-AS1) is associated with cardiovascular diseases, but its roles in myocardial ischemia/reperfusion (I/R) injury and the related signaling pathway have not been fully reported. We aimed to investigate the roles and mechanism of action of FOXD3-AS1 in myocardial I/R injury. An in vivo myocardial I/R injury mouse model and an in vitro hypoxia/reoxygenation (H/R) cardiomyocyte model was established. Quantitative reverse transcription-polymerase chain reaction, western blotting, and immunofluorescent assays were performed to examine the expression levels of FOXD3-AS1, microRNA (miR)-128, thioredoxin-interacting protein/regulation of development and DNA damage response 1/protein kinase B/glycogen synthase kinase 3ß/nuclear factor erythroid 2-related factor 2 (TXNIP/Redd1/AKT/GSK3ß/Nrf2) pathway-related proteins and apoptosis-related proteins. The interactions between FOXD3-AS1 and miR-128 and miR-128 and TXNIP were analyzed by Spearman's correlation test, predicted by ENCORI, and verified by dual-luciferase reporter assay. In addition, the levels of cardiac injury markers and oxidative stress markers were evaluated by corresponding kits. Cell Counting Kit-8 assays and flow cytometry were performed to assess cell viability and apoptosis. Hematoxylin and eosin staining was applied to observe the effect of FOXD3-AS1 on the morphology of myocardial I/R injured tissues. The results showed that the FOXD3-AS1 and TXNIP were highly expressed, whereas miR-128 was expressed at low levels in I/R myocardial tissues and H/R-induced H9c2 cells. FOXD3-AS1 directly targeted miR-128 to reduce its expression. TXNIP was confirmed as a downstream target of miR-128. Knockdown of FOXD3-AS1 led to the alleviation of I/R injury in vivo and in vitro. FOXD3-AS1 enhanced the expression of TXNIP by sponging miR-128, which inhibited the Redd1/AKT/GSK3ß/Nrf2 pathway. Both inhibition of miR-128 and overexpression of TXNIP reversed the cardioprotective effect of FOXD3-AS1 small interfering RNA in H/R-induced H9c2 cells.

The risk factors for delayed recovery in patients with cardiopulmonary bypass: Why should we care?

ABSTRACT: Cardiopulmonary bypass (CPB) is very commonly performed among the cardiovascular surgeries, and delayed recovery (DR) is a kind of serious complications in patients with CPB. It is necessary to assess the risk factors for DR in patients with CPB, to provide evidence into the management of CPB patients.Patients undergoing CPB in our hospital from January 2018 to March 2020 were included. Cases that consciousness has not recovered 12 hours after anesthesia were considered as DR. The preoperative and intraoperative variables of CPB patients were collected and analyzed. Logistic regressions were conducted to analyze the potential influencing factor.A total of 756 CPB patients were included, and the incidence of DR was 9.79%. There were significant differences on the age, aspartate aminotransferase (AST), glutamic pvruvic transaminase (ALT), blood urea nitrogen (BUN), and serum creatinine (SCr) between patients with and without DR (all P < .05); there were no significant differences in the types of surgical procedure (all P > .05); there were significant differences on the duration of CPB, duration of aortic cross clamp (ACC), duration of surgery, minimum nasopharyngeal temperature, and transfusion of packed red blood cells between patients with and without DR (all P < .05). Logistic regression analysis indicated that duration of CPB ≥132 minutes (odds ratio [OR] 4.12, 1.02-8.33), BUN ≥9 mmol/L (OR 4.05, 1.37-8.41), infusion of red blood cell suspension (OR 3.93, 1.25-7.63), duration of surgery ≥350 minutes (OR 3.17, 1.24-5.20), age ≥6 (OR 3.01, 1.38-6.84) were the independent risk factors for DR in patients with CPB (all P < .05).Extra attention and care are needed for those CPB patients with duration of CPB ≥132 minutes, BUN ≥9 mmol/L, infusion of red blood cell suspension, duration of surgery ≥350 minutes, and age ≥60.