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BACKGROUND: Although blood flow is restored after treatment of myocardial infarction (MI), myocardial ischemia and reperfusion (I/R) can cause cardiac injury, which is a leading cause of heart failure. Gastrodin (GAS) exerts protective effects against brain, heart, and kidney I/R. However, its pharmacological mechanism in myocardial I/R injury (MIRI) remains unclear. PURPOSE: GAS regulates autophagy in various diseases, such as acute hepatitis, vascular dementia, and stroke. We hypothesized that GAS could repair mitochondrial damage and regulate autophagy to protect against MIRI. STUDY DESIGN: Male C57BL/6 mice and H9C2 cells were subjected to I/R and hypoxia-reoxygenation (H/R) injury after GAS administration, respectively, to assess the impact of GAS on cardiomyocyte phenotypes, heart, and mitochondrial structure and function. The effect of GAS on cardiac function and mitochondrial structure in patients undergoing cardiac surgery has been observed in clinical practice. METHODS: The effects of GAS on cardiac structure and function, mitochondrial structure, and expression of related molecules in an animal model of MIRI were evaluated using immunohistochemical staining, enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy, western blotting, and gene sequencing. Its effects on the morphological, molecular, and functional phenotypes of cardiomyocytes undergoing H/R were observed using immunohistochemical staining, real-time quantitative PCR, and western blotting. RESULTS: GAS significantly reduces myocardial infarct size and improves cardiac function in MIRI mice in animal models and increases cardiomyocyte viability and reduces cardiomyocyte damage in cellular models. In clinical practice, myocardial injury was alleviated with better cardiac function in patients undergoing cardiac surgery after the application of GAS; improvements in mitochondria and autophagy activation were also observed. GAS primarily exerts cardioprotective effects through activation of the PINK1/Parkin pathway, which promotes mitochondrial autophagy to clear damaged mitochondria. CONCLUSION: GAS can promote mitophagy and preserve mitochondria through PINK1/Parkin, thus indicating its tremendous potential as an effective perioperative myocardial protective agent.

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Objective: The risk factors of postoperative pulmonary complications (PPCs) have been extensively investigated in non-cardiac surgery and non-elderly adult patients undergoing cardiac surgery. However, data on elderly patients after cardiopulmonary bypass (CPB) is limited. This study aimed to evaluate the risk factors and short-term outcomes for PPCs in elderly patients undergoing CPB procedures. Patients and Methods: Data from 660 patients who underwent CPB over a six-year period at a tertiary care hospital were collected. The primary outcome encompassed the incidence of PPCs, including re-intubation, postoperative mechanical ventilation exceeding 48 hours, pulmonary infection, pleural effusion requiring thoracic drainage, and acute respiratory distress syndrome. Missing data were managed using multiple imputation. Univariate analysis and the multiple logistic regression method were utilized to ascertain independent risk factors for PPCs. Results: Among the 660 patients, PPCs were observed in 375 individuals (56.82%). Multiple logistic regression identified serum albumin levels <40 g/L, type of surgery, CPB duration >150 minutes, blood transfusion, and intra-aortic balloon pump use before extubation as independent risk factors for PPCs. Patients experiencing PPCs had prolonged mechanical ventilation, extended hospitalization and ICU stays, elevated postoperative mortality, and higher tracheotomy rates compared to those without PPCs. Conclusion: Elderly patients following CPB displayed a substantially high incidence of PPCs, significantly impacting their prognosis. Additionally, this study identified five prominent risk factors associated with PPCs in this population. These findings enable clinicians to better recognize patients who may benefit from perioperative prevention strategies based on these risk factors.

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Circular RNAs (circRNAs), as a burgeoning sort of non-coding RNAs (ncRNAs), can regulate the expression of parental genes as miRNA sponges. This study was designed to explore the circRNA expression profile of nasopharyngeal carcinoma (NPC). High-throughput sequencing was performed to identify the circRNA expression profile of NPC patients compared with healthy controls. A total of 93 upregulated circRNAs and 77 downregulated circRNAs were identified. The expression levels of the top three upregulated and three downregulated circRNAs annotated by circBase were validated by quantitative real-time PCR (qRT-PCR). GO and KEGG analyses showed that these differentially expressed circRNAs were potentially implicated in NPC pathogenesis. CircRNA-miRNA-target gene network analysis revealed a potential mechanism that hsa_circ_0002375 (circKITLG) may be involved in NPC through sponging up miR-3198 and interfering with its downstream targets. Silencing of circKITLG inhibited NPC cell proliferation, migration, and invasion in vitro. This study provides a leading and fundamental circRNA expression profile of NPC.

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Aims: Remote ischaemic preconditioning (RIPC) by inducing brief ischaemia in distant tissues protects the heart against myocardial ischaemia-reperfusion injury (IRI) in children undergoing open-heart surgery, although its effectiveness in adults with comorbidities is controversial. The effectiveness and mechanism of RIPC with respect to myocardial IRI in children with tetralogy of Fallot (ToF), a severe cyanotic congenital cardiac disease, undergoing open heart surgery are unclear. We hypothesized that RIPC can confer cardioprotection in children undergoing ToF repair surgery. Methods and results: Overall, 112 ToF children undergoing radical open cardiac surgery using cardiopulmonary bypass (CPB) were randomized to either a RIPC group (n = 55) or a control group (n = 57). The RIPC protocol consisted of three cycles of 5-min lower limb occlusion and 5-min reperfusion using a cuff-inflator. Serum inflammatory cytokines and cardiac injury markers were measured before surgery and after CPB. Right ventricle outflow tract (RVOT) tissues were collected during the surgery to assess hypoxia-inducible factor (Hif)-1α and other signalling proteins. Cardiac mitochondrial injury was assessed by electron microscopy. The primary results showed that the length of stay in the intensive care unit (ICU) was longer in the control group than in the RIPC group (52.30 ± 13.43 h vs. 47.55 ± 10.34 h, respectively, P = 0.039). Patients in the control group needed longer post-operative ventilation time compared to the RIPC group (35.02 ± 6.56 h vs. 31.96 ± 6.60 h, respectively, P = 0.016). The levels of post-operative serum troponin-T at 12 and 18 h, CK-MB at 24 h, as well as the serum h-FABP levels at 6 h, after CPB were significantly lower, which was coincident with significantly higher protein expression of cardiac Hif-1α, p-Akt, p-STAT3, p-STAT5, and p-eNOS and less vacuolization of mitochondria in the RIPC group compared to the control group. Conclusion: In ToF children undergoing open heart surgery, RIPC attenuates myocardial IRI and improves the short-term prognosis.

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Mechanical ventilation (MV) may amplify the lung-specific inflammatory response in preinjured lungs by elevating cytokine release and augmenting damage to the alveolar integrity. In this study, we test the hypothesis that MV exerts different negative impacts on inflammatory response at different time points of postlung injury. Basic lung injury was induced by cecal ligation and puncture (CLP) surgery in rats. Physiological indexes including blood gases were monitored during MV and samples were assessed following each experiment. Low V T (tidal volume) MV caused a slight increase in cytokine release and tissue damage at day 1 and day 4 after sepsis induced lung injury, while cytokine release from the lungs in the two moderately ventilated V T groups was amplified. Interestingly, in the two groups where rats received low V T MV, we found that infiltration of inflammatory cells was only profound at day 4 after CLP. Marked elevation of protein leakage indicated a compromise in alveolar integrity in rats that received moderate V T MV at day 4 following CLP, correlating with architectural damage to the alveoli. Our study indicates that preinjured lungs are more sensitive to mechanical MV at later phases of sepsis, and this situation may be a result of differing immune status.

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