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Background: Reperfusion therapy is the most effective approach to resolve coronary occlusion, but myocardial injury caused by excessive inflammation during myocardial ischemia–reperfusion will also pose a new threat to health. Our prior study revealed the expression pattern of interleukin‐38 (IL‐38) in the peripheral blood serum of patients with ischemic cardiomyopathy and the role of IL‐38 in acute myocardial infarction in mice. However, its role and potential mechanisms in myocardial ischemia/reperfusion injury (MIRI) remain to be determined. Methods and Results: The left anterior descending artery of C57BL/6 mice was transiently ligated to induce the MIRI model. We found that MIRI induced the expression of endogenous IL‐38, which was mainly produced by locally infiltrating macrophages. Overexpression of IL‐38 in C57BL/6 mice attenuated inflammatory injury and decreased myocardial apoptosis after myocardial ischemia–reperfusion. Furthermore, IL‐38 inhibited lipopolysaccharide‐induced macrophage inflammation in vitro. Cardiomyocytes cocultured with the supernatant of IL‐38‐ and troponin I‐treated macrophages showed a lower rate of apoptosis than controls. Conclusions: IL‐38 attenuates MIRI by inhibiting macrophage inflammation. This inhibitory effect may be partially achieved by inhibiting the activation of NOD‐like receptor pyrin domain‐related protein 3 inflammasome, resulting in decreased expression of inflammatory factors and reduced cardiomyocyte apoptosis. [ABSTRACT FROM AUTHOR]

Rehmannia glutinosa Libosch, Achyranthes bidentata Bl. ( A. bidentata ), Dioscorea opposita Thunb, and Chrysanthemum morifolium Ramat ( C. morifolium ) are known as the ' Four Huaiqing Chinese Medicine ' in China, which are used as materials for functional foods. In this paper, the constituents of Four Huaiqing Chinese Medicine were identified by UPLC-Q-TOF-MS/MS, and flavones and aromatic compounds are mainly responsible for these herbs. Moreover, C. morifolium exhibited the most significant effect in cobalt chloride-induced HUVECs injury, which could decrease cell apoptosis and the overproduction of ROS, lactic dehydrogenase (LD) and pyruvic acid, and increase the migration capacity of cells. Meanwhile, A. bidentata exhibited the most significant effect in isoproterenol-induced H9C2 cell injury, which could decrease the levels of ROS overproduction, BNP, NO, LD and pyruvic acid. Western blot revealed that C. morifolium and A. bidentata also could decrease the levels of bax/bcl-2 ratio, cleaved caspase-3, cytochrome c, HIF-1ɑ, GLUT1, HKII and PFKFB3, respectively.

Background: The only clinically approved drug that reduces doxorubicin cardiotoxicity is dexrazoxane, but its application is limited due to the risk of secondary malignancies. So, exploring alternative effective molecules to attenuate its cardiotoxicity is crucial. Colchicine is a safe and well-tolerated drug that helps reduce the production of reactive oxygen species. High doses of colchicine have been reported to block the fusion of autophagosomes and lysosomes in cancer cells. However, the impact of colchicine on the autophagy activity within cardiomyocytes remains inadequately elucidated. Recent studies have highlighted the beneficial effects of colchicine on patients with pericarditis, postprocedural atrial fibrillation, and coronary artery disease. It remains ambiguous how colchicine regulates autophagic flux in doxorubicin-induced heart failure., Methods and Results: Doxorubicin was administered to establish models of heart failure both in vivo and in vitro. Prior studies have reported that doxorubicin impeded the breakdown of autophagic vacuoles, resulting in damaged mitochondria and the accumulation of reactive oxygen species. Following the administration of a low dose of colchicine (0.1 mg/kg, daily), significant improvements were observed in heart function (left ventricular ejection fraction: doxorubicin group versus treatment group=43.75%±3.614% versus 57.07%±2.968%, P =0.0373). In terms of mechanism, a low dose of colchicine facilitated the degradation of autolysosomes, thereby mitigating doxorubicin-induced cardiotoxicity., Conclusions: Our research has shown that a low dose of colchicine is pivotal in restoring the autophagy activity, thereby attenuating the cardiotoxicity induced by doxorubicin. Consequently, colchicine emerges as a promising therapeutic candidate to improve doxorubicin cardiotoxicity.

Background: Early recurrence of atrial fibrillation (ERAF) after catheter ablation is common and has been thoroughly studied. However, very late recurrence of atrial fibrillation (VLRAF) is rarely researched, and its characteristics have not been determined., Hypothesis: The aim of this study was to investigate the clinical characteristics of VLRAF after circumferential pulmonary vein ablation (CPVA), and to identify the risk factors for VLRAF., Methods: We retrospectively studied 259 consecutive patients with atrial fibrillation (AF) who were referred for CPVA. Clinical variables were investigated and predictors of VLRAF were identified., Results: A total of 249 patients were enrolled in this study. After a mean follow-up of 18.2 +/- 4.4 mo, 14 patients (5.6%) had VLRAF. Patients with VLRAF were more likely than those without recurrence to have ERAF (78.6% versus 17.8%, p = 0.000) and persistent AF (50.0% versus 13.0%, p = 0.000), but were less likely to achieve pulmonary vein (PV) isolation (78.6% versus 97.6%, p = 0.000). Bivariate analysis demonstrated that ERAF (odds ratio [OR] 8.148, 95% confidence interval [CI] 2.197-30.222; p = 0.002), persistent AF (OR 8.853, 95% CI 1.773-16.155; p = 0.003), and lack of PV isolation (OR 7.530, 95% CI 1.792-33.122; p = 0.006) were related to VLRAF. Multivariate logistic regression analysis only identified ERAF as a predictor of VLRAF after CPVA (OR 7.461, 95% CI 1.696-24.836; p = 0.006)., Conclusions: Very late recurrence of AF is uncommon after CPVA. That occurs more commonly in patients with ERAF., (Copyright (c) 2008 Wiley Periodicals, Inc.)