Abstract:Aim To investigate the effect and mechanism of hydrogen molecule on myocardial injury in severe traumatic brain injury (TBI) rats. Methods Using the fluid percussion injury (FPI)-induced TBI model. 72 SD rats were randomly divided into sham group, TBI group and hydrogen molecule-treated group, with 24 rats in each group, and the rats were executed at 48 h after the operation. HE staining was used to observe the myocardial injury and the infiltration of granulocytes, ELISA was used to detect the level of superoxide dismutase (SOD), Western blot was used to detect the expression of inflammation-related factors myeloperoxidase (MPO) and heme oxygenase-1 (HO-1) protein, RT-qPCR was used to detect the levels of cardiac troponin T (cTnT), inhibitory factor-1 (IF-1), NADH/ubiquinone oxidoreductase core subunit S7 (NDUFS7), nicotinamide adenine dinucleotide phosphate (NADP) and reduced nicotinamide adenine dinucleotide phosphate (NADPH). The changes of post-traumatic echocardiography and the 7-day survival rate and body weight in the rats were observed and recorded. Results Compared with the sham group, rats in the TBI group had significantly higher troponin levels, and the echocardiographic results showed higher left ventricular end-diastolic diameter (LVEDD) and significantly lower left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and the above pathologic changes were significantly improved after treatment with the hydrogen molecule. Myocardial tissue was disorganized with erythrocyte infiltration, and myocardial fibers were infiltrated with granulocytes in the section, which were improved in the hydrogen molecule-treated group. The body weight of the rats decreased dramatically after the operation, and about 5 days later dropped to the lowest level, and then showed a trend of slow recovery. mNSS scores showed that the neurological function of the rats was severely impaired after TBI, and the postoperative myocardial tissues showed an increase in the expression levels of MPO and HO-1 proteins and a decrease in the expression levels of SOD, and the above pathological changes were significantly improved by hydrogen molecule treatment. In the TBI group, the expression levels of NADPH, IF-1 and NDUFS7 were reduced, and the expression levels of the above indicators were significantly increased after hydrogen molecule treatment. Conclusion Hydrogen molecule may be able to increase mitochondrial energy metabolism in cardiomyocytes and reduce myocardial oxidative stress by synergistically enhancing the protein expression of IF-1 and NDUFS7 on the mitochondrial oxidative respiratory chain to increase cardiac function and survival rate in the acute phase of TBI.

Abstract:Aim To explore the effects of yam polysaccharide (RDPS-Ⅰ) on myocardial injury and tyrosine protein kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in septic rats. Methods Ninety rats were randomly divided into:RDPS-Ⅰ low (1.0 g/kg), medium (2.0 g/kg), and high (3.0 g/kg) dose groups, model group, positive control group and sham operation group. The cecal ligation and perforation method was used to establish a sepsis rat model, after the model was completed, RDPS-Ⅰ low, medium and high dose groups were given corresponding dose yam polysaccharide by gavage respectively; The positive control group was given 200 mg/kg subcutaneous injection of 4 mL/kg ampicillin solution; The other two groups were given normal saline, and intervened once every 12 hours, for 6 consecutive days. After the intervention, the hemodynamic indicators of the rats were measured, including mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), and heart rate (HR); Hematoxylin-Eosin (HE) staining was used to observe the pathological changes of septic rat myocardium; TUNEL staining was used to detect cardiomyocyte apoptosis of septic rat; enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of inflammatory cytokines in septic rat serum; Western blot was used to test the expression level of JAK2/STAT3 signaling pathway proteins in rat myocardial tissue. Results Compared with the sham operation group, the myocardial tissue was disordered and occurred with severe inflammatory cell infiltration in the model group; LVSP, HR, MAP decreased by 56%, 54%, 55% (P＜0.05). The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and nuclear factor-κB (NF-κB) in serum and p-JAK2/JAK2, p-STAT3/STAT3 and apoptosis rates in myocardial tissue were increased by 2.5,1.4,1.9,1.9,2.6,2.26 and 3.67 times (P＜0.05), respectively. Compared with model group, the degree of myocardial tissue disorder and inflammatory cell infiltration were gradually relieved after RDPS-Ⅰ intervention; LVSP, HR and MAP increased by 0.4,0.35 and 0.34 times in low dose RDPS-Ⅰ group, respectively; TNF-α, IL-6, IL-1β, NF-κB, p-JAK2/JAK2, p-STAT3/STAT3 and apoptosis rate decreased by 28%, 19%, 18%, 26%, 27%, 29%, 25%, respectively. LVSP, HR and MAP increased by 0.2,0.67 and 0.83 times in medium dose RDPS-Ⅰ group, respectively. TNF-α, IL-6, IL-1β, NF-κB, p-JAK2/JAK2, p-STAT3/STAT3 and apoptosis rate decreased by 45%, 41%, 40%, 50%, 49%, 50%, 50%, respectively. LVSP, HR and MAP increased by 1.1,1.10 and 1.15 times in high dose RDPS-Ⅰ group (P＜0.05), respectively. TNF-α, IL-6, IL-1β, NF-κB, p-JAK2/JAK2, p-STAT3/STAT3 and apoptosis rate decreased by 64%, 63%, 63%, 66%, 70%, 66%, 70% (P＜0.05), respectively. Conclusion Yam polysaccharide can reduce inflammation, and improve myocardial injury and dysfunction in septic rats, which may be related to the inhibition of JAK2/STAT3 signaling pathway.

Abstract:Acute coronary syndrome is a kind of acute cardiac ischemic syndrome. At present, the traditional cardiac markers such as troponin are widely used in clinic, but have limitation of poor specificity, low sensitivity and signal timeliness. This leads to misdiagnosis, missed diagnosis or delayed treatment of patients with acute chest pain, and the best opportunity for rescue treatment is missed. To this end, researchers have found some novel biomarkers with early diagnostic and predictive value for myocardial injury in acute coronary syndrome in recent years. This review will summarize the research progress of these novel myocardial injury markers in the early diagnosis of acute coronary syndrome patients.

Abstract:Aim To investigate the changes of serum miR-1, miR-133a and miR-208a levels in patients undergoing on-pump coronary artery bypass surgery (ONCABG) and off-pump coronary artery bypass grafting (OPCABG). Methods From February 2016 to February 9,4 patients with multiple coronary artery disease requiring CABG in our hospital were selected. According to the operation method, 94 patients were divided into ONCABG group (n＝47) and OPCABG group (n＝47). The serum miR-1, miR-133a and miR-208a levels were detected by quantitative real-time PCR in all patients before operation and at different time after operation. The levels of serum cardiac troponin I (cTnI) and creatine kinase isoenzyme MB (CK-MB) were detected by chemiluminescence immunoassay in all patients before operation and at different time after operation. The correlation between serum miR-1, miR-133a, miR-208a levels and cTnI, CK-MB levels was analyzed. Results Compared with preoperative, the serum levels of miR-1, miR-133a, miR-208a, cTnI and CK-MB were increased in both groups at 4 h and 24 h after operation (P＜0.05). Compared with 4 h after operation, the serum levels of miR-1, miR-133a, miR-208a, cTnI, and CK-MB were decreased in the two groups at 24 h after operation (P＜0.05). Compared with ONCABG group, the serum levels of miR-1, miR-133a, miR-208a, cTnI and CK-MB were lower in OPCABG group at 4 h and 24 h after operation (P＜0.05). Pearson analysis showed that the serum miR-1, miR-133a and miR-208a levels were positively correlated with cTnI and CK-MB levels at 4 h and 24 h after operation in the two groups (P＜0.05). Conclusion miR-1, miR-133a, and miR-208a are expected to be important biomarkers for judging myocardial injury after ONCABG and OPCABG. This study provides a certain reference for the clinical selection of ONCABG and OPCABG.

Abstract:Since the discovery of pneumonia infected by the new coronavirus (SARS-CoV-2), it has brought great pressure to Chinas public health cause. With the in-depth study of the new coronavirus, it was found that SARS-CoV-2 infection is closely related to myocardial injury in patients. More and more attention has been paid to the myocardial damage caused by the new coronavirus in clinic. This article reviews the possible pathogenesis, diagnosis, and treatment of myocardial injury associated with novel coronavirus infection, with a view to providing assistance to the treatment of SARS-CoV-2 infection in patients with cardiovascular disease.

Abstract:Aim To investigate the changes of myocardial injury and cardiac function in severe patients with coronavirus disease 2019 (COVID-19). Methods Retrospective analysis was performed on the clinical datas of 36 COVID-19 patients. According to clinical classification, the patients were divided into severe group (n＝4) and mild group (n＝32). Collect the patientss general clinical datas and the status of the consolidated basis of cardiovascular disease, the patients serum creatinie, myoglobin, lactic dehydrogenase(LDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), troponin T (cTnT),Nü end of B-type natriuretic peptide (NT-ProBNP), c-reactive protein (CRP) levels, and echocardiography measurements of left ventricular and right ventricular function. Results The in-hospital time in the severe group was significantly longer than that in the mild group (Z＝－3.183, P＝0.001), the incidence of diabetes (χ2=13.056, P＜0.001), the serum levels of myoglobin(t＝5.284,P＜0.001), CK(Z＝－2.267,P＝0.023), CK-MB(Z＝－2.140,P＝0.032), cTnT(Z＝－2.134, P＝0.037), CRP(Z＝－1.892,P＝0.041), NT-ProBNP(Z＝－2.467,P＝0.014) and right ventricular Tei index(t＝5.256,P＝0.023) were significantly higher than those in the mild group. There were no significant differences in LVDd, LVSd, LVEF and left ventricular Tei index between the two groups. Conclusion The morbidity of diabetes in patients with severe COVID-19 was significantly higher than that of patients with mild COVID-19, while patients with severe COVID-19 had some extend of myocardiol injury and impaired right ventricular function.

Abstract:Aim To investigate the clinical characteristics and the dynamic changes of myocardial enzymes in patients with severe/critical coronavirus disease 2019 (COVID-19) with cardiac injury. Methods A total of 18 severe/critical COVID-19 patients in our hospital from January 7,0 to March 1,0 were retrospectively analyzed. According to the detection value of cardiac enzyme or troponin I during hospitalization, patients in the normal range were classified as nonmyocardial injury group (n＝13), and patients with abnormal elevation were classified as myocardial injury group (n＝5). The epidemiological and clinical data of the two groups after admission were compared and analyzed, and laboratory indicators such as blood routine, liver and kidney function, myocardial enzyme, C-reactive protein were analyzed, and the changes of creatine kinase, creatine kinase isoenzyme MB, N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin I were dynamically analyzed. Results Of the 18 severe/critical type patients, 27.8% (5/18) had myocardial injury. Compared with the nonmyocardial injury patients, there were no significant differences in age, gender, basic diseases, symptoms and signs, time from onset to hospitalization, body temperature, heart rate, diastolic blood pressure and hospital stay in the myocardial injury group, but the systolic blood pressure in the myocardial injury group was significantly higher than that in the nonmyocardial injury group(P＝0.017 1). There was no significant difference in white blood cell count, neutrocyte count, lymphocyte count and mononuclear cell count between the two groups upon admission. Similarly, there was no significant difference between the two groups in alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, α-hydroxybutyrate dehydrogenase, creatine kinase, creatine kinase isoenzyme MB, blood urea nitrogen, serum creatinine, C-reactive protein and NT-proBNP. Dynamic analysis found that in patients with myocardial injury, creatine kinase, creatine kinase muscle-brain isoenzyme, troponin I, and NT-proBNP gradually increased during the 4～5 days of hospitalization, and gradually returned to normal after 9～11 days. Conclusions Higher systolic blood pressure in patients with severe/critical COVID-19 may be associated with higher risk of heart injury.Abnormalities in myocardial enzyme spectrum occur in the early stage of hospitalization. Early detection and intervention are beneficial to the prognosis of patients with heart injury.

Abstract:Since December 2019, the 2019 novel coronavirus (2019-nCoV) has been raging around the world and causing global panic. 2019-nCoV infection not only leads to lung injury, but also causes myocardial damage in a considerable proportion of patients, which worsens the state of illness and associates with poor prognosis. Heretofore little is known about the characteristic of myocardial damage induced by 2019-nCoV infection. Therefore, this paper will focus on the features, pathological mechanism, prevention and treatment of myocardial damage caused by 2019-nCoV.

Abstract:Severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2) infects host cells through ACE2, CD147 and GRP78 receptors, causing 2019 coronavirus disease (COVID-19), and partially inducing acute myocardial injury and chronic damage to the cardiovascular system. Therefore, special attention should be paid to the protection of the heart during treatment for COVID-19. This issue continues with an expert presentation on SARS- CoV-2 infection and myocardial injury to deepen the understanding of COVID-19 and its cardiovascular injury and improve the prevention and treatment.

Abstract:Aim To investigate the protective effect of crocetin on isoprenaline induced ischemia and hypoxia in rats, and to verify whether its mechanism is related to the C/EBP- β/PGC-1α/UCP3 signaling pathway. Methods The rat model of ischemia and hypoxia was established by subcutaneous injection of isoproterenol, different doses of Crocin(5,0, 100 mg/kg) were given intragastrically. The levels of serum LDH-1, CK-MB, MDA, TNF- α, NO, CI and myocardial infarct size, myocardial Akt, ERK1/2, C/EBP-β, PGC-1α, UCP3 protein and gene expression were compared in each experimental group Results Compared with the blank control group, the survival rate of the model group was significantly decreased(P<0.01), the levels of serum LDH-1, CK-MB, MDA, TNF-α, NO, CI and myocardial infarction area were significantly increased(P<0.01). The arrangement of myocardial fibers was disordered and the infiltration of inflammatory cells was obvious. The expression of Akt and ERK1/2 protein was significantly increased(P<0.05), the expression of C/EBP-β, UCP3 protein and mRNA was significantly increased(P<0.01), and the expression of PGC-1α protein and mRNA was significantly decreased(P<0.01). The levels of serum LDH-1, CK-MB, MDA, TNF-α and NO in the positive control group were significantly higher than those in the control group(P<0.01). The infarct size was significantly decreased(P<0.01), CI was significantly decreased(P<0.05), the myocardial fibers were arranged neatly and the infiltration of inflammatory cells was significantly reduced. The expression of Akt and ERK1/2 protein was significantly increased(P<0.01), the expression of C/EBP-β protein and mRNA was significantly decreased(P<0.01), and the expression of PGC-1α protein was extremely high(P<0.05). The expression of mRNA was significantly increased(P<0.01), the expression of UCP3 protein was not different(P>0.05), but the expression of mRNA was significantly increased(P<0.05), which was compared with that of the model control group. The middle and high doses of Crocin could significantly increase the survival rate of rats(P<0.05), significantly decrease the levels of serum LDH-1, CK-MB, MDA, TNF-α and NO(P<0.05), and significantly decrease the areas of CI and myocardial infarction(P<0.05). Reduce inflammatory infiltration and improve the integrity of cardiomyocytes; The expression of Akt and ERK1/2 protein was significantly increased(P<0.05), the expression of C/EBP-β protein and mRNA was significantly decreased(P<0.05), and the expression of PGC-1α, UCP3 protein and mRNA was significantly increased(P<0.05). The comprehensive effect of high dose group was better than that of high dose group. Conclusion Crocin has obvious protective effect on myocardial ischemia and hypoxia injury in rats, and its mechanism may be related to the regulation of C/EBP-β/PGC-1α/UCP3 signaling pathway.