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Objective To observe the protective effect of different doses of left carnitine on cardiomyocyte function in children with viral myocarditis.Methods94 cases of children with viral myocarditis were selected and divided into observation group and control group according to the random number table, 47 cases in each group.Both groups were treated with fructose 1,6-diphosphate(100~250mg/kg, add 150mL of 10% glucose in intravenous infusion, 1times/d) combined with left carnitine.Large dose group of left carnitine 100 mg/kg, low dose group 50mg/kg, all added 150mL of 5% glucose intravenous infusion, 1 times/d.The total effective rate, creatine kinase(CK), creatine kinase isoenzyme (CK-MB),lactate dehydrogenase (LDH), cardiac ejection fraction(EF), ventricular short axis shortening (FS) And the total incidence of adverse reactions were compared between two groups.ResultsThe total effective rates of two group were 93.62% and 87.23%.The level of CK,CK-MB,LDH in two groups were significantly decreased after treatment of two weeks(P<0.05), EF, FS were increased after treatment of two weeks(P<0.05).There was no significant difference in CK, CK-MB, LDH, EF and FS between the high dose group and the low dose group after treatment of two weeks.The overall incidence of adverse reactions in the high dose group was 25.53%, which was lower than that in the low dose group (8.51%,P<0.05).ConclusionThe use of low-dose left carnitine in children with viral myocarditis can effectively remove free radicals, protect cardiomyocyte function and improve myocardial energy metabolism and cardiac function, and safer than high-dose groups.
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Objective@#To explore the impact of hydrogen sulfide (H2S) on the heme oxygenase-1/carbon monoxide pathway in Coxsackie virus B3 (CVB3)-induced murine myocarditis (VMC) model.@*Method@#A total of 70 inbred male Balb/c mouse (4-6 weeks old) were randomized into the following four groups: Normal, VMC, PAG and NaHS (n=10 for Normal, n=20 for VMC, PAG and NaHS groups). Mice in Normal group were non-infected mice treated with intraperitoneal injection of sterile phosphate-buffered saline daily for 10 days.Mice in VMC group received intraperitoneal CVB3 injection (0.1 ml 10-5.69TCID50m·ml-1·d-1 and PBS for 10 days), and mice in PAG group received additional intraperitoneal DL-proparglygylcine injection (40 mg·kg-1·d-1 for 10 days), mice in NaHS group received additional intraperitoneal NaHS injection (50 μmol·kg-1·d-1 for 10 days). All mice were sacrificed on day 10th, and body weight and heart weight, the ratio of heart weight to body weight were compared among groups.Pathological changes of heart tissues were observed microscopically by HE and the histopathologic scores were valued.The content of COHb was tested after the gathering of blood specimens while reverse transcription-polymerase chain reaction was used to detect myocardial HO-1 mRNA expression.@*Results@#(1) Pathological findings in myocardium: hearts sections in Normal group were normal and no inflammatory cells and necrosis were found.A notable cellular infiltration, interstitial edema, vascular hyperemia and necrosis were observed in heart section of VMC, PAG and NaHS group.Extensive inflammations and larger area of myocardial cells necrosis were evidenced in PAG group and above changes were significantly reduced in NaHS group.(2) Comparison of the ratio of heart weight to body weight and histological scores of myocardium: the ratio was significantly higher in the VMC, PAG, NaHS groups than in Normal group (P<0.05), which was higher in PAG group and lower in NaHS group as compared with VMC group (both P<0.05). The histopathologic scores of all CVB3 innoculation groups were higher than in the Normal group, which was higher in PAG group and lower in NaHS group as compared to VMC group (both P<0.05). (3) The content of blood COHb in VMC, PAG or NaHS group was significantly higher than that in Normal group (P<0.05), which was significantly lower in PAG group, and higher in NaHS group as compared to VMC group (both P<0.05). (4) The mRNA expression of myocardial HO-1 detected by RT-PCR: weak expression was observed in Normal group, which was significantly upregulated in VMC, PAG and NaHS groups (P<0.05), which was downregulated in PAG group and upregulated in NaHS group as compared to VMC group (both P<0.05). (5) Correlation analysis: blood COHb concentration was positively correlated with myocardial HO-1 mRNA expression(r=0.927, P=0.000), negatively correlated with histopathologic scores(r=-0.753, P=0.000)and the histopathologic scores were negatively correlated with the myocardial HO-1 mRNA expression (r=-0.754, P=0.000).@*Conclusions@#H2S could play a protective role in murine CVB3 myocarditis model through inducing HO-1 expression and upregulating HO-1/CO pathway.
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<p><b>OBJECTIVE</b>To explore the effects of tanshinone and JAK2/STAT1 signaling pathway related mechanism in CVB3-induced myocarditis in murine.</p><p><b>METHODS</b>A total of 110 inbred male Balb/c mice which were 4 to 6 weeks-old were randomly divided into five groups: normal control (N, n = 10), myocarditis control (C, n = 25), tanshinone group (T, 15 mg · kg⁻¹ · d⁻¹, i.p., n = 25), janus kinase 2 inhibitor AG490 group (A, 10 mg · kg⁻¹ · d⁻¹, i.p., n = 25), T+A group (H, n = 25). Myocarditis was induced by 0.5 ml 10(-9.51) TCID50/ml CVB3 i.p. injection for 10 days in group C, T and H. Myocardial histopathologic changes were observed and phospho-STAT1 expressions were detected by immunohistochemistry and Western blot analysis. The levels of serum cardiac troponin I were detected with chemiluminescence immunoassay.</p><p><b>RESULTS</b>(1) Compared with group C, the histopathologic scores were significantly higher in group A and H (3.35 ± 0.57 and 3.34 ± 0.54 vs. 2.12 ± 0.39, P < 0.01), but lower in group T (1.40 ± 0.34 vs.2.12 ± 0.39, P < 0.01). (2) The expression of p-STAT1 protein was similar in group A and H compared to group N (P > 0.05), but was significantly lower than that in group C (0.017 ± 0.010 and 0.020 ± 0.010 vs. 0.246 ± 0.010, P < 0.01). The expression of p-STAT1 protein was significantly higher in group T than in group C (P < 0.01). (3) The levels of serum cardiac troponin I in group C, A, T and H were significantly higher than in group N ((0.42 ± 0.06), (1.17 ± 0.25), (0.23 ± 0.05) and (1.04 ± 0.19) µg/L vs. (0.02 ± 0.01) µg/L, all P < 0.01). The levels of serum cardiac troponin I were significantly higher in group A and H compared with group C ((1.17 ± 0.25) and (1.04 ± 0.19) µg/L vs. (0.42 ± 0.06) µg/L, P < 0.01), but were significantly lower in group T than in group C ((0.23 ± 0.05) µg/L vs. (0.42 ± 0.06) µg/L, P < 0.01). (4) There was a negative correlation between the expression level of p-STAT1 and the histopathologic scores (y = -4.503 x + 3.371, R² = 0.738, P < 0.01), but a positive correlation between the levels of serum cardiac troponin I and the histopathologic scores (y = 1.935x + 1.165, R² = 0.766, P < 0.01).</p><p><b>CONCLUSION</b>Tanshinone could attenuate myocardial injury via upregulating the JAK2/STAT1 signaling pathway in this murine viral myocarditis model.</p>
Subject(s)
Animals , Male , Mice , Blotting, Western , Coxsackievirus Infections , Disease Models, Animal , Abietanes , Pharmacology , Heart Injuries , Janus Kinase 2 , Mice, Inbred BALB C , Myocarditis , Drug Therapy , Virology , Myocardium , STAT1 Transcription Factor , Signal Transduction , Troponin IABSTRACT
Objective To explore the clinical features and treatment of children with acute severe viral myocarditis.Methods The clinical data of presentation,diagnosis,therapy and prognosis of children who were admitted in our hospital from Jan 2005 to Jan 2012 with acute severe viral myocarditis(severe myocarditis group) were analyzed retrospectively.Twenty-three cases of normal healthy children in the same period were selected as control group.The levels of serum cardiac troponin(CTn)-Ⅰ and N-terminal pro-brain natriuretic peptide(NT-proBNP) were detected by ELISA method,the changes of left ventricular ejection fraction and left ventricular fraction shortening were understood by color doppler echocardiography.Results The level of CTn-Ⅰin severe myocarditis group was significantly higher than that of control group,the difference was statistically significant [(18.67 ± 12.31) ng/ml vs (0.02 ±0.01) ng/ml,P ＜0.05].Compared with the acute phase,the level of CTn-Ⅰshowed a trend of gradual decline in 7 d [(0.55 ±0.24) ng/ml],basic close to normal in 14 d [(0.06 ±0.03) ng/ml] (P ＜0.05).The level of NT-proBNP increased significantly in severe myocarditis group compared with control group [(3 067.26 ± 902.79) pg/ml vs (80.04 ± 17.79) pg/ml,P ＜0.05].Compared with acute phase,the levels of NT-proBNP were closed to normal in 7 d [(648.63 ±342.37) pg/ml] and 14 d [(213.58 ± 129.51) pg/ml] (P ＜ 0.05).The left ventricular ejection fraction [(52.63 ± 6.98) ％ vs (71.39 ± 2.41) ％] and left ventricular fraction shortening [(32.1 ± 2.97) ％ vs (40.04 ± 2.31) ％] in severe myocarditis group were significantly lower than those in control group (P ＜ 0.05).Conclusion Acute severe viral myocarditis of children was characterized by rapid onset,severe illness and high mortality.Early use of adrenal cortical hormone and gamma globulin under the comprehensive treatment and application temporary pacemaker can help patients to recover from the disease.