Association between congenital hypothyroidism and in-hospital adverse outcomes in very low birth weight infants / 中华儿科杂志

Objective: To investigate the association between congenital hypothyroidism (CH) and the adverse outcomes during hospitalization in very low birth weight infants (VLBWI). Methods: This prospective, multicenter observational cohort study was conducted based on the data from the Sino-northern Neonatal Network (SNN). Data of 5 818 VLBWI with birth weight <1 500 g and gestational age between 24-<37 weeks that were admitted to the 37 neonatal intensive care units from January 1st, 2019 to December 31st, 2022 were collected and analyzed. Thyroid function was first screened at 7 to 10 days after birth, followed by weekly tests within the first 4 weeks, and retested at 36 weeks of corrected gestational age or before discharge. The VLBWI were assigned to the CH group or non-CH group. Chi-square test, Fisher exact probability method, Wilcoxon rank sum test, univariate and multivariate Logistic regression were used to analyze the relationship between CH and poor prognosis during hospitalization in VLBWI. Results: A total of 5 818 eligible VLBWI were enrolled, with 2 982 (51.3%) males and the gestational age of 30 (29, 31) weeks. The incidence of CH was 5.5% (319 VLBWI). Among the CH group, only 121 VLBWI (37.9%) were diagnosed at the first screening. Univariate Logistic regression analysis showed that CH was associated with increased incidence of extrauterine growth retardation (EUGR) (OR=1.31(1.04-1.64), P<0.05) and retinopathy of prematurity (ROP) of stage Ⅲ and above (OR=1.74(1.11-2.75), P<0.05). However, multivariate Logistic regression analysis showed no significant correlation between CH and EUGR, moderate to severe bronchopulmonary dysplasia, grade Ⅲ to Ⅳ intraventricular hemorrhage, neonatal necrotizing enterocolitis in stage Ⅱ or above, and ROP in stage Ⅲ or above (OR=1.04 (0.81-1.33), 0.79 (0.54-1.15), 1.15 (0.58-2.26), 1.43 (0.81-2.53), 1.12 (0.70-1.80), all P>0.05). Conclusion: There is no significant correlation between CH and in-hospital adverse outcomes, possibly due to timely diagnosis and active replacement therapy.

Panax quinquefolium saponin Optimizes Energy Homeostasis by Modulating AMPK-Activated Metabolic Pathways in Hypoxia-Reperfusion Induced Cardiomyocytes / 中国结合医学杂志

OBJECTIVE@#To investigate the effects and underlying mechanisms of Panax quinquefolium saponin (PQS) on energy deficiency in hypoxia-reperfusion (H/R) induced cardiomyocytes.@*METHODS@#The H/R injury involved hypoxia for 3 h and then reperfusion for 2 h. Cardiomyocytes recruited from neonatal rat ventricular myocytes (NRVMs) were randomly divided into control, H/R, H/R+compound C (C.C), H/R+PQS, and H/R+C. C+PQS groups. BrdU assay, lactase dehydrogenase (LDH) leakage and early apoptosis rate were evaluated to assess cell damages. Contents of high energy phosphate compounds were conducted to detect the energy production. Protein expression levels of adenosine monophosphate-activated protein kinase a (AMPKα), glucose transporter 4 (GLUT4), phosphate fructose kinase 2 (PFK2), fatty acid translocase/cluster of differentiation 36 (FAT/CD36), and acetyl CoA carboxylase 2 (ACC2) in the regulatory pathways were measured by Western blotting. Immunofluorescence staining of GLUT4 and FAT/CD36 was used to observe the mobilization of metabolic transporters.@*RESULTS@#PQS (50 mg/L) pretreatment significantly alleviated H/R-induced inhibition of NRVMs viability, up-regulation of LDH leakage, acceleration of early apoptosis, and reduction of energy production (P<0.05). Compared with the H/R group, up-regulated expression of AMPKα, GLUT4, PFK2, FAT/CD36 and ACC2 were observed, and more GLUT4 and FAT/CD36 expressions were detected on the membrane in the H/R+PQS group (P<0.05). These effects of PQS on H/R-induced NRVMs were eliminated in the H/R+C.C+PQS group (P<0.05).@*CONCLUSION@#PQS has prominent advantages in protecting NRVMs from H/R-induced cell damages and energy metabolic disorders, by activation of AMPKα-mediated GLUT4-PFK2 and FAT/CD36-ACC2 pathways.

Effects of niacin on cell adhesion and early atherogenesis: involvement of the p38 mitogen-activated protein kinases pathway / 中华儿科杂志

<p><b>OBJECTIVE</b>To examine the effects of niacin on lysophosphatidylcholine (LPC)-induced intercellular adhesion molecule-1 (ICAM-1), and gained insight to the mechanisms.</p><p><b>METHOD</b>Human umbilical vein endothelial cell line was cultured using Medium 200 medium in incubator at 37 °C and 5% CO2 condition.Experimental groups:(1) the negative control group:medium; (2) LPC different time groups:the medium added with 20 µmol/L final concentration of LPC, were cultured for 10 min and 8 h, 24 h; (3) LPC+ p38-mitogen-activated protein kinase (p38MAPK) inhibitor (SB203580) group:the medium added with 10 µmol/L p38MAPK inhibitor (SB203580) was cultured for 1 h, then human umbilical vein endothelial cells (HUVECs) added with the LPC were cultured for 10 min, 8 h and 24 h.(4) LPC+different niacin dose group:after separately adding with 0.25, 0.5, 1 mmol/L niacin, the cells were cultured for 18 h, then HUVECs added with the LPC were cultured for 10 min, 8 h and 24 h. Cell concentration in each group was 5×10(5)/ml, inoculated in 6-well plates, each well 1 ml. Detected by Western blot analysis of pp38MAPK, ICAM-1 protein content, real-time quantitative PCR to detect endothelial cell ICAM-1 mRNA expression, cell immunofluorescence to detect LPC-induced ICAM-1 protein expression.</p><p><b>RESULT</b>In LPC 24 h group, the expression of ICAM-1 protein was significantly increased 0.786 ± 0.02, the LPC+niacin group, ICAM-1 protein levels (0.487 ± 0.015) was significantly lower than the LPC 24 h group (P < 0.01), in LPC+SB203580 intervention group, ICAM-1 protein levels (0.461 ± 0.011) was significantly lower than that of the LPC 24 h group (P < 0.01), but did not reach the level of the control group. Adding LPC to culture for 10 min, phosphorylation of p38MAPK (pp38MAPK) reached its peak (0.47 ± 0.02), niacin could reduce the pp38MAPK (0.07 ± 0.02), SB203580 could also reduce its activity (0.11 ± 0.02). Adding LPC to culture for 8 h, ICAM-1 mRNA expression (8.16 ± 0.15) compared with the control group (1.00 ± 0.02) had a significant increase (t = 24.34, P < 0.01). Compared with the LPC 8 h, niacin reduced LPC-induced ICAM-1 mRNA expression (3.85 ± 0.14), and showed a dose-dependent manner (F = 8.06, P < 0.01), while SB203580 could not effectively reduce the ICAM-1 mRNA (8.09 ± 0.11).</p><p><b>CONCLUSION</b>Niacin prevented LPC-induced endothelial dysfunction by reducing expression of ICAM-1. These mechanisms appeared to be at least partly mediated by suppression of the pp38MAPK in endothelial cells. These pleiotropic effects of niacin may potentially contribute to the beneficial effects of risk reduction for atherosclerotic disease.</p>

Effects of early intervention with taurine on oxLDL/LOX-1 system and vascular endothelial dysfunction in young streptozotocin-induced diabetic rats / 中华儿科杂志

<p><b>OBJECTIVE</b>As an endogenous antioxidant, taurine could retard the development of diabetic cardiovascular complications. Whereas, whether TAU has a protective effect on diabetic vascular endothelium in young patients is still unclear. This study aimed to investigate the protective effect of taurine on early vascular endothelial dysfunction and its possible mechanism by detecting the changes of oxLDL/LOX-1 system in young STZ-induced diabetic rats. Doing so, the authors expect to find an effective approach in clinical practice to the prevention and treatment of diabetic vascular complication.</p><p><b>METHOD</b>Six-week-old rats were divided randomly into normal control (CN group, n=8), diabetes mellitus group (DM group, n=8) and taurine supplement group (DM+TAU group, n=8). Diabetes was induced in the rats by intraperitoneal injection of streptozotocin (STZ, 60 mg/kg) and after the onset of diabetes, the rats in DM+TAU group were given free access to drinking water containing 1% taurine. At the end of 4 weeks, blood glucose, serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL) and high-density lipoprotein (HDL), oxidized low density lipoprotein (oxLDL) and sICAM-1 levels were determined, meanwhile LOX-1 and ICAM-1 expression on abdominal aortas were examined by immunostaining, Western blotting and reverse transcription PCR, respectively. The results were quantified by densitometry.</p><p><b>RESULT</b>Compared to normal control, in STZ-induced diabetic rats, the levels of serum TC, TG, LDL, oxLDL and sICAM-1 were all increased (P<0.01 for all), meanwhile LOX-1 and ICAM-1 expression (protein and mRNA) in the endothelium layers of abdominal aortas were also markedly enhanced (P<0.01 for all); while in taurine supplemented rats, the levels of serum TG (0.64+/-0.12 vs. 0.97+/-0.18), TC (0.82+/-0.18 vs. 1.01+/-0.23), oxLDL (3.1+/-0.6 vs. 4.2+/-0.6), sICAM-1 (108.3+/-18.0 vs. 130.7+/-17.4), expression of LOX-1 and ICAM-1 protein (1.02+/-0.19 vs. 2.60+/-0.33, 1.21+/-0.22 vs. 2.98+/-0.31) as well as mRNA (0.45+/-0.09 vs. 0.96+/-0.15, 0.50+/-0.07 vs. 0.87+/-0.16) were all markedly lower than those of untreated diabetic rats (P<0.05 for all). Also, the level of LOX-1 protein expression was positively correlated with levels of serum oxLDL (r=0.922, P=0.001), sICAM-1 (r=0.753, P=0.031) and ICAM-1 expression on abdominal aorta (r=0.849, P=0.008).</p><p><b>CONCLUSION</b>Vascular endothelial dysfunction was present in early stage of young diabetic rats and taurine supplement could protect against this early endothelial dysfunction by its antioxidation to inhibit the role of oxLDL/LOX-1 system in young rats with diabetes mellitus.</p>

Influence on antidiuretic hormone secretion in children with obstructive sleep apnea hypopnea syndrome / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To explore the influence of obstructive sleep apnea hypopnea syndrome (OSAHS) in children on the secretion of antidiuretic hormone (ADH).</p><p><b>METHODS</b>Thirty pediatric patients with OSAHS were examined with polysomnography (PSG) and urinary volume was recorded during sleep, and vein blood was sampled in deep sleep to detect the level of ADH in serum using radioimmunoassay technique, which were performed before and after adenotonsillectomy. Among twenty heath children were also detected the secretion of ADH as normal controls.</p><p><b>RESULTS</b>After surgery, apnea-hypopnea index (AHI) decreased (from 17.4 +/- 2.6 to 3.3 +/- 1.4, t = 27.68, P < 0.001), lowest SaO2 increased (from 0.783 +/- 0.134 to 0.954 +/- 0.062, t = 6.45, P < 0.001). The level of ADH in OSAHS patients (63.1 +/- 35.2) ng/L was much lower than that in health children (85.1 +/- 22.2) ng/L (t = 2.75, P < 0.01). The serum ADH level in postoperative patients (83.1 +/- 21.2) ng/L was increased significantly compared with that of preoperative (t = 2.56, P < 0.05), and no statistical difference versus that of health children (t = 0.17, P > 0.05). Nycturia volume of preoperative OSAHS children (492 +/- 90) ml was significant higher than that of postoperative (332 +/- 56) ml or normal controls (346 +/- 62) ml (t was 7.85 and 6.43, both P < 0.001). There was no significance in nycturia volume between postoperative group and control group (t = 0.77, P > 0.05).</p><p><b>CONCLUSIONS</b>After adenotonsillectomy in children with OSAHS caused by adenotonsillar hypertrophy, the sleep pattern and ADH secretion could become normal.</p>

Intervention of Tongxinluo capsule against vascular lesion of atherosclerosis and its effect on lectin-like oxidized low density lipoprotein receptor-1 expression in rabbits / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the prevention by Tongxinluo capsule (TXL) of vascular lesions and its effect on the levels of protein and gene expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) of vascular wall in rabbits with atherosclerosis (AS), and to explore its possible mechanism against AS.</p><p><b>METHODS</b>AS models were established by feeding New Zealand white rabbits with high-cholesterol diet, and 24 immature rabbits were randomly divided into the control group, model group and treated group (treated with TXL capsule). The indexes of total cholesterol (TC) and low density lipoprotein (LDL) levels were measured at the 16th week. The intima thickness and the plaque area of abdominal aorta were quantitatively analyzed by pathological morphological analysis, the expression of macrophage and smooth muscle cell (SMC) in intima were detected by immunohistochemical method and histologic segments were stained by Hematoxilin-Eosin (HE) to identify the degree of atherosclerotic lesion in the model group and the prevention by TXL. The LOX-1 gene and protein expression in abdominal aorta was detected by semi-quantitative RT-PCR and immunohistochemistry, respectively.</p><p><b>RESULTS</b>In the model group, the levels of TC and LDL were significantly elevated, aortic intima thickened extensively, the intima area enhanced, and macrophages expression increased; the levels of LOX-1 gene and protein expression was up-regulated in endothelium and neo-intima of the abdominal aorta. The treatment with TXL reduced blood lipids, attenuated arterial intimal proliferation, markedly inhibited the expression of macrophage and excessively expressed the level of LOX-1.</p><p><b>CONCLUSION</b>TXL has an inhibitory effect on blood lipids, and it can prevent the occurrence of vascular lesion and cure its development, and its protection against AS was possibly associated with a crucial endothelial protective action through lowering the expression of LOX-1 in vascular walls.</p>

Effects of different interventional modalities on vascular endothelial dysfunction of obese rats / 中华儿科杂志

<p><b>OBJECTIVE</b>To observe the effect of diet-control only, diet-control with swimming training or with polysaccharide sulfate (PSS), a kind of blood lipid-lowering drug on the serum lipid level and vascular endothelial function in obese rats fed by fat-rich-diet.</p><p><b>METHODS</b>Forty Wistar rats were randomly divided into the following 5 groups: group F (n = 8), group N (n = 8), group A (n = 8), group B (n = 8) and group C (n = 8), where the rats were given fat-rich-diet, basic-diet, 12 weeks of diet-control after 8 weeks of fat-rich-diet, 12 weeks of diet-control with swimming training after 8 weeks of fat-rich-diet and 12 weeks of diet-control with PSS after 8 weeks of fat-rich-diet, respectively. All rats were sacrificed after 12 weeks of intervention. Then the levels of Lee index, serum total cholesterol (TC), triglyceride (TG), plasma endothelin (ET), nitric oxide (NO) and von Willebrand Factor (vWF) were measured. The protein expression of intercellular adhesion molecule-1 (ICAM-1) in artery endothelium was evaluated by immunohistochemistry (IHC) and the gene expression of ICAM-1 was examined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>After the interventions for 12 weeks, the levels of serum TC, TG and ET decreased in group A (P < 0.05). The levels of Lee index, TC, TG, ET, vWF, ICAM-1 protein and ICAM-1 mRNA decreased in group B and C (P < 0.05). Three interventions increased serum NO production (P < 0.05) in group B.</p><p><b>CONCLUSIONS</b>Diet-control could a meliorate the hyperlipidemia and vascular function. Diet-control with swimming training and diet-control with PSS could result in weight loss of rats and meliorate the hyperlipidemia, vascular endothelial function, coagulatory activities and adhesive dysfunction. The effects of diet-control with swimming on vascular endothelial function were prominent.</p>

Effects of benazepril on renal function and kidney expression of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 in diabetic rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Excessive deposition of extracellular matrix (ECM) in the kidney is the hallmark of diabetic nephropathy. Increased matrix synthesis has been well documented but the effects of diabetes on degradative pathways, particularly in the in vivo setting. The renal protective effect of these pathways on matrix accumulation has not been fully elucidated. The present study was undertaken to investigate the activity of matrix metalloproteinase-2 (MMP-2), the expression of MMP-2 and tissue inhibitor of metalloproteinase-2 (TIMP-2) in kidney tissues of diabetic rats, and to explore the degradative pathway of type IV collagen (IV-C) and the renal protective effects of ACE inhibition-benazepril.</p><p><b>METHODS</b>Twenty-four healthy male Wistar rats were divided randomly into normal control group (NC group), untreated diabetes mellitus group (DM group), and diabetes mellitus group treated with benazepril (DL group). The rat model of diabetes mellitus was induced by intraperitoneal injection of streptozocin (60 mg/kg). After the establishment of DM model, benazepril (10 mg.kg(-1).d(-1)) was given to the DL group for 12 weeks, and the same volume of water was given to the other two groups. At the end of 12 weeks, renal function was evaluated with 24-hour urinary protein (Upro), clearance of creatinine (Ccr), and blood urea nitrogen (BUN). MMP-2 activity was determined by gelatin zymography. The levels of MMP-2, TIMP-2 and collagen IV (IV-C) protein in the kidney tissue were assessed by immunohistochemistry. The gene expression of MMP-2 and TIMP-2 was measured by reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The levels of BUN, Upro and Ccr in the DM group were higher than those in the NC group. In the DM group, the mRNA, enzymatic activity and proteins of MMP-2 decreased, but the expressions of IV-C and TIMP-2 increased. All diabetes-associated changes in renal function and MMP/TIMP were attenuated after benazepril treatment with reduced IV-C accumulation.</p><p><b>CONCLUSIONS</b>The changes of MMP-2 and TIMP-2 expressions in kidney tissues of diabetes rats may contribute to the occurrence and progression of diabetic nephropathy. Benazepril could exert protective effects on diabetic nephropathy, owing to the upregulation of MMP-2 and downregulation of TIMP-2 expressions, which further inhibits the excessive deposition of extracellular matrix in the glomerulus.</p>

Fluvastatin prevents renal injury and expression of lactin-like oxidized low-density lipoprotein receptor-1 in rabbits with hypercholesterolemia / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Lipid abnormalities are often complicated by renal dysfunction. 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are the first-line choice for lowering cholesterol levels. The present study was designed to investigate whether statins could prevent and invert the development of renal injury in cholesterol-fed rabbits and to find the possible mechanism of their effects by detecting gene and protein expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the renal artery.</p><p><b>METHODS</b>Twenty-four male New Zealand white rabbits were divided into three groups: (1) control group, regular granules chow; (2) HC-diet group, granules chow with 1% cholesterol and 5% lard oil; and (3) fluvastatin group, 1% cholesterol and 5% lard oil diet plus fluvastatin [10 mg.kg(-1).d(-1)]. After 16 weeks, serum total cholesterol (TC), low-density lipoprotein (LDL) and creatinine (Cr) levels were measured. Renal hemodynamics and function, mainly including glomerular filtration rate (GFR) in vivo were quantified using (99m)Tc-DTPA single photon emission computed tomograph ((99m)Tc-DTPA SPECT). The thickness of the renal artery intima was quantitated in HE-stained segments by histomorphometry. Gene expression of LOX-1 in the renal artery was examined by semi-quantitative RT-PCR and its protein expression was evaluated by immunohistochemistry.</p><p><b>RESULTS</b>High cholesterol diet induced hypercholesterolemia (HC) complicated by renal dysfunction with increased levels of serum lipid and Cr, decreased GFR and delayed excretion and extensively thickened renal arterial intima in the HC-diet group. Rabbits in the control group showed a minimal LOX-1 expression (mRNA and protein) in the endothelium and neointima of the renal artery. Intimal proliferation of the renal artery in the HC-diet group was associated with a marked increase of LOX-1 expression (protein and mRNA). Treatment with fluvastatin improved renal function, attenuated intimal proliferation of the renal artery and markedly decreased the enhanced LOX-1 expression in the endothelium and neointima of the renal artery in rabbits.</p><p><b>CONCLUSIONS</b>Fluvastatin treatment could prevent the development of renal injury in patients with HC and early atherosclerosis (AS). This beneficial effect might be mediated by its pleiotropic effects including a decrease in total cholesterol exposure level and prevention of LOX-1 expression in atherosclerotic arteries.</p>

Early intervention on atherosclerosis by fluvastatin and lectin-like oxidized low-density lipoprotein receptor-1 expression in atherosclerotic arteries in immature rabbits / 中华儿科杂志

<p><b>OBJECTIVE</b>The present study was designed to investigate the preventive and therapeutic effect of 3-hydroxy-3-methylglutanyl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on the development of atherosclerosis (AS) in immature rabbits and its possible mechanism by detecting the expression level of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the abdominal aorta.</p><p><b>METHODS</b>A model of hypercholesterolemia (HC) was established by high-cholesterol diet and 24 immature rabbits were divided randomly and equally into control group, HC-diet group and fluvastatin group. At the beginning of the study and after 12 weeks, the body height (BH) and body weight (BW) of the rabbits were measured and their body mass index (BMI) was calculated. At the end of 12 weeks, serum total cholesterol (TC) and low-density lipoprotein (LDL) levels were examined. The intima-medial thickness of the abdominal aorta (aIMT) was measured by using non-invasive high-resolution (14 MHz) B-mode ultrasound imaging. Histological changes in abdominal arteries were studied by H&E-staining and histomorphometric analysis. The gene expression of LOX-1 in abdominal aorta was evaluated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and its protein expression was examined by immunohistochemistry.</p><p><b>RESULTS</b>High cholesterol diet induced hypercholesterolemia and early AS in immature rabbits. In HC-diet group serum TC and LDL levels in rabbits elevated. B mode echocardiography showed that aIMT was thickened and pathomorphology indicated that extensive aortic intima (I) and intima and media (I + M) became thickened and the ratio of the area of intima to media (S(I)/S(M)) was increased. Aortic intimal proliferation in HC-diet group was associated with a marked increase in LOX-1 expression (protein and mRNA) in endothelium and neointima of the abdominal aorta. Treatment with fluvastatin at a dosage of 10 mg/(kg.d) deduced serum lipid, attenuated artery intimal proliferation and markedly decreased the enhanced LOX-1 expression level in endothelium and neointima in immature rabbits. There were no significant differences of BH, BW or BMI among the three groups.</p><p><b>CONCLUSIONS</b>These findings suggested that early treatment with fluvastatin not only induced a significant regression of arterial lesions of HC and early AS in immature rabbits, but also had a crucial endothelial protective effect by down-regulating LOX-1 expression level in atherosclerotic arteries in early AS.</p>

Dynamic changes in myocardial matrix metalloproteinase activity in mice with viral myocarditis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Matrix metalloproteinases (MMPs) are the major regulators of collagen degradation involved in the pathogenesis of several diseases of the heart. The purpose of this study was to investigate the dynamic changes in myocardial MMP activity in mice with viral myocarditis (VM), the relationship between MMP activity and both cardiac function and the quantity of myocardial collagen, and the role MMPs playing in the pathological lesions of VM.</p><p><b>METHODS</b>Sixty-five six-week-old male DBA/2 mice were divided into two groups. Mice in the infected group (n = 50) were inoculated intraperitoneally with 0.14 ml of Coxsackievirus B3 (CVB3, Nancy strain). Control mice (n = 15) were inoculated intraperitoneally with 0.14 ml of Eagle's medium. Eight infected mice and three control mice were sacrificed on each of days 3, 7, 10, 21 and 30 after inoculation. MMP activity was measured on an SDS-PAGE substrate gel embedded with type I gelatin (zymography). Echocardiographic studies were performed under anesthesia with 3% chloralhydrate administered intraperitoneally (0.01 ml/g - 0.015 ml/g). Cardiac systolic function indices, such as peak velocity of the aorta (Vp), flow velocity integral of the aorta (Vi), ejection fraction (EF), and fractional shortening (FS) were determined by echocardiography. Histological cross sections of the hearts were stained with hematoxylin-eosin and myocardial histopathological scores were determined under an optical microscope. The amount of myocardial collagen was measured by means of hydroxyproline quantification.</p><p><b>RESULTS</b>In virus-infected mice, both MMP-2 and MMP-9 activities were significantly higher than in control mice, reaching a peak on day 10 (P < 0.01). On day 10, cardiac systolic function indices (EF, FS, Vp, and Vi) were all significantly lower compared both to other stages following viral inoculation and to the control group (P < 0.05). In the acute stage, the amount of myocardial collagen in mice with VM was not significantly different from normal control mice (P > 0.05). However, the amount of myocardial collagen in infected mice at the recovery stage (on days 21 and 30) was significantly greater than those of the control mice. MMP-2 and MMP-9 activities positively correlated with myocardial histopathological scores (r = 0.801, 0.821, P < 0.01) and negatively correlated with Vp (r = -0.649, -0.683, P < 0.01) and Vi (r = -0.711, -0.755, P < 0.01). However, Vp negatively correlated with myocardial histopathological scores (r = -0.756, P < 0.01).</p><p><b>CONCLUSIONS</b>In mice with VM, the activities of myocardial MMP-2 and MMP-9 increase significantly during the acute stage, and the total quantity of myocardial collagen increases by the time of recovery. These changes are associated with myocardial interstition remodeling and cardiac dysfunction. MMP activity is an important reference marker for myocardial pathological lesions and can be used to evaluate the severity of myocardial interstitial damage and cardiac dysfunction.</p>

Effects of Intravenous Immunoglobulin on Apoptosis and Necrosis of Myocytes in Viral Myocarditis / 实用儿科临床杂志

Objective To investigate the effects of intravenous immunoglobulin(IVIG) on apoptosis and necrosis of myocytes in mice with viral myocarditis.Methods Three hundreds and twenty Balb/c mice were randomly divided into 8 groups.Different courses of IVIG were given in varying time after virus inoculation,Chinese medicine Huangqi given in control group.The virus titer in myocardium、percentage of apoptosis and necrosis of myocytes were detected, myocardial histopathologic scores were counted.Results In every IVIG treatment group,the above 3 items were all significantly lower than that in virus control group and Huangqi group,as IVIG early long course group had the best effect.Conclusion IVIG may reduce the percentage of apoptosis and necrosis of myocytes and virus titer in myocardium in mice with viral myocarditis,the effects are better than that of Huangqi.