| ObjectivesGalectin-1(Gal-1) and Galectin-3(Gal-3) are belong to the family of galactose, which distribute in lots of organisms and tissues. They possess special affinity toβ-galactoside sugars and are involved in cell adhesion, growth, differentiation, apoptosis, inflamation, immunomodulation and so on. The dynamic changes and roles of the Gal-1 and Gal-3 in Myocarditis mice induced by Coxsackie virus B3 (CVB3) were investigated.MethodsA total of 58 healthy male Balb/C mice were randomly divided into CVB3 group (n=50) and control group (n=8). The former was treated with 0.10 ml 10"5/L CVB3 and every time eight infected mice were respectively sacrificed on 7,10,14 and 28d, the latter was inoculated intraperitoneally with 0.10 ml eagle reagent and sacrificed at 28d. The myocardial pathological changes were observed by light microscope and histopathology scores were calculated. In addition, myocardial and serum expressions of Gal-1 and Gal-3 were respectively detected by real-time quantitative-polymerase chain reaction (RQ-PCR) and ELISA, and then linear correlation analysis with myocardial histopathology scores was applied.Results1. After 3 days, the CVB3 group showed less activity, less eating, towering hair and so on. Some died after 4 d and mortality peak arrived from 7d to 9d. In addition, the symptoms became alleviated (12 d) and appeared (18 d) as well as the weight increased. The control group showed good condition:smooth hair, good sense and increasing weight. The CVB3 group showed 30% mortality rate. Meanwhile, none of control group died.2. The CVB3 group revealed different level of myocardial pathology and 100% incidence of myocarditis. Myocardial cells became swell, degenerate or necrotic and there were inflammatory cells infiltration (mainly mononuclear cells) in the myocardium at 7 d. And from 10 to 14 d, there were lots of inflammatory cells infiltration, myocardial fibers fracture, and extensive necrotic lesions. It was not until 28 d that most necrotic lesions were absorbed. Cardiac muscle cells were normal and muscle fibers were in an order in control group.3. The myocardial expression of Galectin-1 mRNA in CVB3 group obviously increased at 7d (0.92±0.13 vs 2.86±3.46) and lOd (0.92±0.13 vs 3.10±3.49) compared with control group (p< 0.05).4. The myocardial expression of Galectin-3 mRNA in CVB3 group obviously increased on 7d, (0.91±0.64 vs 10.09±2.78), lOd (0.91±0.64 vs 12.49±6.08) and 14d (0.91±0.64 vs 2.86±2.90) compared with control group (p< 0.05).5. The serum concentration of Galectin-1 in CVB3 group obviously increased on 7d(2.65±0.46 vs 11.07±2.39),10d(2.65±0.46 vs 9.64±3.76) and 14d(2.65±0.46 vs 6.92±3.98) compared with control group (p< 0.05).6. The serum concentration of Galectin-3 in CVB3 group obviously increased on 7d(5.27+1.11 vs 9.70±2.39), 10d (5.27±1.11 vs 8.98±3.03) and 14d (5.27±1.11 vs 7.73±1.88) compared with control group (p< 0.05).7. There was significantly positive correlation between the expression of Galectin-1 mRNA and Galectin-3 mRNA and myocardial histopathological scores(r=0.54,p<0.05; r=0.77,p<0.05).8. There was significantly positive correlation between the serum concentration of Galectin-1 and Galectin-3 and myocardial histopathological scores (r=0.73,p<0.05; r=0.69,p<0.05). Conclusions1. The expressions of Gal-1 and Gal-3 genes in myocardium and proteins in serum dynamically changes, which could be involved in the pathogenesis and development of viral myocarditis.2. There was significantly positive correlation between the expression of myocardial Gal-1 mRNA and Gal-3 mRNA and histopathological scores, which was also found between the serum concentration of Gal-1 and Gal-3 and histopathological scores. It was inferred that they should be related with the extent of viral myocarditis. They might be used as new detection indexs of viral myocarditis. |
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