论文部分内容阅读
目的观察慢性病毒性心肌炎(CVMC)小鼠血清抗心肌肌球蛋白抗体(AMA)的表达和心肌胶原容积积分(CVF),以及氧化苦参碱对其的干预作用和对心肌的保护作用。方法以柯萨奇病毒B3株(CVB3)重复增量感染BALB/c小鼠,建立CVMC模型(n=60)。正常对照组(n=8)同期腹腔注射等体积9 g.L-1盐水。42 d将CVMC模型组存活小鼠随机分为CVMC对照组(n=8)、氧化苦参碱干预组(n=8)。氧化苦参碱干预组小鼠给予氧化苦参碱100 mg.kg-1.d-1灌胃,1次.d-1。CVMC对照组及正常对照组同期给予9 g.L-1盐水灌胃。干预28 d后处死各组小鼠。计算各组小鼠心脏/体质量比(HW/BW);心肌切片行胶原组织特异性染色,计算心肌组织中CVF;ELISA法检测其血清AMA的表达。结果CVMC对照组小鼠HW/BW(0.007 9±0.000 3)、CVF[(15.30±1.08)%]及血清中AMA吸光度(A)值(0.286±0.053)较正常对照组HW/BW(0.005 5±0.000 2)、CVF[(6.84±1.11)%]及AMAA值(0.160±0.050)均显著增高(Pa<0.01)。AMA阳性组HW/BW[(0.007 60±0.000 68)%]、CVF[(14.328±2.63)%]及AMAA值(0.313±0.028)较阴性组HW/BW[(0.006 30±0.000 91)]、CVF[(9.195±3.061)%]及AMAA值(0.189±0.051)均显著增高(Pa<0.01)。氧化苦参碱干预后HW/BW(0.006 8±0.000 4)、CVF[(9.94±1.35)%]及血清中AMAA值(0.229±0.054)均较CVMC对照组HW/BW(0.007 9±0.000 3)、CVF[(15.30±1.08)%]及血清中AMAA值(0.286±0.053)显著降低(Pa<0.05)。结论CVMC小鼠血清AMA和CVF表达均增高,氧化苦参碱可下调二者的表达,抑制CVMC小鼠的心肌重构。
Objective To observe the anti-cardiac myosin antibody (AMA) expression and myocardial collagen volume integral (CVF) in serum of chronic viral myocarditis (CVMC) mice, as well as the protective effect of oxymatrine on its intervention and myocardial protection. METHODS: BALB/c mice were infected in duplicate with Coxsackievirus B3 strain (CVB3) to establish a CVMC model (n=60). The normal control group (n=8) was intraperitoneally injected with an equal volume of 9 g.L-1 saline. Forty-two days, mice in CVMC model group were randomly divided into CVMC control group (n=8) and oxymatrine intervention group (n=8). Oxymatrine intervention group mice were given oxymatrine 100 mg.kg-1.d-1 intragastrically once a day. D-1. The CVMC control group and normal control group were given 9 g.L-1 saline gavage at the same time. After 28 days of intervention, each group of mice was sacrificed. The heart/body mass ratio (HW/BW) of each group of mice was calculated. Collagen-specific staining of myocardial tissue was performed to calculate CVF in cardiac muscle tissue. Serum AMA expression was detected by ELISA. Results The HW/BW (0.007 9±0.000 3), CVF [(15.30±1.08)%] and AMA absorbance (A) values (0.286±0.053) in the CVMC control group were higher than those in the normal control group (HW/BW, 0.005 5). ± 0.000 2), CVF [(6.84±1.11)%] and AMAA (0.160±0.050) were significantly higher (Pa<0.01). HW/BW [(0.007 60±0.000 68)%], CVF [(14.328±2.63)%], and AMAA (0.313±0.028) in the AMA positive group were higher than those in the negative group (HW/BW [(0.006 30±0.000 91)], CVF [(9.195±3.061)%] and AMAA (0.189±0.051) were both significantly higher (Pa<0.01). The HW/BW (0.006 8±0.000 4), CVF [(9.94±1.35)%] and serum AMAA (0.229±0.054) were significantly higher than those of the CVMC control group (HW/BW, 0.007 9±0.000 3) after intervention with oxymatrine. ), CVF [(15.30±1.08)%] and serum AMAA (0.286±0.053) were significantly reduced (Pa<0.05). Conclusion The expressions of AMA and CVF in serum of CVMC mice are all increased. Oxymatrine can down-regulate the expression of AMA and CVF and inhibit myocardial remodeling in CVMC mice.