抗柯注射液对柯萨奇B_3病毒感染小鼠自然杀伤细胞活性的影响

Effects of RSF on natural killer cell activity of mice infected by coxB_3 virus

目的 :检测 BAL B/ c小鼠在感染柯萨奇 (cox) B3病毒后自然杀伤 (NK)细胞活性的动态变化以及抗柯注射液 (RSF)对其影响。方法 :将小鼠分为正常对照组、病毒对照组、10 m g/ kg RSF组、2 0 mg/ kg RSF组和 30m g/ kg RSF组 ,每组 17只 ,分别在病毒感染后第 3天、8天、12天用乳酸脱氢酶释放法 ,检测各组小鼠外周血的NK细胞活性 ,并将心脏行组织病理检查。结果 :病毒感染后第 3天 NK细胞活性显著升高 (6 7.11± 2 .5 2 ) % ,之后进行性下降 ,第 12天时低于正常 [(42 .2 6± 1.6 1) %∶ (47.79± 4.0 3) % ];RSF对 cox B3病毒感染小鼠的 NK细胞活性有双向调节作用。大剂量 (2 0 mg/ kg和 30 mg/ kg) RSF在第 3天时对增高的 NK细胞活性有抑制作用 ,第 12天时可使降低的 NK细胞活性恢复至正常水平 ;小剂量 (10 mg/ kg) RSF在第 3天时对增高的 NK活性无抑制作用 ,但第 12天时也能使降低的 NK活性恢复至正常。病毒感染第 8天时心肌病变最重 ,小剂量 RSF组心肌病变改善较少 ,大剂量 RSF组改善明显。结论 :RSF调节 cox B3病毒感染后机体的 NK细胞活性可能是其防治病毒性心肌炎的重要机制之一。

Objective:To determine natural killer cell (NK) activity of peripheral blood of BALB/c mice infected with coxB 3 virus on different days after infection and the effects of (RSF) on it.Method:BALB/c mice were divided into five groups:normal control group,virus control group,10 mg/kg RSF group,20 mg/kg RSF group and 30 mg/kg RSF group.NK cell activity was determined by LDH release assays.Result:NK cell activity was increased significantly in virus control mice on day 3( 67.11 ± 2.52 ),subsequently decreased continuously,and lower than normal control on day 12[( 42.26 ± 1.61 )%,normal level was( 47.79 ± 4.03 )].RSF had dual regulatory effects on NK cell activity of mice infected by coxB 3.High doses (20 mg/kg and 30 mg/kg) inhibited the increase in NK cell activity on day 3[( 54.88 ± 1.25 ) and ( 52.90 ± 3.80 ) respectively] and elevated the decreased NK activity to normal level on day 12[( 49.37 ± 4.07 ) and ( 49.48 ± 4.72 ) respectively],while low dose (10 mg/kg) failed to inhibit the increase in it on day 3( 67.92 ± 1.21 ) but could also elevate it to normal level on day 12( 45.91 ± 2.51 ).Myocardial damages were most serious on day 8 and were improved more largely in high dose group than in low dose group.Conclusion:It suggested that that RSF regulated NK cell activity of peripheral blood of infected mice may be one of the mechanisms of RSF preventing viral myocarditis.