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目的探讨柯里拉京对单纯疱疹病毒型脑炎(HSE)炎性因子分泌和神经元凋亡的影响。方法建立HSV-1接种BV2细胞模型,随机分为正常组、单纯疱疹病毒1型(HSV-1)感染组、柯里拉京干预组、地塞米松干预组、黄芪多糖干预组,采用ELISA法检测各组炎性因子白细胞介素1β(IL-1β)、肿瘤坏死因子(TNF-a)的表达水平;25只Balb/c小鼠按上述分组分成五组,除正常组外其它各组应用HSV-1感染小鼠建立病毒性脑炎模型,治疗4d后采用TUNEL法观察各组小鼠神经元凋亡的情况。结果与病毒感染组比较,柯里拉京和地塞米松干预组HSV-1感染后IL-1b和TNF-a的分泌(P<0.01)和神经元凋亡数(P<0.01)均明显减少。结论柯里拉京可能通过减少HSV-1感染后IL-1b和TNF-a的分泌,并同时抑制神经元的凋亡来发挥其脑保护作用。
Objective To investigate the effects of corilagin on the secretion of inflammatory cytokines and neuronal apoptosis in herpes simplex virus encephalitis (HSE). Methods The HSV-1 inoculated BV2 cell model was established and randomly divided into normal group, HSV-1 infection group, Corilagin intervention group, dexamethasone intervention group and Astragalus polysaccharide intervention group. Twenty-five Balb / c mice were divided into five groups according to the above groups. All groups except the normal group were given HSV -1 infected mice to establish a viral encephalitis model, after 4 days of treatment by TUNEL method to observe the neuronal apoptosis in each group. Results Compared with the virus-infected group, the secretion of IL-1b and TNF-α (P <0.01) and the number of apoptotic neurons (P <0.01) were significantly decreased after HSV-1 infection in corilagin and dexamethasone groups. CONCLUSION Corilagin exerts its neuroprotective effect by decreasing the secretion of IL-1b and TNF-a after HSV-1 infection and simultaneously inhibiting neuronal apoptosis.