QING-YI WANG1, WEI ZHAO2, QUI-LING LI2, MEI-YING ZHANG2, MING LI2, EN-QIN GUAN2, RUI-YUN ZHANG2
1Department of Pain, Qingdao Municipal Hospital of Hospital, Qingdao 266071, China - 2Department of Pediatrics, Qingdao Municipal Hospital, Qingdao 266011, China
Aims: to investigate fluctuations in serum nitric oxide (NO) and interleukin-1β levels, as well as pathological changes in mice treated by ganciclovir, in order to explore curative effect and mechanism of ganciclovir on Herpes simplex encephalitis (HSE).
Methods: the model of viral encephalitis mice infected by herpes simplex virus type 1 was established. This model was divided into five groups (model group, acyclovir treatment group, ganciclovir treatment group, control group and saline treatment group). Mortality rate, fluctuations of serum NO and interleukin-1β in mice and the morphological changes of neural cells, were observed and compared.
Results: the herpes simplex virus DNA of mice brain tissues in model group was positive whereas it was negative in normal con- trol group. Furthermore, herpes simplex virus type 1 particles were found in nerve cells in model group. Mortality rates and levels of serum NO and interleukin-1β remarkably decreased in acyclovir treatment group and ganciclovir treatment group compared to normal control group and the difference was statistically significant (P<0. 01). Furthermore, the level of interleukin-1β significantly decreased in ganciclovir treatment group, compared with the acyclovir treatment group (P<0.01). Lesions in nerve cells and the myelin of mice in the ganciclovir treatment group were mild.
Conclusion: By reducing the level of serum NO and interleukin-1β in mice with herpes simplex virus type-1 encephalitis, ganci- clovir may reduce nerve cell inflammatory reactions and neural toxicity induced by cytokines, which showed that ganciclovir may provi- de protection to nerve cells.
Serum nitric oxide, interleukin-1β, herpes simplex virus type-1 encephalitis, ganciclovir.
10.19193/0393-6384_2019_2_104