临床儿科杂志
臨床兒科雜誌
림상인과잡지
2013年
7期
650-654
,共5页
赵园园%华青%陈兆红%马凯%徐以凤%王甜甜
趙園園%華青%陳兆紅%馬凱%徐以鳳%王甜甜
조완완%화청%진조홍%마개%서이봉%왕첨첨
单纯疱疹病毒型脑炎%阿昔洛韦%糖皮质激素%小鼠
單純皰疹病毒型腦炎%阿昔洛韋%糖皮質激素%小鼠
단순포진병독형뇌염%아석락위%당피질격소%소서
herpes simplex virus encephalitis%acyclovir%glucocorticoid%mouse
目的探讨单纯疱疹病毒性脑炎(HSE)的发病机制以及阿昔洛韦和地塞米松的作用机制。方法雄性小鼠共102只,随机分为对照组、病毒感染组、阿昔洛韦组和联合用药组。采用颅内注射单纯疱疹病毒-1型建立HSE小鼠模型;颅内注射后第1天,阿昔洛韦组和联合用药组小鼠给予阿昔洛韦灌胃,对照组和病毒感染组给予生理盐水灌胃;颅内注射后第3天,联合用药组给予地塞米松腹腔注射,余组给予生理盐水腹腔注射。分别于模型建立后第3、6、9天行神经症状评分,并用免疫组化法测定小鼠脑组织中IL-2、IL-10的表达, HE染色比较脑组织病理变化。结果病毒感染组生存率最低,阿昔洛韦组次之,联合用药组最高(P<0.05)。第3、6、9天的神经症状评分均以病毒感染组最高,阿昔洛韦组次之,联合用药组最低(P<0.05)。小鼠脑组织病理和HE染色也显示同样的情况。第3、6、9天,小鼠脑内IL-2呈现先升高后下降的趋势,而IL-10呈逐渐上升趋势;在各时间点,各组小鼠间IL-2、IL-10表达差异均有统计学意义(P<0.05),其中均以病毒感染组高于阿昔洛韦组,阿昔洛韦组高于联合用药组(P均<0.05);而联合用药组与对照组差异无统计学意义(P>0.05)。结论糖皮质激素联合抗病毒药物治疗HSE,较单纯阿昔洛韦治疗更能减少脑组织中IL-2、IL-10的分泌,减轻临床症状,提高生存率。
目的探討單純皰疹病毒性腦炎(HSE)的髮病機製以及阿昔洛韋和地塞米鬆的作用機製。方法雄性小鼠共102隻,隨機分為對照組、病毒感染組、阿昔洛韋組和聯閤用藥組。採用顱內註射單純皰疹病毒-1型建立HSE小鼠模型;顱內註射後第1天,阿昔洛韋組和聯閤用藥組小鼠給予阿昔洛韋灌胃,對照組和病毒感染組給予生理鹽水灌胃;顱內註射後第3天,聯閤用藥組給予地塞米鬆腹腔註射,餘組給予生理鹽水腹腔註射。分彆于模型建立後第3、6、9天行神經癥狀評分,併用免疫組化法測定小鼠腦組織中IL-2、IL-10的錶達, HE染色比較腦組織病理變化。結果病毒感染組生存率最低,阿昔洛韋組次之,聯閤用藥組最高(P<0.05)。第3、6、9天的神經癥狀評分均以病毒感染組最高,阿昔洛韋組次之,聯閤用藥組最低(P<0.05)。小鼠腦組織病理和HE染色也顯示同樣的情況。第3、6、9天,小鼠腦內IL-2呈現先升高後下降的趨勢,而IL-10呈逐漸上升趨勢;在各時間點,各組小鼠間IL-2、IL-10錶達差異均有統計學意義(P<0.05),其中均以病毒感染組高于阿昔洛韋組,阿昔洛韋組高于聯閤用藥組(P均<0.05);而聯閤用藥組與對照組差異無統計學意義(P>0.05)。結論糖皮質激素聯閤抗病毒藥物治療HSE,較單純阿昔洛韋治療更能減少腦組織中IL-2、IL-10的分泌,減輕臨床癥狀,提高生存率。
목적탐토단순포진병독성뇌염(HSE)적발병궤제이급아석락위화지새미송적작용궤제。방법웅성소서공102지,수궤분위대조조、병독감염조、아석락위조화연합용약조。채용로내주사단순포진병독-1형건립HSE소서모형;로내주사후제1천,아석락위조화연합용약조소서급여아석락위관위,대조조화병독감염조급여생리염수관위;로내주사후제3천,연합용약조급여지새미송복강주사,여조급여생리염수복강주사。분별우모형건립후제3、6、9천행신경증상평분,병용면역조화법측정소서뇌조직중IL-2、IL-10적표체, HE염색비교뇌조직병리변화。결과병독감염조생존솔최저,아석락위조차지,연합용약조최고(P<0.05)。제3、6、9천적신경증상평분균이병독감염조최고,아석락위조차지,연합용약조최저(P<0.05)。소서뇌조직병리화HE염색야현시동양적정황。제3、6、9천,소서뇌내IL-2정현선승고후하강적추세,이IL-10정축점상승추세;재각시간점,각조소서간IL-2、IL-10표체차이균유통계학의의(P<0.05),기중균이병독감염조고우아석락위조,아석락위조고우연합용약조(P균<0.05);이연합용약조여대조조차이무통계학의의(P>0.05)。결론당피질격소연합항병독약물치료HSE,교단순아석락위치료경능감소뇌조직중IL-2、IL-10적분비,감경림상증상,제고생존솔。
Objectives To investigate the pathogenic mechanism of herpes simplex encephalitis (HSE) and the mecha-nism of action of dexamethasone and acyclovir. Methods 102 male mice were randomly assigned to normal control group, HSV-1 infection group, acyclovir-treated group and combination-treated group. The model of HSE was established by in-tracranial injection of HSV-1 in mice except normal controls. One day after intracranial injection, mice in acyclovir-treated group and combination-treated group were intragastrically administrated with acyclovir, and mice in normal control group and HSV-1 infection group were intragastrically administrated with normal saline. Three days after intracranial injection, mice in combination-treated group were intraperitoneally injected with dexamethasone and mice in other groups were in-traperitoneally injected with normal saline. The neurological injury score and the expressions of IL-2 and IL-10 of the mice brain tissues in each group were compared at 3, 6 and 9 days after model establishment. Results The survival rate of mice was lowest in HSV-1 infection group and highest in combination-treated group (P<0.05). The neurological injury scores at 3, 6 and 9 days were highest in HSV-1 infection group and lowest in the combination-treated group (P<0.05). The changes in brain tissue pathology and HE staining were closely corresponded to the neurological injury scores. At 3, 6 and 9 days, the expression of IL-2 was increased at first and then decreased, but the expression of IL-10 was gradually increased. The expressions of IL-2 and IL-10 were highest in HSV-1 infection group and lowest in combination-treated group. And differ-ences were significant among all groups at each time point (P<0.05) except between combination-treated group and normal control group (P>0.05). Conclusions In comparison with acyclovir monotherapy, combined treatment with dexamethasone and acyclovir for HSE can reduce the expression of IL-2 and IL-10, relieve the clinical symptoms, and increase the survival rate.