河北医药
河北醫藥
하북의약
HEBEI MEDICAL JOURNAL
2015年
9期
1285-1289
,共5页
党泽方%李金霞%张秋云%崔利娟%穆凌云%高连印%杜宇琼
黨澤方%李金霞%張鞦雲%崔利娟%穆凌雲%高連印%杜宇瓊
당택방%리금하%장추운%최리연%목릉운%고련인%두우경
截断逆挽方%肝衰竭,慢加急性%超微结构,Cyclin E%DP-1
截斷逆輓方%肝衰竭,慢加急性%超微結構,Cyclin E%DP-1
절단역만방%간쇠갈,만가급성%초미결구,Cyclin E%DP-1
truncation and inversion prescription%acute-on-chronic liver failure%ultrastructure%Cyclin E%DP-1
目的:观察截断逆挽方对慢加急性肝衰竭(ACLF)模型大鼠肝细胞超微结构,周期蛋白 Cyclin E 及转录因子 DP-1表达的影响,并考察模型24 h 病死率和生存时间,从提高疗效、降低死亡、改善肝细胞超微结构损伤和调控肝细胞代偿性增殖的角度,分析该方干预 ACLF 的部分疗效和作用机制。方法 Wistar 大鼠61只,随机分为正常组、模型组及截断逆挽方组。采用猪血清免疫诱导大鼠肝纤维化或肝硬化模型,再给予 D-GalN/LPS 一次性联合腹腔注射进行急性攻击,建立慢加急性肝衰竭大鼠模型。截断逆挽方组在急性攻击后给予水煎液灌胃连续3 d,模型组和截断逆挽方组大鼠分别在4、8、12 h 处死,取肝组织,进行电镜超微结构观察,Elisa 法测定 Cyclin E 及其转录因子 DP1的表达,运用 IPP 6.0软件进行图像分析,自动计算出阳性物质的 IOD 值。结果截断逆挽方可以延长模型的存活时间,与模型组比较,差异有统计学意义( P <0.05),在一定程度上减轻 ACLF 大鼠肝细胞超微结构的损伤;截断逆挽方组 Cyclin E 、DP1 IOD 值在8 h 时比4 h 低,12 h 比8 h 有增加( P <0.01),而模型组 Cyclin E 、DP1 IOD 则呈持续下降( P <0.05)。结论截断逆挽方可以延长模型大鼠的存活时间,并能改善肝细胞超微结构,对肝细胞代偿性增殖有一定的调控作用。
目的:觀察截斷逆輓方對慢加急性肝衰竭(ACLF)模型大鼠肝細胞超微結構,週期蛋白 Cyclin E 及轉錄因子 DP-1錶達的影響,併攷察模型24 h 病死率和生存時間,從提高療效、降低死亡、改善肝細胞超微結構損傷和調控肝細胞代償性增殖的角度,分析該方榦預 ACLF 的部分療效和作用機製。方法 Wistar 大鼠61隻,隨機分為正常組、模型組及截斷逆輓方組。採用豬血清免疫誘導大鼠肝纖維化或肝硬化模型,再給予 D-GalN/LPS 一次性聯閤腹腔註射進行急性攻擊,建立慢加急性肝衰竭大鼠模型。截斷逆輓方組在急性攻擊後給予水煎液灌胃連續3 d,模型組和截斷逆輓方組大鼠分彆在4、8、12 h 處死,取肝組織,進行電鏡超微結構觀察,Elisa 法測定 Cyclin E 及其轉錄因子 DP1的錶達,運用 IPP 6.0軟件進行圖像分析,自動計算齣暘性物質的 IOD 值。結果截斷逆輓方可以延長模型的存活時間,與模型組比較,差異有統計學意義( P <0.05),在一定程度上減輕 ACLF 大鼠肝細胞超微結構的損傷;截斷逆輓方組 Cyclin E 、DP1 IOD 值在8 h 時比4 h 低,12 h 比8 h 有增加( P <0.01),而模型組 Cyclin E 、DP1 IOD 則呈持續下降( P <0.05)。結論截斷逆輓方可以延長模型大鼠的存活時間,併能改善肝細胞超微結構,對肝細胞代償性增殖有一定的調控作用。
목적:관찰절단역만방대만가급성간쇠갈(ACLF)모형대서간세포초미결구,주기단백 Cyclin E 급전록인자 DP-1표체적영향,병고찰모형24 h 병사솔화생존시간,종제고료효、강저사망、개선간세포초미결구손상화조공간세포대상성증식적각도,분석해방간예 ACLF 적부분료효화작용궤제。방법 Wistar 대서61지,수궤분위정상조、모형조급절단역만방조。채용저혈청면역유도대서간섬유화혹간경화모형,재급여 D-GalN/LPS 일차성연합복강주사진행급성공격,건립만가급성간쇠갈대서모형。절단역만방조재급성공격후급여수전액관위련속3 d,모형조화절단역만방조대서분별재4、8、12 h 처사,취간조직,진행전경초미결구관찰,Elisa 법측정 Cyclin E 급기전록인자 DP1적표체,운용 IPP 6.0연건진행도상분석,자동계산출양성물질적 IOD 치。결과절단역만방가이연장모형적존활시간,여모형조비교,차이유통계학의의( P <0.05),재일정정도상감경 ACLF 대서간세포초미결구적손상;절단역만방조 Cyclin E 、DP1 IOD 치재8 h 시비4 h 저,12 h 비8 h 유증가( P <0.01),이모형조 Cyclin E 、DP1 IOD 칙정지속하강( P <0.05)。결론절단역만방가이연장모형대서적존활시간,병능개선간세포초미결구,대간세포대상성증식유일정적조공작용。
Objective To observe the effects of truncation and inversion prescription on the ultrastructure,Cyclin E and its transcription factor DP-1 in liver cells of model rats with acute-on-chronic liver failure (ACLF), to explore 24-hour mortality and survival time of rat models and to analyze the therapeutic effects and action mechanism of the prescription on ACLF.Me thods Sixty -one Wistar rats were randomly divided into three groups: normal control group, model group and Chinese traditional medicine group (TCM group).The rat models with hepatic fibrosis or hepatic cirrhosis were established by immune induction of pig serum,then D-GalN/LPS one-time combination intraperitoneal injection was performed to establish the rat models with acute hepatic failure.After the animal models were established,the rats were treated by truncation and inversion prescription decoction through gavage for 3 days,then the rats in model group and TCM group were sacrificed respectively at 4h,8h,12h,and the ultrastructure changes of liver tissues were observed by electron microscopy, and the expression levels of Cyclin E and its transcription factors DP-1 were detected by ELISA.The images were analyzed by IPP6.0 software, and IOD value in positive substance was automatically calculated.Results The survival time in TCM group was significantly longer than that in model group ( P <0.05), furthermore,the ultrastructural injury of liver cells in TCM group was relieved at some extent; the IOD vlue and levels of Cyclin E ,DP-1 in TCM group at 8h were obviously lower than those at 4h,however,which in 12h were significantly increased,as compared with those at 8h ( P <0.01),but IOD value and levels of Cyclin E, DP-1 in model group were decreased continually.Conclusion Truncation and inversion prescription can prolong survival time of model rats, and can improve the ultrastructure of liver cells, which has regulative effects on compensatory proliferation of liver cells at some extent.