中华肝脏病杂志
中華肝髒病雜誌
중화간장병잡지
CHINESE JOURNAL OF HEPATOLOGY
2015年
8期
609-615
,共7页
刘舒%黄文祥%辛小娟%赵金秋%时正雨%刘成伟%唐君
劉舒%黃文祥%辛小娟%趙金鞦%時正雨%劉成偉%唐君
류서%황문상%신소연%조금추%시정우%류성위%당군
肝炎,酒精性%炎症因子%肝功能%细胞凋亡%人参皂苷Rg1
肝炎,酒精性%炎癥因子%肝功能%細胞凋亡%人參皂苷Rg1
간염,주정성%염증인자%간공능%세포조망%인삼조감Rg1
Alcoholic hepatitis%Inflammatory factor%Liver function%Apoptosis%Rg1
目的 观察人参皂苷Rg1对大鼠酒精性肝炎的疗效,分析可能的作用机制.方法 采取连续酒精灌胃的方式构建酒精性肝炎大鼠模型:将雌性SD大鼠随机分为正常组(10只)、模型组(20只)、Rg1组(20只)、地塞米松组(20只),模型组、Rg1组、地塞米松组分别给予同等剂量的等渗盐水、Rg1及地塞米松灌胃治疗.采集大鼠血清检测肝功能生物化学及炎症因子相关指标,观察肝脏炎性变和脂肪变及凋亡程度,免疫组织化学、Western blot及RT-PCR分别检测caspase3、caspase8、NF-κ B蛋白水平及mRNA水平表达改变.组间比较用t检验. 结果 模型构建完成后,病理检查证实模型组大鼠肝脏1/3以上的肝细胞出现脂肪变性,呈现典型的酒精性脂肪肝病理表现.治疗120h后,Rg1组及地塞米松组的肝功能生物化学指标及炎症因子水平均低于模型组,Rg1组与模型组比较,ALT为(69.19±8.00) U/L对比(102.88±5.16) U/L,TBil为(0.36±0.07)μmol/L对比(1.20±0.18)μmol/L,白细胞介素6为(126.50±6.50) U/ml对比(169.19±7.68) U/ml,肿瘤坏死因子α为(268.31±13.19) ug/L对比(318.94±7.87) μg/L,P值均＜0.05.免疫组织化学检测caspase3、caspase8、NF-κB,模型组表达量明显高于Rg1组和地塞米松组(P＜0.05).TUNEL染色示模型组凋亡指数高于地塞米松组及Rg1组(P＜0.05).RT-PCR检测caspase3、caspase8、NF-κ B mRNA,Rg1组及地塞米松组均低于模型组(P＜ 0.05),Rg1组以上各项水平低于地塞米松组(P＜0.05).Western blot检测caspase3、caspase8、NF-κB蛋白表达,Rg1组及地塞米松组均低于模型组(P＜ 0.05).Rg1组以上各项水平低于地塞米松组(P＜0.05).结论 人参皂苷Rg1通过阻断凋亡通路以及抑制炎症因子的释放,可显著缓解酒精性肝炎大鼠的病理损伤,改善肝脏功能.
目的 觀察人參皂苷Rg1對大鼠酒精性肝炎的療效,分析可能的作用機製.方法 採取連續酒精灌胃的方式構建酒精性肝炎大鼠模型:將雌性SD大鼠隨機分為正常組(10隻)、模型組(20隻)、Rg1組(20隻)、地塞米鬆組(20隻),模型組、Rg1組、地塞米鬆組分彆給予同等劑量的等滲鹽水、Rg1及地塞米鬆灌胃治療.採集大鼠血清檢測肝功能生物化學及炎癥因子相關指標,觀察肝髒炎性變和脂肪變及凋亡程度,免疫組織化學、Western blot及RT-PCR分彆檢測caspase3、caspase8、NF-κ B蛋白水平及mRNA水平錶達改變.組間比較用t檢驗. 結果 模型構建完成後,病理檢查證實模型組大鼠肝髒1/3以上的肝細胞齣現脂肪變性,呈現典型的酒精性脂肪肝病理錶現.治療120h後,Rg1組及地塞米鬆組的肝功能生物化學指標及炎癥因子水平均低于模型組,Rg1組與模型組比較,ALT為(69.19±8.00) U/L對比(102.88±5.16) U/L,TBil為(0.36±0.07)μmol/L對比(1.20±0.18)μmol/L,白細胞介素6為(126.50±6.50) U/ml對比(169.19±7.68) U/ml,腫瘤壞死因子α為(268.31±13.19) ug/L對比(318.94±7.87) μg/L,P值均＜0.05.免疫組織化學檢測caspase3、caspase8、NF-κB,模型組錶達量明顯高于Rg1組和地塞米鬆組(P＜0.05).TUNEL染色示模型組凋亡指數高于地塞米鬆組及Rg1組(P＜0.05).RT-PCR檢測caspase3、caspase8、NF-κ B mRNA,Rg1組及地塞米鬆組均低于模型組(P＜ 0.05),Rg1組以上各項水平低于地塞米鬆組(P＜0.05).Western blot檢測caspase3、caspase8、NF-κB蛋白錶達,Rg1組及地塞米鬆組均低于模型組(P＜ 0.05).Rg1組以上各項水平低于地塞米鬆組(P＜0.05).結論 人參皂苷Rg1通過阻斷凋亡通路以及抑製炎癥因子的釋放,可顯著緩解酒精性肝炎大鼠的病理損傷,改善肝髒功能.
목적 관찰인삼조감Rg1대대서주정성간염적료효,분석가능적작용궤제.방법 채취련속주정관위적방식구건주정성간염대서모형:장자성SD대서수궤분위정상조(10지)、모형조(20지)、Rg1조(20지)、지새미송조(20지),모형조、Rg1조、지새미송조분별급여동등제량적등삼염수、Rg1급지새미송관위치료.채집대서혈청검측간공능생물화학급염증인자상관지표,관찰간장염성변화지방변급조망정도,면역조직화학、Western blot급RT-PCR분별검측caspase3、caspase8、NF-κ B단백수평급mRNA수평표체개변.조간비교용t검험. 결과 모형구건완성후,병리검사증실모형조대서간장1/3이상적간세포출현지방변성,정현전형적주정성지방간병리표현.치료120h후,Rg1조급지새미송조적간공능생물화학지표급염증인자수평균저우모형조,Rg1조여모형조비교,ALT위(69.19±8.00) U/L대비(102.88±5.16) U/L,TBil위(0.36±0.07)μmol/L대비(1.20±0.18)μmol/L,백세포개소6위(126.50±6.50) U/ml대비(169.19±7.68) U/ml,종류배사인자α위(268.31±13.19) ug/L대비(318.94±7.87) μg/L,P치균＜0.05.면역조직화학검측caspase3、caspase8、NF-κB,모형조표체량명현고우Rg1조화지새미송조(P＜0.05).TUNEL염색시모형조조망지수고우지새미송조급Rg1조(P＜0.05).RT-PCR검측caspase3、caspase8、NF-κ B mRNA,Rg1조급지새미송조균저우모형조(P＜ 0.05),Rg1조이상각항수평저우지새미송조(P＜0.05).Western blot검측caspase3、caspase8、NF-κB단백표체,Rg1조급지새미송조균저우모형조(P＜ 0.05).Rg1조이상각항수평저우지새미송조(P＜0.05).결론 인삼조감Rg1통과조단조망통로이급억제염증인자적석방,가현저완해주정성간염대서적병리손상,개선간장공능.
Objective To observe the effect of Rgl treatment on prognosis of alcoholic hepatitis using a rat model.Methods Female Sprague-Dawley rats were radomly divided into four groups:unmodeled control,untreated model,Rgl-treated model,and dexamethasone (DXM)-treated model.The model groups were generated by intragastric injection of alcohol.The unmodeled control group was given an equal dosage of normal saline by the same route.After model establishment,the Rg1 treatment group and the DXM treatment group were administered a 120-hour treatment of Rgl or DXM;the unmodeled controls were administered normal saline on the same schedule.All rats were then fasted for 120 hours and venous blood samples were collected for detection of serum aspartate aminotransferase (AST),alanine transaminase (ALT),total bilirubin (TBil),albumin (Alb),tumor necrosis factor-alpha (TNFαt) and interleukin 6 (IL-6).Markers of liver inflammation were measured by immunohistochemistry,western blotting,and real-time quantitative reverse transcription PCR.Fat and apoptosis indices were assessed by hematoxylin-eosin staining and TUNEL assay,respectively.The t-test and F test were used for statistical analyses.Results The model group showed remarkably more liver steatosis (over one-third of the tissue) than the unmodeled control group,indicating proper establishment of alcoholic liver disease in the modeled rats.The AST,ALT,TBil,and IL-6 levels were significantly higher in the untreated model group than in the Rgl-treated group and the DXM-treated group.The values were significantly different between the Rg1-treated group and the DXM-treated group:ALT,69.19±8.00 U/L vs.102.88±5.16 U/L;TBil,0.36±0.07 μmol/L vs.1.20±0.18 μmol/L;IL-6,126.50±6.50 U/ml vs.169.19±7.68 U/ml;TNFα,268.31±13.19 μg/L vs.318.94±7.87 μg/L (all P ＜ 0.05).Expression of caspase3 and caspase8 was significantly higher in the model group than in the Rgltreated group and the DXM-treated group (bothP ＜ 0.05).The apoptosis index was significantly lower in the Rgltreated group and the DXM-treated group than in the model group (bothP ＜ 0.05).The mRNA and protein expression of caspase3,caspase8 and NF-kB were significantly lower in the Rgl-treated group and the DXM-treated group than in the model group (allP ＜ 0.05),and the levels of all were significantly lower in the Rgl-treated group cornered to the DXM-treated group (allP ＜ 0.05).Conehision In rats with alcoholic hepatitis,Rg1 can significantly relieve pathological injury,improve liver function by blocking the apoptotic pathway,and inhibit release of inflammatory cytokines.
