郑州大学学报（医学版）
鄭州大學學報（醫學版）
정주대학학보（의학판）
JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES)
2014年
5期
719-722
,共4页
黄芪总苷%肝细胞癌%抗炎%抗氧化%大鼠
黃芪總苷%肝細胞癌%抗炎%抗氧化%大鼠
황기총감%간세포암%항염%항양화%대서
astragalosides%hepatocellular carcinoma%anti-inflammatory%anti-oxidative%rat
目的：探讨黄芪总苷（ AT）对二乙基亚硝胺（ DEN）诱导的大鼠肝细胞癌生长的影响及其可能的作用机制。方法：将50只大鼠随机分为正常组、模型组和低、中、高剂量AT组，每组10只。模型组和AT组大鼠每天灌胃DEN，正常组给予等量生理盐水，共16周。从造模第1天开始，低、中、高剂量AT组分别按照10、20、40 mg/kg的剂量灌胃AT。末次给药后，测算大鼠肝脏指数、肿瘤体积和肝表面结节数，测定大鼠血清 AST、ALT、甲胎蛋白（AFP）、IL-6、TNF-α水平，测定肝组织中丙二醛（MDA）含量和SOD、GSH-Px活性。结果：5组大鼠肝脏指数，血清AST、ALT、AFP水平差异均有统计学意义（F＝17．481，47．975，76．390，52．312，P＜0．001）；模型组大鼠上述指标均较正常组升高（P＜0．05），AT组较模型组降低（P＜0．05）。5组大鼠血清IL-6、TNF-α水平，肝组织MDA含量和SOD、GSH-Px活性差异均有统计学意义（F＝20．998，9．359，38．233，15．638，17．475，P＜0．001）；与正常组比较，模型组大鼠血清IL-6、TNF-α水平和肝组织MDA含量升高，肝组织SOD、GSH-Px活性降低（ P＜0．05）；与模型组比较，AT组血清IL-6、TNF-α水平和肝组织中MDA含量降低，肝组织SOD和GSH-Px活性升高（P＜0．05）。结论：AT可能通过抗炎和抗氧化作用抑制DEN诱发的大鼠肝癌的生长。
目的：探討黃芪總苷（ AT）對二乙基亞硝胺（ DEN）誘導的大鼠肝細胞癌生長的影響及其可能的作用機製。方法：將50隻大鼠隨機分為正常組、模型組和低、中、高劑量AT組，每組10隻。模型組和AT組大鼠每天灌胃DEN，正常組給予等量生理鹽水，共16週。從造模第1天開始，低、中、高劑量AT組分彆按照10、20、40 mg/kg的劑量灌胃AT。末次給藥後，測算大鼠肝髒指數、腫瘤體積和肝錶麵結節數，測定大鼠血清 AST、ALT、甲胎蛋白（AFP）、IL-6、TNF-α水平，測定肝組織中丙二醛（MDA）含量和SOD、GSH-Px活性。結果：5組大鼠肝髒指數，血清AST、ALT、AFP水平差異均有統計學意義（F＝17．481，47．975，76．390，52．312，P＜0．001）；模型組大鼠上述指標均較正常組升高（P＜0．05），AT組較模型組降低（P＜0．05）。5組大鼠血清IL-6、TNF-α水平，肝組織MDA含量和SOD、GSH-Px活性差異均有統計學意義（F＝20．998，9．359，38．233，15．638，17．475，P＜0．001）；與正常組比較，模型組大鼠血清IL-6、TNF-α水平和肝組織MDA含量升高，肝組織SOD、GSH-Px活性降低（ P＜0．05）；與模型組比較，AT組血清IL-6、TNF-α水平和肝組織中MDA含量降低，肝組織SOD和GSH-Px活性升高（P＜0．05）。結論：AT可能通過抗炎和抗氧化作用抑製DEN誘髮的大鼠肝癌的生長。
목적：탐토황기총감（ AT）대이을기아초알（ DEN）유도적대서간세포암생장적영향급기가능적작용궤제。방법：장50지대서수궤분위정상조、모형조화저、중、고제량AT조，매조10지。모형조화AT조대서매천관위DEN，정상조급여등량생리염수，공16주。종조모제1천개시，저、중、고제량AT조분별안조10、20、40 mg/kg적제량관위AT。말차급약후，측산대서간장지수、종류체적화간표면결절수，측정대서혈청 AST、ALT、갑태단백（AFP）、IL-6、TNF-α수평，측정간조직중병이철（MDA）함량화SOD、GSH-Px활성。결과：5조대서간장지수，혈청AST、ALT、AFP수평차이균유통계학의의（F＝17．481，47．975，76．390，52．312，P＜0．001）；모형조대서상술지표균교정상조승고（P＜0．05），AT조교모형조강저（P＜0．05）。5조대서혈청IL-6、TNF-α수평，간조직MDA함량화SOD、GSH-Px활성차이균유통계학의의（F＝20．998，9．359，38．233，15．638，17．475，P＜0．001）；여정상조비교，모형조대서혈청IL-6、TNF-α수평화간조직MDA함량승고，간조직SOD、GSH-Px활성강저（ P＜0．05）；여모형조비교，AT조혈청IL-6、TNF-α수평화간조직중MDA함량강저，간조직SOD화GSH-Px활성승고（P＜0．05）。결론：AT가능통과항염화항양화작용억제DEN유발적대서간암적생장。
Aim:To investigate the effect of astragalosides ( AT) on hepatocellular carcinoma growth induced by diethyl-nitrosamines(DEN) in rat and the possible mechanisms .Methods:A total of 50 rats were randomly divided into normal group,model group and the low,middle and high dose of AT groups ,10 in each group.The rat in model group and AT group were intragastricly administrated with DEN for 16 weeks to prepare the hepatocellular carcinoma model .The rats in normal group was given equal normal saline .From the 1st day of the modeling ,the low,middle and high dose of AT groups were in-tragastricly administrated with AT at dose of 10,20,40 mg/kg,respectively.After the last delivery,the liver index,tumor size,the nodule number on liver surface were measured and calculated ,the serum levels of AST ,ALT,AFP,IL-6,and TNF-αwere detected .MDA content and SOD ,GSH-Px activities in liver tissue were determined .Results:The differences in liver index,serum levels of AST,ALT,AFP among the 5 groups were significant ( F=17.481,47.975,76.390,52.312,P<0.001);the above indicators of model group were higher than those of the normal group (P<0.05),while AT groups were lower than those of the model group (P<0.05).The differences in the serum levels of IL-6,TNF-α,MDA content and SOD,GSH-Px activity among the 5 groups were significant(F=20.998,9.359,38.233,15.638,17.475,P<0.001).Com-pared with the normal group ,serum IL-6,TNF-αlevels and MDA content of model group increased ,while SOD,GSH-Px ac-tivity reduced(P<0.05);compared with the model group,the serum IL-6 and TNF-αlevels and MDA content of AT groups were lower,SOD and GSH-Px activity were higher(P<0.05).Conclusion:AT may inhibit the growth of hepatocellular car-cinoma induced by DEN through anti-inflammatory and anti-oxidative .
