浙江中医药大学学报
浙江中醫藥大學學報
절강중의약대학학보
Journal of Zhejiang Chinese Medical University
2015年
9期
666-670
,共5页
金祖汉%金捷%毛培江%杨毅%黄晶晶
金祖漢%金捷%毛培江%楊毅%黃晶晶
금조한%금첩%모배강%양의%황정정
角鲨烯%四氯化碳%急性肝损伤%抗氧化%护肝作用
角鯊烯%四氯化碳%急性肝損傷%抗氧化%護肝作用
각사희%사록화탄%급성간손상%항양화%호간작용
Squalene%CCl4%acute liver injury%antioxidation%hepatoprotective effect
[目的]观察角鲨烯对四氯化碳急性肝损伤模型小鼠的抗氧化和护肝作用。[方法]60只雄性ICR小鼠随机分成6组,分别为角鲨烯0.4g·kg-1、0.2g·kg-1、0.1 g·kg-1组,阳性组,模型组和对照组,每组10只。角鲨烯0.4g·kg-1、0.2g·kg-1、0.1g·kg-1组分别给予角鲨烯0.4g·kg-1、0.2g·kg-1、0.1g·kg-1灌胃,阳性组给予联苯双酯片1mg·kg-1灌胃,模型组和对照组给予等体积的食用植物油灌胃,连续给予30d。第29d除对照组外各组小鼠给予CCl480mg·kg-1灌胃。第31d眼内眦取血(取血前禁食不禁水12h),分离血清,检测血清中谷丙转氨酶(alanine aminotransferase,ALT)和谷草转氨酶(as-partate aminotransferase,AST)水平;取血后处死小鼠,解剖取肝,检测肝组织中的丙二醛(malondialdehyde,MDA)、谷胱甘肽(glutathione,GSH)和超氧化物歧化酶(superoxide dismutase,SOD)的含量及肝组织的病理变化。[结果]与对照组比较,模型组MDA显著增高(P<0.001),GSH、SOD显著降低(GSH:P<0.01,SOD:P<0.001),说明本实验抗氧化动物模型成功,而角鲨烯0.4g·kg-1剂量能显著提高肝组织中的GSH水平(P<0.01),显著降低肝组织中MDA水平(P<0.05);0.4g·kg-1和0.2g·kg-1能显著提高肝组织中的SOD水平(P<0.05),说明角鲨烯有明显抗氧化作用。与对照组比较,模型组血清ALT、AST均显著升高(P<0.001),肝组织气球样变、脂肪性变性、胞浆凝聚、水样变性及细胞坏死等病理变化的分级积分显著高于对照组(气球样变、脂肪性变性、胞浆凝聚:P<0.001;水样变性、细胞坏死:P<0.01),说明急性肝损伤动物模型成功,而角鲨烯0.4g·kg-1剂量能显著降低血清ALT、AST水平(ALT:P<0.01, AST:P<0.05);角鲨烯0.4g·kg-1和0.2g·kg-1剂量能显著改善肝细胞的气球样变(0.4g·kg-1:P<0.001,0.2g·kg-1:P<0.01);角鲨烯0.4g·kg-1剂量能显著改善肝细胞的脂肪性变性、胞浆凝聚、水样变性及细胞坏死等病理改变(P<0.05),说明角鲨烯有明显护肝效果。[结论]角鲨烯对小鼠因四氯化碳引起的肝组织中GSH、SOD下降和MDA升高有显著拮抗作用,对因四氯化碳引起的血清ALT、AST水平升高和肝组织病变等急性肝损伤表现也有显著的改善作用,且有明显的剂量相关性,0.4g·kg-1剂量的角鲨烯与1mg ·kg-1的联苯双酯作用效果相当,表明角鲨烯有较好的抗氧化和护肝作用。
[目的]觀察角鯊烯對四氯化碳急性肝損傷模型小鼠的抗氧化和護肝作用。[方法]60隻雄性ICR小鼠隨機分成6組,分彆為角鯊烯0.4g·kg-1、0.2g·kg-1、0.1 g·kg-1組,暘性組,模型組和對照組,每組10隻。角鯊烯0.4g·kg-1、0.2g·kg-1、0.1g·kg-1組分彆給予角鯊烯0.4g·kg-1、0.2g·kg-1、0.1g·kg-1灌胃,暘性組給予聯苯雙酯片1mg·kg-1灌胃,模型組和對照組給予等體積的食用植物油灌胃,連續給予30d。第29d除對照組外各組小鼠給予CCl480mg·kg-1灌胃。第31d眼內眥取血(取血前禁食不禁水12h),分離血清,檢測血清中穀丙轉氨酶(alanine aminotransferase,ALT)和穀草轉氨酶(as-partate aminotransferase,AST)水平;取血後處死小鼠,解剖取肝,檢測肝組織中的丙二醛(malondialdehyde,MDA)、穀胱甘肽(glutathione,GSH)和超氧化物歧化酶(superoxide dismutase,SOD)的含量及肝組織的病理變化。[結果]與對照組比較,模型組MDA顯著增高(P<0.001),GSH、SOD顯著降低(GSH:P<0.01,SOD:P<0.001),說明本實驗抗氧化動物模型成功,而角鯊烯0.4g·kg-1劑量能顯著提高肝組織中的GSH水平(P<0.01),顯著降低肝組織中MDA水平(P<0.05);0.4g·kg-1和0.2g·kg-1能顯著提高肝組織中的SOD水平(P<0.05),說明角鯊烯有明顯抗氧化作用。與對照組比較,模型組血清ALT、AST均顯著升高(P<0.001),肝組織氣毬樣變、脂肪性變性、胞漿凝聚、水樣變性及細胞壞死等病理變化的分級積分顯著高于對照組(氣毬樣變、脂肪性變性、胞漿凝聚:P<0.001;水樣變性、細胞壞死:P<0.01),說明急性肝損傷動物模型成功,而角鯊烯0.4g·kg-1劑量能顯著降低血清ALT、AST水平(ALT:P<0.01, AST:P<0.05);角鯊烯0.4g·kg-1和0.2g·kg-1劑量能顯著改善肝細胞的氣毬樣變(0.4g·kg-1:P<0.001,0.2g·kg-1:P<0.01);角鯊烯0.4g·kg-1劑量能顯著改善肝細胞的脂肪性變性、胞漿凝聚、水樣變性及細胞壞死等病理改變(P<0.05),說明角鯊烯有明顯護肝效果。[結論]角鯊烯對小鼠因四氯化碳引起的肝組織中GSH、SOD下降和MDA升高有顯著拮抗作用,對因四氯化碳引起的血清ALT、AST水平升高和肝組織病變等急性肝損傷錶現也有顯著的改善作用,且有明顯的劑量相關性,0.4g·kg-1劑量的角鯊烯與1mg ·kg-1的聯苯雙酯作用效果相噹,錶明角鯊烯有較好的抗氧化和護肝作用。
[목적]관찰각사희대사록화탄급성간손상모형소서적항양화화호간작용。[방법]60지웅성ICR소서수궤분성6조,분별위각사희0.4g·kg-1、0.2g·kg-1、0.1 g·kg-1조,양성조,모형조화대조조,매조10지。각사희0.4g·kg-1、0.2g·kg-1、0.1g·kg-1조분별급여각사희0.4g·kg-1、0.2g·kg-1、0.1g·kg-1관위,양성조급여련분쌍지편1mg·kg-1관위,모형조화대조조급여등체적적식용식물유관위,련속급여30d。제29d제대조조외각조소서급여CCl480mg·kg-1관위。제31d안내자취혈(취혈전금식불금수12h),분리혈청,검측혈청중곡병전안매(alanine aminotransferase,ALT)화곡초전안매(as-partate aminotransferase,AST)수평;취혈후처사소서,해부취간,검측간조직중적병이철(malondialdehyde,MDA)、곡광감태(glutathione,GSH)화초양화물기화매(superoxide dismutase,SOD)적함량급간조직적병리변화。[결과]여대조조비교,모형조MDA현저증고(P<0.001),GSH、SOD현저강저(GSH:P<0.01,SOD:P<0.001),설명본실험항양화동물모형성공,이각사희0.4g·kg-1제량능현저제고간조직중적GSH수평(P<0.01),현저강저간조직중MDA수평(P<0.05);0.4g·kg-1화0.2g·kg-1능현저제고간조직중적SOD수평(P<0.05),설명각사희유명현항양화작용。여대조조비교,모형조혈청ALT、AST균현저승고(P<0.001),간조직기구양변、지방성변성、포장응취、수양변성급세포배사등병리변화적분급적분현저고우대조조(기구양변、지방성변성、포장응취:P<0.001;수양변성、세포배사:P<0.01),설명급성간손상동물모형성공,이각사희0.4g·kg-1제량능현저강저혈청ALT、AST수평(ALT:P<0.01, AST:P<0.05);각사희0.4g·kg-1화0.2g·kg-1제량능현저개선간세포적기구양변(0.4g·kg-1:P<0.001,0.2g·kg-1:P<0.01);각사희0.4g·kg-1제량능현저개선간세포적지방성변성、포장응취、수양변성급세포배사등병리개변(P<0.05),설명각사희유명현호간효과。[결론]각사희대소서인사록화탄인기적간조직중GSH、SOD하강화MDA승고유현저길항작용,대인사록화탄인기적혈청ALT、AST수평승고화간조직병변등급성간손상표현야유현저적개선작용,차유명현적제량상관성,0.4g·kg-1제량적각사희여1mg ·kg-1적련분쌍지작용효과상당,표명각사희유교호적항양화화호간작용。
Objective] To observe the antioxidative and hepatoprotective effects of squalene on acute liver injury mice induced by CCl4. [Methods] 60 male ICR mice were randomly divided into 6 groups(n=10). Three groups were orally administered with 0.4g·kg-1, 0.2g·kg-1 and 0.1g·kg-1 dosages of squalene respectively, one group with 1mg·kg-1 dosage of biphenyldicarboxylate, the others(control group and model group) with edible vegetable oil once a day for 30d. At the 29th day, all mice were orally administered with 80mg·kg-1 dosage of CCl4 except the control mice. The levels of ALT and AST in serum were detected, the levels of MDA, GSH and SOD in liver were detected, and the pathology changes of hepatic were observed after 16h fasting at the 31th day. [Results] Compared with the control group, the levels of MDA of model mice are higher(P<0.001), the levels of GSH, SOD of model mice are lower(GSH:P<0.01,SOD:P<0.001), indicating the antioxidation model is effective. Compared with the model group, 0.4g·kg-1 dosage of squalene can raise the levels of GSH(P<0.01) and reduce the levels of MDA(P<0.05) in liver, 0.4g·kg-1 and 0.2g·kg-1 dosage can raise the levels of SOD(P<0.05) in liver. Compared with the control group, the levels of ALT, AST on model mice are higher(P<0.001), and the pathology changes of model mice are significant(P<0.001), indicating the liver injury model is effective. 0.4g·kg-1 dosage of squalene can reduce the serum levels of ALT, AST(ALT:P<0.01, AST:P<0.05), 0.4g·kg-1 dosage can ameliorate the pathology changes of hepatic by CCl4. [Conclusion] Squalene has significant antagonistic effects on GSH, SOD decreasing and MDA increasing in liver tissue of mice induced by carbon tetrachloride. The effects on acute liver injury such as Serum AST, ALT abnormality and liver pathology changes by carbon tetrachloride are also improved. Squalene is of antioxidation and hepatoprotective effects on CCl4 induced acute liver injury in mice. These effects are of dose dependency.