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纸质出版日期:2016
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张慧, 裴志东, 陈莹, 等. 18,18-甘草酸对小鼠急性肝损伤的保护作用及其联合用药配伍比例探讨[J]. 中国实验方剂学杂志, 2016,22(2):103-106.
ZHANG Hui, PEI Zhi-dong, CHEN Ying, et al. Protective Effect and Combination Proportion of 8,8Glycyrrhizic Acid on Acute Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(2): 103-106.
张慧, 裴志东, 陈莹, 等. 18,18-甘草酸对小鼠急性肝损伤的保护作用及其联合用药配伍比例探讨[J]. 中国实验方剂学杂志, 2016,22(2):103-106. DOI: 10.13422/j.cnki.syfjx.2016020103.
ZHANG Hui, PEI Zhi-dong, CHEN Ying, et al. Protective Effect and Combination Proportion of 8,8Glycyrrhizic Acid on Acute Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(2): 103-106. DOI: 10.13422/j.cnki.syfjx.2016020103.
目的:对比研究18α-甘草酸
18β-甘草酸及二者联合用药对小鼠急性肝损伤的保护作用
并筛选二者联合用药的最佳配伍比例。方法:小鼠随机被分为正常组
模型组
18α-甘草酸
18β-甘草酸低、中、高剂量组(15
30
60 mg·kg-1)
联合用药给药剂量均为60 mg·kg-1
联合用药1(18α-甘草酸-18β-甘草酸1:3)组、联合用药2(18α-甘草酸-18β-甘草酸2:3)组、联合用药3(18α-甘草酸:18β-甘草酸1:1)组。在造模前各治疗组ip给药7 d
1次/d
其他各组ip生理盐水;末次给药1 h后
除正常组ip生理盐水外
其他各组均ip 0.1%四氯化碳(CCl4)花生油(20 mL·kg-1)建立CCl4诱导小鼠急性肝损伤模型
观察18α-
18β-甘草酸高、中、低剂量(15
30
60 mg·kg-1)组
联合用药3个不同配伍比例组对急性肝损伤小鼠血清中和肝组织中丙氨酸转氨酶(ALT)
天冬氨酸转氨酶(AST)水平的影响
并检测肝组织匀浆中超氧化物歧化酶(SOD)活力及丙二醛(MDA)含量
同时筛选二者联合用药的最佳配伍比例。结果:与正常组比较
模型组血清AST
肝组织AST
ALT
MDA水平明显升高
SOD活力显著降低(P<0.01)
提示造模成功。与模型组比较
18α-甘草酸组
18β-甘草酸组均可降低小鼠血清中AST
肝组织AST
ALT活力
MDA含量
升高肝组织中SOD活力;比较二者对急性肝损伤小鼠的保护作用
结果18β-甘草酸组对肝组织中AST
ALT水平影响优于18α-甘草酸组
其他指标无显著性差异;二者联合用药的最佳配伍比例为2:3
其对肝组织中AST活力及MDA含量的影响均优于单用18α-或18β-甘草酸治疗组。结论:18α-与18β-甘草酸可保护急性肝损伤小鼠
后者保护作用比前者强
二者配伍的最佳比例是2:3
其对AST
MDA水平影响优于单用18α-或18β-甘草酸。
Objective:To compare the protective effect of 18α-and 18β-glycyrrhizic acid on acute liver injury in mice
and screen out their optimal combination proportion. Method:The mice were randomly divided into normal group
model group
high dose group (60 mg·kg-1)
middle dose group (30 mg·kg-1)
low dose group (15 mg·kg-1) of 18α-and 18β-glycyrrhizic acid. With the drug dose of combined medication groups of 60 mg·kg-1
combined medication 1 groups (18α-glycyrrhizic acid-18β-glycyrrhizic acid 1:3)
combined medication 2 groups (18α-glycyrrhizic acid-18β-glycyrrhizic acid 2:3)
combined medication 3 groups (18α-glycyrrhizic acid-18β-glycyrrhizic acid 1:1). Before the modeling
the drugs were injected once everyday for 7 days
the same volume of saline was given to normal group and model group. At 1 h after the last administration
the treated groups and model group were ip given 0.1%CCl4 peanut oil (20 mL·kg-1) to establish mouse model of acute liver injury induced by CCl4 .The samples of blood and liver from high does group
middle dose group
low dose group and three combination proportion groups of 18α-and 18β-glycyrrhizic acid were analyzed
and level of alanine aminotransferase (ALT)
aspartate aminotransferase (AST)
superoxide dismutase (SOD) and malondialdehyde (MDA) were measured. Result:Compared with the normal group
the serum levels of AST
liver homogenate levels of AST
ALT
MDA in model group were remarkably higher (P<0.01)
levels of SOD was remarkably lower. Compared with the model group
18α-and 18β-glycyrrhizic acid remarkably reduced the serum levels of AST
reduced liver homogenate levels of AST
ALT and MDA
and increased liver homogenate content of SOD. 18β-glycyrrhizic acid had a better effect on liver homogenate levels of AST
ALT than 18α-glycyrrhizic acid
and showed no significant difference in other indexes compared with 18β-glycyrrhizic acid. The optimal combination proportion of 18α-and 18β-glycyrrhizicacid is 2:3
with a better effect on liver homogenate levels of AST
MDA than simple 18α-or 18β-glycyrrhizic acid. Conclusion:18α-and 18β-glycyrrhizic acid can protect acute liver injury in mice. The latter had a better protective effect than the former. Their optimal combination proportion is 2:3
with a better effect on liver homogenate levels of AST
MDA than simple 18α-or 18β-glycyrrhizic acid.
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