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作 者:刘红杰[1,2] 李天昊[1] 詹莎[1] 陈亮[1] 陈灵修 唐树杰[1,2]
机构地区:[1]暨南大学医学院中医学系 [2]暨南大学中西医结合研究所
出 处:《中国临床药理学与治疗学》2017年第3期248-252,共5页Chinese Journal of Clinical Pharmacology and Therapeutics
基 金:国家自然科学基金青年科学基金项目(30901936);广东省中医药局科研项目(20151185)
摘 要:目的:研究艾叶挥发油致小鼠急性肝毒性作用及其可能的机制。方法:水蒸气蒸馏法制备艾叶挥发油。52只SPF级ICR小鼠,雌雄各半,随机分为5组:空白对照组,四氯化碳组,艾叶挥发油1.9 g/kg组、2.3 g/kg组和2.7 g/kg组。一次性灌服等容量药物或溶媒,6 h后取标本,检测血清丙氨酸转氨酶(ALT)、碱性磷酸酶(ALP)、总胆红素(TB),观察肝脏病理组织学变化并进行Ridit分析,检测肝脏组织产生超氧阴离子自由基活力、超氧化物歧化酶(SOD)和丙二醛(MDA)含量、还原型谷胱甘肽(GSH)和氧化型谷胱甘肽(GSSG)含量。结果:与空白对照组比较,不同剂量的艾叶挥发油组血清ALT、ALP含量显著升高(P<0.05);肝脏组织具有变性、坏死等不同程度的损伤,且Ridit积分显著升高(P<0.05);肝组织产生超氧阴离子活力、MDA含量和GSSG含量显著升高(P<0.05),SOD含量和GSH含量显著降低(P<0.05)。结论:艾叶挥发油可通过直接或间接损伤肝细胞而导致小鼠急性肝毒性,其机制可能与氧化应激有关。AIM:To explore the effect and mechanism of acute liver injury induced by volatile oils from artemislae argyi folium in mice.METHODS:Volatile oil from folium artemislae argyi was obtained through hydro-distillation extraction.52 SPF ICR mice (half male and half female) were randomized into five groups,i,e.control group,carbon tetrachloride group,different doses (1.9 g/kg,2.3 g/ kg and 2.7 g/kg) of volatile oils from folium artemislae argyi groups.Biological samples were obtained 6 hours after gavaging equal volume drugs or solvents to mice at a single dose.Alanine amino transferase (ALT),alkaline phosphatase (ALP) and total bilirubin (TB) in serum were detected.Morphologic changes of hepatic tissues were observed and analyzed by Ridit.Superoxide anion free radical,superoxide dismutase (SOD),malondialdehyde (MDA),reduced glutathione (GSH) and oxidized glutathione (GSSG) of hepatic tissues were examined.RESULTS:Compared to those of control group,ALT,ALP,MDA,GSSG,scores of Ridit and superoxide anion free radical of all volatile oil groups increased (P 〈 0.05),while SOD and GSH decreased (P 〈 0.05).Damage of hepatic tissues,such as degeneration,necrosis were observed in the poisoned groups.CONCLUSION:The acute liver injury induced by volatile oil from folium artemislae argyi might directly or indirectly relate to hepatic cells,and the mechanism may be related to oxidative stress.
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