灵芝的改善效应对碳tetrachloride-induced在大鼠肝纤维化。

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林WC,林西城

灵芝的改善效应对碳tetrachloride-induced在大鼠肝纤维化。

世界杂志。2006年1月14日,12 (2):265 - 70。

PubMed ID

16482628 (在PubMed

]

文摘

目的:探讨灵芝、灵芝提取物(GLE)对四氯化碳引起的肝纤维化大鼠(亚兰)。方法:大鼠肝纤维化是由亚兰。四十Wistar鼠随机分为4组:控制、亚兰,和两个GLE组。除了对照组老鼠,老鼠口服药物与亚兰(20%,0.2毫升/ 100克体重)8周的每周两次。老鼠在GLE治疗组每日GLE(1600或600毫克/公斤)通过gastrogavage整个实验周期。肝功能参数,如ALT, AST,白蛋白,白蛋白/球蛋白(A / G)比,肝脾重量和数量的蛋白质,malondiladehyde (MDA)和羟脯氨酸(HP)测定。小天狼星红染色。转化生长因子的表达beta1 (TGF-beta1),蛋氨酸adenosyltransferase (MAT1) 1和MAT2A mRNA利用rt - pcr检测。结果:亚兰导致肝纤维化,增加血浆转氨酶、肝脏MDA和惠普的内容,和脾脏重量;和血浆白蛋白降低,A / G比值和肝脏蛋白质水平。 Compared with CCl4 group, GLE (600, 1,600 mg/kg) treatment significantly increased plasma albumin level and A/G ratio (P < 0.05) and reduced the hepatic HP content (P < 0.01). GLE (1,600 mg/kg) treatment markedly decreased the activities of transaminases (P < 0.05), spleen weight (P < 0.05) and hepatic MDA content (P < 0.05); but increased hepatic protein level (P < 0.05). Liver histology in the GLE (1,600 mg/kg)-treated rats was also improved (P < 0.01). RT-PCR analysis showed that GLE treatment decreased the expression of TGF-beta1 (P < 0.05-0.001) and changed the expression of MAT1A (P < 0.05-0.01) and MAT2A (P < 0.05-0.001). CONCLUSION: Oral administration of GLE significantly reduces CCl4-induced hepatic fibrosis in rats, probably by exerting a protective effect against hepatocellular necrosis by its free-radical scavenging ability.

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药物酶

药物	酶	类	生物	药理作用	行动
蛋氨酸	S-adenosylmethionine合成酶同种型2型	蛋白质	人类	未知的	底物	细节