维生素E抗大鼠上氯化碳所致肝纤维化的实验研究

目的 为探讨维生素（ＶＥ）对肝纤维化的治疗作用。方法 观察了ＶＥ对四氯化碳的诱导的肝纤维化大鼠肝功能，脯氨酸肽酶（ＰＬＤ），透明质酸（ＨＡ）、丙二醛（ＭＤＡ）、氧化物歧化酶（ＳＯＤ）及肝脏组织学的影响，同时设有正常对照、溶剂对照及空白组。结果维生素Ｅ治疗１０周后，上述生化指标除ＨＡ（３８７．５７±１２９．３９ｎｇ／ｍｌ）仍示达正常外，其余各指标均恢复正常，其中ＡＬＴ干第２周后、ＰＬＤ和ＭＤＡ于第４     

维生素E与肝纤维化

维生素E具有抗肝纤维化作用,详细作用机制不明,可能与其影响肝细胞、枯否细胞、贮脂细胞等有关。     

维生素E对肝纤维化大鼠肝脏病变及血型胶原表达的影响

为了解补充维生素E(VE)对肝纤维化的影响,以四氯化碳(CCl_4)诱导大鼠肝纤维化模型,对VE(100mg/kg,2次/周,连续10～20周)抗肝纤维化的作用进行了研究。于治疗后10周、20周取肝组织作病理检查及Ⅲ型胶原免疫组化染色,同时设溶剂对照组及盐水对照组。结果表明,经VE治疗后,肝纤维化大鼠肝脏胶原纤维及网状纤维由粗大变纤细并有缩短及断裂;免疫组化染色发现肝纤维化大鼠肝内Ⅲ型胶原主要位于肝细胞浆,呈弥漫性分布,VE治疗组含量较对照组减少,经真彩色图像系统分析与对照组差异显著(P<0.01)。提示VE治疗有助于实验性肝纤维化的恢复。     

促肝细胞生长素、维生素E联用对大鼠实验性肝纤维化影响的研究

目的：观察促肝细胞生长素（HGF），维生素E（Vit E)联合应用抑制大鼠实验性肝纤维化的可行性。方法：以20％CCl4豆油溶液腹腔注射和高脂食物喂养制备SD大鼠肝纤维化模型，设HGF组，VitE组，HGF＋VitE组和非治疗组，疗程结束后（6周）对受试各组进行血清学和肝组织学检查。结果：HGF＋VitE组在血清学（ALT，HA，HYP）和组织学的改善均优于HGF组或VitE组，结论：HGF和VitE联用对大鼠实验性肝纤维化的防治作用优于单一用药。     

联用阿米洛利与维生素E预防大鼠肝纤维化的实验研究

新近关于肝纤维化形成机制的研究表明,氧应激和Na^ ／H^ 交换泵在肝纤维化形成中起重要作用,为抗肝纤维化的研究提供了新靶点。本实验通过建立二甲基亚硝胺诱导的肝纤维化模型,观察联用Na^ ／H^ 交换泵抑制剂阿米洛利(amiloride,Am)与抗氧化剂维生素E联用对大鼠纤维化形成的影响,以探索临床抗肝纤维化的新途径。     

中西药抗四氯化碳实验性大鼠肝纤维化研究

目前，中西药抗肝纤维化的实验研究已取得可喜进展，四氯化碳(CCl4)诱导的大鼠肝纤维化模型是经典的研究肝纤维化的模型，本文将近几年中西药抗CCl4中毒性肝纤维化的实验研究综述如下。     

维生素E与肝纤维化

目前 ,关于维生素Ｅ抗肝纤维化作用屡有报道〔1,2〕,本文就维生素Ｅ的组成和体内代谢 ,它的抗氧化性及其对肝纤维化的影响作一综述。1　维生素Ｅ的组成及体内代谢维生素Ｅ是具有α -生育酚 (α -ＴＨ)生物活性化合物的总称 ,可分二类 :生育酚 (ｔｏｃｏｐｈｅｒｏｌ)和三烯生育酚 (ｔｏｃｏｔｒｉｅｎｄｓ)。自然界共有 8种化合物 ,即α、β、γ、δ -生育酚和α、β、γ、δ -三烯生育酚。其中α-生育酚具有 3个甲基定位于色满醇环的 5、7、8位上 ,是生物活性最强的生育酚。维生素Ｅ在体内主要分布于脂蛋白中。正常人为 6 5%在低密度脂蛋白…     

维生素E与肝纤维化

维生素Ｅ具有抗肝纤维化作用，详细作用机制不明，可能与其影响肝细胞、枯否细胞、贮脂细胞等有关。     

硒和维生素E对实验性肝纤维化的协同保护作用

目的：观察硒(Se)和维生素E(Vit．E)单独应用和联合应用对肝纤维化的影响。方法：以40％ CCl4制备大鼠肝纤维化模型，分别以单纯和联合补充Se和Vit．E的形式，观察血清肝功能指标(ALT、AST、Glb)、肝纤维化指标(HA)、抗氧化指标(SOD)和肝脏组织学变化。结果：单纯补充Se或Vit．E能够降低大鼠血清ALT、AST和Glb的含量，减轻肝细胞变性及肝纤维化增生程度，对SOD活性无显著性影响，单纯补充Vit.E能降低HA水平。联合补充Se和Vit．E对以上指标均有明显改善，且能显著提高SOD活性。结论：Se和Vit．E联合应用优于单一应用，二者具有协同保护效应。     

川芎嗪抗肝纤维化作用的实验研究

目的:观察川芎嗪的抗肝纤维化作用。方法:用50％四氯化碳油剂腹腔注射6周诱导大鼠肝纤维化模型并用川芎嗪治疗,观察其对肝纤维化各项指标的影响。结果:川芎嗪能显著降低大鼠血清谷丙转氨酶(ALT)、丙二醛(MDA)、透明质酸(HA)、Ⅲ型前胶原(PCⅢ)及肝组织中MDA;提高肝组织中超氧化物歧化酶(SOD)活性;显著减轻肝脏胶原纤维增生程度。结论:川芎嗪有抗脂质过氧化作用及抗肝纤维化作用。     

Antioxidants vitamin E and C attenuate hepatic fibrosis in biliary-obstructed rats

INTRODUCTION Hepatic fibrosis is a highly integrated cellular response to tissue injury[1]. It is essentially characterized by activation of hepatic stellate cells, secretion and accumulation of extracellular matrix proteins[2]. Various causes of cholesta…     

A comparative study of grape seed extract and vitamin E effects on silica-induced pulmonary fibrosis in rats

Due to the production of reactive oxygen species (ROS), oxidative stress has been implicated in the pathogenesis of silica-induced lung fibrosis. So it is hypothesized that grape seed extract (GSE) or vitamin E (Vit E) as antioxidants may ameliorate some symptoms of the disease. Male Wistar albino rats were divided into 7 groups: rats in group I instilled intratracheally (IT) with a single dose of silica suspension (50mg/rat) as positive control (PC). Treatment groups (II-IV) received Vit E (20 IU/kg/day), GSE (150 mg/kg/day), or Vit E+GSE simultaneously orally 1 day after instillation of silica. Groups V and VI were given oral GSE or Vit E after instillation of the equivalent volume of saline (IT) as controls for GSE or Vit E. Rats of group VII only instilled saline (IT) as negative control. After 90 days animals were sacrificed and plasma-malondialdehyde (p-MDA) and lung tissue hydroxyproline (HP) were quantified. The lungs were also investigated for histopathological changes. The mean concentrations of p-MDA and HP in studied groups (I-VII) were 1.95, 2.77, 0.72, 0.81, 0.64, 0.94, 1.02 micromolMDA/L(plasma) and 28.476, 27.85, 22.83, 22.64, 15.40, 18.31, 18.51 mgHP/g(tissue), respectively. Silica caused a significant increase in HP content of lungs and MDA levels in the plasma except in GSE-treated groups (III and IV). According to the results of this study GSE could reduce the fibrogenic effect of silica. However; no synergistic effect was observed after co-administration of GSE and Vit E.     

Effects of extract from Ginkgo biloba on carbon tetrachloride-induced liver injury in rats

AIM: To study the effects of extract from Ginkgo biloba (EGb) containing 22% flavonoid and 5% terpenoid on chronic liver injury and liver fibrosis of rats induced by carbon tetrachloride (CCl4). METHODS: All rats were randomly divided into control group, CCl4-treated group, colchicine-treated group and EGb-protected group. Chronic liver injury was induced in experimental groups by subcutaneous injection of CCl4 and fed with chows premixed with 79.5% corn powder, 20% lard and 0.5% cholesterol (v/v). EGb-protected group was treated with EGb (0.5 g/kg body weight per day) for 7 wk. At the end of wk 8, all the rats were killed. Liver function, liver fibrosis, oxidative stress and expression of transforming growth factorβ1 (TGF-β1), a-smooth muscle actin (α-SMA) and typeⅠcollagens in liver were determined. In addition, pathology changes of liver tissue were observed under light microscope. RESULTS: The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and albumin (Alb) in EGb-protected group were notably improved as compared with the CCL4-treated group (P < 0.01). The contents of serum hyaluronic acid (HA), typeⅢprocollagen (PCⅢ), typeⅣcollagen (CIV) and the expression of hepatic tissue TGF-β1,α-SMA and typeⅠcollagen in EGb-protected group were significantly lower than those in CCL4-treated groups (P < 0.05, P < 0.01). The degrees of liver fibrosis in EGb-protected groups were lower than those in CCL4-treated groups (6.58±1.25 vs 9.52±2.06, P < 0.05). Compared to the CCL4-treated group, the levels of plasma glutathoine peroxidase (Se-GSH-Px), superoxide dismutase (SOD) and malondialdehyde (MDA) were strikingly improved also in EGb-protected group (P < 0.05, P < 0.01). CONCLUSION: EGb resists oxidative stress and thereby reduces chronic liver injury and liver fibrosis in rats with liver injury induced by CCl4     

Effects of vitamin E deficiency on bleomycin-induced pulmonary fibrosis in the hamster

The effects of vitamin E deficiency on bleomycin (BLM)-induced pulmonary fibrosis have been studied by analyses of pressure volume (PV) curves and morphological examinations. Golden hamsters were divided into groups on a control diet (group C), vitamin E-deficient diet (E), control diet with BLM treatment (CB), and vitamin E-deficient diet with BLM treatment (EB). Group EB showed PV curves shifted downward and to the right soon after BLM administration (10 days) and gradually shifted upward and to the left compared to group CB in the later period (30 and 60 days after BLM treatment). Histologically group EB was characterized by relatively severe interstitial pneumonitis in the early stages. In later stages, emphysematous changes were induced in combination with a lesser degree of fibrosis in group EB. Mean thickness of the alveolar wall of group CB was larger than group C while that of group EB was smaller at 30 days after BLM treatment. These results indicate that, with BLM treatment, vitamin E-deficient hamsters show increased distensibility on the PV curve and emphysematous changes mixed with focal fibrosis on morphological examination. This means that by adding other modulating factors, such as vitamin E deficiency, BLM, an agent known to produce pulmonary fibrosis, acts to induce an emphysematous lesion in the lung. Although pulmonary fibrosis and emphysema have been considered to be final and different forms of parenchymal injury, each may proceed to the other under the influence of some modulating factors.     

砷中毒对小鼠脏器脂质过氧化的影响及VE干预作用的研究

目的研究不同水平的砷对小鼠脏器组织脂质过氧化的影响,并观察维生素E(VE)对砷毒作用的干预作用。方法昆明种小鼠按2因素3水平析因实验设计分为9组,不同实验组的动物通过喂饲法给三氧化二砷和VE复制亚慢性砷中毒动物模型。三氧化二砷的分组剂量按照其对小鼠经口半数致死量LD50进行分组,VE按照我国青少年每日推荐量进行分组。2个月后,采用试剂盒,研究砷对小鼠脏器组织中超氧化物歧化酶(SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量的影响以及给于VE处理后的干预作用。结果染毒组动物脏器组织中SOD、GSH-Px活力低于正常对照组动物(P<0.05),MDA含量高于正常对照组(P<0.05);VE处理后动物脏器组织中SOD、GSH-Px活力增强,MDA含量降低(P<0.05)。结论砷能引起小鼠脏器组织中氧化与抗氧化系统失衡,VE可拮抗砷对小鼠脏器氧化水平与抗氧化能力的影响。     

Lipid peroxidation in lung of rat stressed by immobilization: Effects of vitamin E supplementation

This study was carried out to examine the possibility of initiation of lipid peroxidation in the lung of Wistar albino male rats stressed by immobilization. The effects of vitamin E supplementation were also investigated. We found that immobilization of rats with normal pulmonary content of vitamin E caused lipid peroxidation in the lung. Decrease of the lung content of unsaturated fatty acids and vitamin E was also established. The immobilization-induced changes of all of these parameters were significantly inhibited by vitamin E injection (100 mg/kg body weight) for 7 days. A possible sequence of events leading to the initiation of lipid peroxidation and lung cell membrane damage in rats stressed by immobilization is discussed. Offprint requests to: Stefan Ribarov, PhD     

Effects of dietary supplementation with vitamin E and selenium on rat hepatic stellate cell apoptosis

AIM: To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells (HSCs), in acute liver injury induced by CCl4, and to explore their role in the recovery from hepatic fibrosis phase. METHODS: An acute liver damage model of rats was established by intraperitoneal injection of carbon tetrachloride (0.3 mL/100 g body weight) twice a week, then the rats were killed at 6, 24, 48, and 72 h after the first and third injection, respectively. A liver fibrosis model was established by the same injection for 8 wk. Then three rats were killed at 3, 7,14, and 28 d after the last injection, respectively. The rats from the intervention group were fed with chow supplemented with vitamin E (250 mg/kg) and selenium (0.2 mg/kg), and the rats in the normal control group and pathological group were given standard chow. Livers were harvested and stained with hematoxylin and eosin, Sirius red. Activated HSCs were determined by α-smooth muscle actin immunohistochemistry staining. Apoptotic HSCs were determined by dual staining with the terminal deoxynucleotidyl transferase UTP nick end labeling (TUNEL) and α-smooth muscle actin immunohistochemistry. Serum alanine aminotransferase and aspartate aminotransferase were also analyzed. RESULTS: In the acute liver damage model, the degree of liver injury was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, while the number of apoptotic HSCs was more in the intervention group than in the pathological group. In the liver fibrosis model, the degree of liver fibrosis was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, and the number of apoptotic HSCs was more in the intervention group than in the pathological group. CONCLUSION: Vitamin E and selenium supplementation at the given level can inhibit CCl4-induced activation and proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage phase. Vitamin E and selenium can also effectively decrease the degree of hepatic fibrosis and promote the recovery process.     

罗汉果甜苷对四氯化碳诱导的肝纤维化大鼠的保护作用

目的研究罗汉果甜苷对大鼠肝纤维化的保护作用。方法除正常组外,其余各组采用四氯化碳(CCL4)诱导肝纤维化模型,于造模第7周起,给药组分别灌胃给予相应的受试药,疗程6周。实验结束后,观察罗汉果甜苷对大鼠血清ALT、AST活性,HA、PⅢP、CⅣ含量,肝组织SOD活性及MDA含量的影响,观察罗汉果甜苷对肝组织转化生长因子β1(TGF-β1)表达的影响及对肝组织病理变化的影响。结果罗汉果甜苷各剂量组能明显降低肝纤维化大鼠ALT、AST、MDA、CⅣ、PⅢNP含量,升高SOD水平,减轻肝组织病理损伤程度,抑制肝组织中TGF-β1表达。结论罗汉果甜苷对CCL4诱导的肝纤维化大鼠有很好的保护作用。