氢盐水对大鼠酒精性肝损伤的保护作用

目的:研究肝脏病理形态学、肝功能、氧化应激因子的变化,探讨氢盐水(hydrogen-rich saline,HS)对大鼠酒精性肝损伤的保护作用.方法:将40只SD大鼠随机分为空白对照组、模型组、低剂量HS治疗组、高剂量HS治疗组;采用梯度酒精灌胃方法建立大鼠慢性酒精性肝损伤模型,模型组及治疗组给予酒精灌胃12wk,低剂量HS治疗组和高剂量HS治疗组同时分别给予HS5g/kg、10g/kg体质量,腹腔注射;空白对照组给予等热量、等体积的糖水灌胃.12wk后检测大鼠血清谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate aminotransferase,AST)、总胆红素(total bilirubin,TBIL)、甘油三酯(triglyceride,TG)、肝组织匀浆丙二醛(malonyldialdehyde,MDA)、还原型谷胱甘肽(reduced glulathione hormone,GSH)、超氧化物歧化酶(superoxide dismutase,SOD)的含量,肝组织HE染色观察肝组织形态学变化.结果:灌酒12wk后模型组大鼠血清ALT、AST、TG、TBIL水平均明显上升(65.82±16.14vs36.43±4.92,180.45±35.51vs110.53±18.43,0.92±0.13vs0.35±0.07,1.92±0.34vs0.74±0.12,P<0.01);肝脏GSH含量、SOD活性下降(78.56±16.45vs135.43±19.81,93.14±21.05vs181.53±30.13,P<0.01),而MDA含量增加显著(8.04±1.12vs3.25±0.83,P<0.01);HS低剂量组和高剂量组大鼠血清ALT、AST、TG、TBIL下降显著(43.26±8.81,41.15±8.89vs65.82±16.14;130.42±11.64,125.81±10.84vs180.45±35.51;0.44±0.09,0.38±0.08vs0.92±0.13;1.03±0.21,0.89±0.15vs1.92±0.34;P<0.01);SOD、GSH活性明显增加(162.51±28.56,164.24±30.07vs93.14±21.05;105.42±17.32,110.67±20.51vs78.56±16.45;P<0.01),MDA含量明显上升(4.56±0.98,4.21±1.05vs8.04±1.12;P<0.01).HE染色结果显示,模型组大鼠肝组织可见中重度肝细胞变性,胞质内见大小不一的脂滴空泡,窦内皮细胞肿胀,汇管区炎细胞浸润;HS低、高剂量组肝组织脂肪变性、炎细胞浸润程度减轻.结论:HS可有效地抗氧化应激和脂质过氧化,改善肝功能,减轻酒精诱导的大鼠慢性肝损伤.     

甜菜碱对酒精性肝损伤大鼠高同型半胱氨酸血症和肝脂质过氧化的影响

目的：观察甜菜碱对大鼠高同型半胱氨酸血症（hyperhomoeysteinemia，HHcy）和肝脏脂质过氧化的作用和影响。方法：将60只SD大鼠随机分为5组（每组12只）：正常对照组，模型组，甜菜碱低、高剂量组，腺苷蛋氨酸（S-adenosylmethionine，SAM）组。除对照组外，其余4组给予酒精、鱼油灌胃配合高脂饮食构建酒精性肝损伤大鼠模型，药物治疗于造模4周后开始，第8周处死全部大鼠，测定血浆总同型半胱氨酸（total plasma homoeysteine，tHcy）浓度、血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、白蛋白（Alb）、白／球蛋白比值（A／G）、肝匀浆丙二醛（MDA）、超氧化物歧化酶（SOD）和还原型谷胱甘肽（GSH）含量，并进行肝脏病理组织学检查。结果：与对照组比较，模型组大鼠tHcy、ALT、AST、MDA含量均明显升高（P〈0．01），SOD、GSH水平明显降低（P〈0．01）。与模型组对比，甜菜碱低、高剂量组大鼠tHcy、ALT、AST、MDA均显著降低（P〈0．01），肝组织SOD含量明显上升（P〈0．01），GSH含量无显著变化（P〉0．05），甜菜碱低、高剂量组之间无明显差异（P〉0．05）；SAM组能显著增加肝组织GSH贮量（P〈0．01），但对血浆tHcy水平无显著影响（P〉0．05），余治疗作用均与甜菜碱治疗无显著差别（P〉0．05）。结论：甜菜碱可防治酒精性肝损伤，其机制可能为降低高同型半胱氨酸血症，改善肝组织脂质过氧化。本文结果显示，甜菜碱的作用优于腺苷蛋氨酸。     

腺苷蛋氨酸对酒精性脂肪肝大鼠治疗效果及机制的研究

目的观察腺苷蛋氨酸（SAM）对酒精性肝损伤的防治作用及机制。方法将48只SD大鼠随机分为对照组（Ⅰ组）、模型组（Ⅱ组）及SAM低剂量组（Ⅲ组）、SAM高剂量组（Ⅳ组）,每组12只。除对照组外,其余三组给予酒精、鱼油灌胃配合高脂饮食诱导酒精性肝损伤,4周后Ⅰ、Ⅱ组腹腔注射生理盐水,Ⅲ、Ⅳ组分别腹腔注射SAMl00mg／kg、200mg／kg,第8周均处死。测定血浆总同型半胱氨酸（tHcy）浓度、血清丙氨酸转移酶（ALT）、天冬氨酸转移酶（AST）浓度;测定肝匀浆丙二醛（MDA）、超氧化物歧化酶（SOD）和还原型谷胱甘肽（GSH）含量,行肝脏病理组织学检查。结果与Ⅰ组比较,Ⅱ组肝损伤明显,表现为ALT、AST、tHcy水平升高,肝脂肪变性,MDA含量增加,SOD和GSH水平下降;Ⅲ、Ⅳ组MDA降低、GSH升高,但tHcy水平和肝组织SOD含量无显著变化,Ⅲ、Ⅳ组间无明显差别。结论SAM可防治大鼠酒精性肝损伤,其机制可能与调节肝脏内氧化抗氧化系统的平衡有关;SAM对血浆tHcy水平无明显影响。     

Protective effect of melatonin against alpha-naphthylisothiocyanate-induced liver injury in rats

The protective effect of melatonin against alpha-naphthylisothiocyanate (ANIT)-induced liver injury with cholestasis was examined in rats injected once with the toxicant (75 mg/kg body weight (BW)). In rats injected with ANIT alone, liver injury with cholestasis did not occur 12 hr after the injection but appeared at 24 hr, judging from the serum levels of marker enzymes and components. When melatonin (10 or 100 mg/kg BW) was orally administered to the ANIT-injected rats at 12 hr after the injection, the administered indoleamine dose-dependently prevented the formation of liver injury with cholestasis. In rats injected with ANIT alone, serum lipid peroxide (LPO) concentration increased 24 hr after the injection, while liver LPO concentration increased 12 hr after the injection and further increased at 24 hr. Myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration, in the liver of the ANIT-injected rats increased 12 hr after the injection and further increased at 24 hr. The oral administration of melatonin (10 or 100 mg/kg BW) to the ANIT-injected rats attenuated the increases in serum and liver LPO concentrations and liver MPO activity found at 24 hr after the injection in a dose-dependent manner. These results indicate that orally administered melatonin at pharmacological doses protects against ANIT-induced liver injury with cholestasis in rats, and suggest that this protective effect of melatonin could be due to its antioxidant action and its inhibitory action against neutrophil infiltration in the liver of ANIT-injected rats.     

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     

Betaine inhibits Toll-like receptor 4 expression in rats with ethanol-induced liver injury

AIM:To test whether ethanol feeding could induce Toll-like receptor 4(TLR4)responses,assess the hepatoprotective effect of betaine and its inhibitive effect on TLR4 in animal models of alcoholic liver injury.METHODS:Forty-eight female Sprague-Dawley rats were randomly divided into four groups as control,model,low and high dose betaine groups.Except control group,all rats were fed with high fat-containing diet plus ethanol and fish oil gavages for 8 wk.Betaine was administered intragastrically after exposure...     

三七总甙对非酒精性脂肪肝大鼠肝组织细胞色素P450 2E1表达的影响

目的研究三七总甙对非酒精性脂肪肝大鼠肝组织细胞色素P450 2E1表达的影响。方法用脂肪乳剂灌胃法诱导大鼠非酒精性脂肪肝模型，并给予三七总甙干预，观察肝组织病理学形态的变化，采用免疫组化法检测肝组织细胞色素P450 2E1的表达，酶标仪法测定肝内丙二醛（MDA）、超氧化物岐化酶（SOD）、游离脂肪酸（FFA）含量。结果与模型组比较，三七总甙干预组肝细胞的脂肪变程度明显减轻，脂滴减少，CYP 2E1的表达受到明显抑制，肝内SOD活性升高，MDA、FFA显著降低。结论三七总甙能显著抑制大鼠脂肪肝CYP 2E1的表达，减轻脂质过氧化反应，因而具有防治脂肪肝的作用。     

柳叶蜡梅提取物对小鼠急性酒精性肝损伤的保护作用

目的：研究柳叶蜡梅提取物对小鼠急性酒精性肝损伤是否具有保护作用。方法雄性C57BL/6小鼠分为4组,每组10只。对照组为正常C57BL/6小鼠;模型组用75％酒精溶液（8 mL/kg）灌胃,每天一次,连续4 d ,建立急性酒精性肝损伤模型;柳叶蜡梅组用柳叶蜡梅提取物（12 g/kg ）溶于生理盐水后灌胃,每天两次,连续11 d;实验组先按柳叶蜡梅组方法灌胃11 d ,同时在最后4 d按模型组方法建立急性酒精性肝损伤模型。通过比较各组血清ALT和AST水平,并评价肝组织病理损伤程度,观察柳叶蜡梅提取物对小鼠急性酒精性肝损伤的保护作用。结果柳叶蜡梅提取物可明显减轻酒精所致急性肝损伤,实验组小鼠血清ALT[（148．75±13．30） U/L]、AST [（170．75±16．96） U/L]与模型组ALT[（260．75±27．35） U/L]、AST[（337．75±37．68） U/L]相比明显降低,肝组织病理损伤和炎症反应减轻（P＜0．05）。结论柳叶蜡梅提取物在小鼠急性酒精性肝损伤中起到保护作用,可能成为急性酒精性肝损伤的新的治疗策略。     

乙醇诱导脂肪肝过程中肝组织一氧化氮合酶的表达及作用

目的　观察乙醇诱导脂肪肝过程中肝组织一氧化氮合酶 (NOS)的表达 ,探讨不同亚型NOS表达与脂质过氧化的关系。方法　在大鼠饮水中加入乙醇建立乙醇性脂肪肝模型 ,采用免疫组化和逆转录多聚酶链反应 (RT PCR)的方法动态观察肝组织中NOS的蛋白及基因表达 ,同时检测肝组织中一氧化氮 (NO)、丙二醛 (MDA)含量。结果　成功建立乙醇性脂肪肝大鼠模型。与正常对照组相比 ,造模大鼠肝组织在第 4周时诱导型一氧化氮合酶 (iNOS)表达已显著增加 (P <0 .0 5 ) ,第 12周达高峰 ,而后有所下降 ,第 2 0周时又明显上升 (P <0 .0 1)。内皮型一氧化氮合酶 (eNOS)在第 4周时表达无明显改变 (P >0 .0 5 ) ,随造模时间延长而逐渐降低 (P <0 .0 5 )。肝组织中NO水平在第 4周时无明显升高 (P>0 .0 5 ) ,以后显著增加 ,第 12周达高峰 ,而后有所下降 ,第 2 0周时又明显上升 (P <0 .0 1)。肝组织中MDA含量在第 4周已显著升高 (P <0 .0 5 ) ,随饮用乙醇时间延长进行性增加。肝组织中NO、MDA含量与iNOS表达成正相关 (P <0 .0 1) ,与eNOS表达成负相关 (P <0 .0 1)。结论　乙醇诱导脂肪肝过程中肝组织NO水平升高主要与iNOS的活化有关 ,iNOS产生的NO可能与脂质过氧化损伤有关 ,而eNOS产生的NO可能起抗脂质过氧化损伤的保护作用。     

Adenosine and cytokine levels following treatment of rheumatoid arthritis with dipyridamole

Adenosine can suppress the release of tumour necrosis factor-α (TNF-α) from activated monocytes and macrophages, and may contribute to the anti-inflammatory activities of methotrexate and sulphasalazine. Dipyridamole inhibits the cellular uptake and metabolism of adenosine and we have, therefore, examined the effects of dipyridamole in patients with rheumatoid arthritis in an attempt to alleviate their symptoms. Forty patients aged 18–75 years were randomised to receive dipyridamole 400 mg/day or placebo. Blood samples were taken at baseline and at monthly intervals for 6 months. Purines were determined by HPLC and cytokines by ELISA. After 3 months of treatment there were significant reductions in neopterin levels and in the modified Health Assessment Questionnaire score, but these were not maintained. Dipyridamole had no effect on disease severity or the levels of purine metabolites, interleukin-1β (IL-1β), IL-6, TNF-α, lipid peroxidation products, erythrocyte sedimentation rate or C-reactive protein. In conclusion, rheumatoid arthritis patients showed no clinical improvement following treatment with dipyridamole for 6 months.     

Hepatoprotective effect of the aqueous extract of the roots of Decalepis hamiltonii against ethanol-induced oxidative stress in rats.

The hepatoprotective activity of the aqueous extract of the roots of Decalepis hamiltonii was investigated against ethanol-induced oxidative stress and liver damage. Pretreatment of rats with aqueous extract of the roots of D. hamiltonii, single (50, 100 and 200mg/kg b.w.) and multiple doses (50 and 100mg/kg b.w. for 7 days) significantly prevented the ethanol (5g/kg b.w.) induced increases in the activities of the serum enzymes, aspartate and alanine transaminases, alkaline phosphatase and lactate dehydrogenase in a dose dependent manner. Parallel to these changes, the root extract inhibited the ethanol-induced oxidative stress in the liver by suppressing lipid peroxidation and protein carbonylation and maintaining the levels of antioxidant enzymes and glutathione. The biochemical changes were consistent with histopathological observations suggesting marked hepatoprotective effect of the root extract. The protective effect of the root extract against hepatotoxicity of alcohol was more pronounced by the multiple dose pretreatment. Hepatoprotective activity of the aqueous extract of the roots of D. hamiltonii could be attributed to the antioxidant effect of the constituents and enhanced antioxidant defenses.     

甜菜碱对酒精性肝损伤大鼠凋亡基因caspase-12表达的影响

目的:研究甜菜碱对凋亡基因caspase-12表达的影响,探讨其抗酒精性肝损伤(ALD)大鼠肝细胞凋亡的机制.方法:采用酒精加鱼油灌胃配合高脂饮食建立酒精性肝损伤模型,应用半定量逆转录聚合酶链反应(RT-PCR)法和免疫组化法检测大鼠肝组织凋亡基因caspase-12mRNA和蛋白水平.结果:与正常组比较,模型组大鼠肝组织caspase-12表达明显增强(mRNA:1.00vs0.18,P<0.01;蛋白:0.2969±0.0451vs0.0526±0.0234,P<0.01),但高、低剂量甜菜碱能抑制其表达(mRNA:0.10,0.12vs1.00,P<0.01;蛋白:0.1215±0.0130,0.1850±0.0085vs0.2969±0.0451,P<0.01).甜菜碱高、低剂量组之间有显著差异(mRNA:0.10vs0.12,P<0.05;蛋白:0.1215±0.0130vs0.1850±0.0085,P<0.05).结论:甜菜碱能抑制凋亡基因caspase-12mRNA和蛋白的表达,可能是其减少凋亡的机制之一.     

酒精性肝损伤大鼠肠道屏障功能改变及谷氨酰胺的保护作用观察

目的 观察酒精性肝损伤大鼠肠道屏障功能的改变,并探讨谷氨酰胺的保护作用。方法 36只SD大鼠随机分为正常对照组（A组）、模型组（B组）和谷氨酰胺治疗组（C组）,分别检测肠道细菌易位率、肠粘膜通透性,同时观察血生化、肝脏和末段回肠粘膜病理学改变。结果 与A组比,B组大鼠血清AST和ALT水平显著升高（AST：256．6±50．8U／L对175．2±16．2U／L,P〈0．05;ALT：86．5±5．4U／L对53．7±13．2U／L,P〈0．05）,C组无显著变化（P〉0．05）;B组肠道细菌易位率明显增高（62．5％,P〈0．05）,C组无显著变化（35．0％,P〉0．05）;B组肠粘膜通透性显著升高（235．1±26．4ml·min^-1·cm^2对30．1±33．6ml·min^-1·cm^2,P〈0．05）,C组肠粘膜通透性比B组明显下降（190．9±19．8ml·min^-1·cm^2对235．1±26．4ml·min^-1·cm^2,P〈0．05）：B组大鼠末段回肠病理损伤明显加重（3．8±0．9对0．4±0．5,P〈0．05）,C组比B组明显下降（2．7±0．7对3．8±0．9,P〈0．05）。结论 大鼠酒精性肝损伤伴有肠道屏障功能改变,谷氨酰胺对大鼠酒精性肝损伤及肠道屏障功能具有双重保护作用。     

内质网分子伴侣糖调节蛋白94在大鼠酒精性肝损伤中的高表达和意义

目的检测酒精性肝损伤大鼠肝组织内质网分子伴侣糖调节蛋白94的表达情况,探讨酒精性肝损伤的发病机制.方法24只SD雌性大鼠分成对照组和模型组.模型组大鼠给予乙醇加鱼油灌胃配合高脂饮食8周,建立酒精性肝损伤模型,应用半定量逆转录聚合酶链反应(RT-PCR)法和免疫组化法检测大鼠肝组织内质网分子伴侣糖调节蛋白94 mRNA和蛋白水平.结果与正常组比较,模型组大鼠肝组织糖调节蛋白94 mRNA和蛋白表达明显增强(P＜0.01).结论酒精性肝损伤大鼠存在糖调节蛋白94高表达,这可能是该病的发病机制之一.     

The effect of ethanol, ethanol metabolizing enzyme inhibitors, and Vitamin E on regulating glutathione, glutathione S-transferase, and S-adenosylmethionine in mouse primary hepatocyte.

We studied changes in the antioxidant systems involved in hepatoprotection after ethanol exposure in primary culture of mouse hepatocytes. Ethanol decreased glutathione (GSH) levels and the S-adenosylmethionine (SAMe) to S-adenosylhomocysteine (SAH) ratio by 53% and 22%, respectively. Cytosolic glutathione S-transferase (GST) activity was significantly lower in ethanol exposed hepatocytes, which was accompanied by an increase in GST activity in the culture medium. When specific substrates for mu- and pi-class GST were utilized, ethanol significantly decreased the mu- and pi-class GST activity by 53% and 13%, respectively. Lipid peroxidation (LPO), assessed by the thiobarbituric acid assay, increased to 221% of control by ethanol and was potentiated by cyanamide, an aldehyde dehydrogenase inhibitor. The changes in LPO, cytosolic GST activity, GSH levels and SAMe/SAH ratio in ethanol exposed hepatocytes were completely or partially reversed by either Vitamin E or 4-methylpyrazole, an alcohol dehydrogenase (ADH) inhibitor. Retinoid X receptor alpha-deficient (RXRalpha KO) mice, which are more susceptible to ethanol-induced liver toxicity, have decreased pi-class GST (56%), mu-class GST (28%), and glutathione peroxidase (35%) activities compared with wild type. Taken together, primary hepatocyte provides a valuable model to analyze ethanol-induced oxidative stress. The inhibition of mu-class GST activity by ethanol and the decreased pi-class GST activity in RXRalpha KO mice implicate the importance of these isozymes in ethanol detoxification process.     

Effects of granulocyte colony stimulating-factor in a rat model of acute liver injury

BACKGROUND/AIM: Controversial experimental observations suggest that granulocyte colony stimulating-factor may promote hepatic regeneration after hepatectomy and chemical injury either by directly stimulating adult liver cells or facilitating the mobilization of bone marrow cells and their homing to the liver. We investigated whether different schedules of granulocyte colony stimulating-factor administration protect against experimental acute liver injury. METHODS: Acute liver injury was induced in Sprague-Dawley fed rats by injecting a single intraperitoneal dose of carbon tetrachloride. Recombinant human granulocyte colony stimulating-factor or vehicle was given daily after intoxication (4 days) or before (7 days) and after carbon tetrachloride administration. Liver injury and regeneration were assessed 2 and 4 days after damage. Bone marrow cells mobilization was evaluated by the white blood cell count and the assessment of circulating clonogenic haematopoietic progenitors (colony forming unit-cells). RESULTS: In this experimental model, although granulocyte colony stimulating-factor induced the significant mobilization of colony forming unit-cells, the study cytokine had no effect on liver injury (serum alanine amino transaminase level and necrotic index) and liver regeneration (mitotic index and bromodeoxyuridine incorporation), regardless of the administration schedule. CONCLUSIONS: This study does not support the conclusion that: (1) granulocyte colony stimulating-factor exerts a protective effect against toxic-induced, non-lethal acute liver injury and (2) promotes hepatocyte regeneration.     

Preventive effect of melatonin on the progression of alpha-naphthylisothiocyanate-induced acute liver injury in rats

The preventive effect of melatonin on the progression of alpha-naphthylisothiocyanate (ANIT)-induced acute liver injury with cholestasis was examined in rats treated once with the hepatotoxin [75 mg/kg body weight (BW), i.p.]. In rats treated with ANIT alone, liver injury with cholestasis occurred 24 hr after treatment and progressed at 48 hr, judging from the serum levels of hepatobiliary marker enzymes and components. Melatonin (10 or 100 mg/kg BW) was orally administered to the ANIT-treated rats, 24 hr after the hepatotoxin treatment at which time hepatic injury had already developed. The administered indoleamine prevented the progression of liver cell damage rather than biliary cell damage more effectively at the higher dose than at the lower dose. In rats treated with ANIT alone, the serum and hepatic concentrations of thiobarbituric acid reactive substances, an index of lipid peroxidation, and the hepatic activity of myeloperoxidase, an index of tissue neutrophil infiltration, increased 24 hr after treatment and further increased at 48 hr. In the liver of rats treated with ANIT alone, Cu,Zn-superoxide dismutase activity decreased 24 hr after treatment and was further reduced at 48 hr, although there was no change in Mn-superoxide dismutase activity. Catalase and Se-glutathione peroxidase activities also decreased at 48 hr, while reduced glutathione concentrations remained increased at 24 and 48 hr. The melatonin administered to the ANIT-treated rats attenuated the increases in serum and hepatic concentrations of thiobarbituric acid reactive substances and the decreases in hepatic activities of Cu,Zn-superoxide dismutase, catalase, and Se-glutathione peroxidase found at 48 hr after the hepatotoxin treatment more effectively at the higher dose than at the lower dose; on the other hand, melatonin treatment had no effect on the increases in hepatic myeloperoxidase activity and reduced glutathione concentration found at 48 h. These results indicate that orally administered melatonin at pharmacological doses prevents the progression of ANIT-induced acute liver injury, mainly liver cell damage, in rats, and suggest that the administered melatonin exerts these preventive effects through its direct and indirect antioxidant actions.     

枳黄方对急性酒精性肝损伤大鼠肝脂质过氧化水平的影响及其机制研究

目的:观察枳黄方对急性酒精性肝损伤大鼠肝脂质过氧化水平的影响,并探讨其机制。方法:通过酒精灌胃法制造急性酒精性肝损伤大鼠模型,采用HE染色观察肝病理变化;羟胺法检测肝脏SOD活力;TBA法检测肝脏MDA含量;采用RT-PCR技术检测肝脏NADPH氧化酶gp-91phox mRNA的表达量。结果:枳黄方能改善急性酒精性肝损伤之肝脏病理变化;下调肝脏NADPH氧化酶gp-91phox mRNA的表达;显著降低肝脏MDA含量(P<0.05);显著提高肝脏SOD活力(P<0.01)。结论:枳黄方能对抗酒精性肝损伤大鼠肝脏脂质过氧化,这可能与其能降低肝脏NADPH氧化酶gp-91phox mRNA的表达有关。     

Energy metabolism and survival of liver grafts from non-heart-beating donor rats with warm ischemia injury

Introduction The quality of liver graft is a key factor for liver transplantation. Organs from non- heart-beating donors (NHBDs) seem to bean effective option to alleviate the problem of liver donor shortage.[1-3] However, the main obstacle to the use of livers from NHBDs is that warm ischemia injury to the liver is related to cardiac arrest.[4-6] Moreover, in liver transplantation, the allograft sustains inevitable cold ischemia in addition to re- warming injury during liver reperfusion. …