硒与金属硫蛋白及对小鼠肝损伤的防护作用研究

应用蛋白质芯片和RT-PCR技术研究硒对小鼠肝脏金属硫蛋白（Metallothionein, MT）的诱导表达;以蛋白质芯片技术为主要实验手段研究CCl4诱导的小鼠肝脏损伤后血清及肝脏蛋白质图谱变化,寻找小鼠血清及肝脏组织损伤标志物,同时观察有机硒(麦硒康,Organ-Se)对损伤的防护作用,结果表明与对照组相比给予有机硒后的小鼠肝脏MT表达明显;比较肝损伤组及用药组（Organ-Se）组的血清及组织蛋白质表达图谱变化,发现血清中存在3个具有统计学意义的标志物：5062.5Da 、5566.5Da、6358.5Da;肝脏组织中有4个具有统计学意义的标志物：5449.6Da、7131.5Da、9903.2Da和10767.3Da;与损伤组相比预先保护组（Organ-Se）的血清及肝脏标志物的表达水平接近正常组。本实验表明非金属元素硒,尤其是有机硒同金属元素（如锌）一样,能够有效诱导MT的表达,为今后进一步开展硒代金属硫蛋白的机制研究奠定了基础;同时在对小鼠肝损伤保护的研究中发现,有机硒具有明显的肝损伤保护作用,是一种较有前途的值得开发的肝损伤防护药。     

藻蓝蛋白复合物对酒精性肝损伤的保护作用

本文对藻蓝蛋白复合物保护化学性肝损伤的功效学进行了研究.以Wistar大鼠建立酒精性肝损伤模型,将藻蓝蛋白复合物分为高、中、低三个剂量组,以联苯双酯作为阳性对照组,灌胃给药42 d,分别测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、血清丙二醛(MDA)、谷胱甘肽(CSH)、肝匀浆丙二醛(MDA)和谷胱甘肽(GSH)的含量,并对肝脏切片进行病理检查.结果表明:藻蓝蛋白复合物对血清ALT、AST具有显著的抑制作用,显著拮抗肝脏MDA的升高,显著提高肝脏GSH-Px含量.出现肝细胞浊肿、脂肪变性、点状坏死的大鼠数目极少.从而表明藻蓝蛋白复合物具有显著的保护酒精性肝损伤的功效.     

久肝胶囊解酒作用的研究

目的:研究久肝胶囊的解酒作用及其机制.方法:用白酒直接灌胃建立小鼠醉酒模型,分别进行致醉、防醉、解酒试验,观察久肝胶囊的药效;长期给酒造成酒精性肝损伤模型,测定小鼠血清中及肝脏中乙醇脱氢酶(ADH)和谷丙转氨酶(GPT)活性.结果:小鼠最适致醉量为0.16 ml/10g;久肝胶囊对醉酒能起到预防作用,且使醉酒小鼠翻正反射恢复时间缩短;对酒精性肝损伤小鼠,久肝胶囊能使血清ADH、GPT活性及肝中ADH活性恢复正常.结论:久肝胶囊具有较好的预防醉酒和解酒作用,对酒精性肝损伤亦有较好的保护作用,其机制可能与恢复ADH和GPT活性有关.     

七味净肝灵对酒精性肝损伤大鼠的保护作用研究

探讨七味净肝灵(QWJGL)对酒精性肝损伤大鼠的保护作用及作用机制。将60只大鼠随机分为正常组、模型组、水飞蓟宾组(0.18 g/kg)、QWJGL高、中、低剂量组(8、4、2 g/kg),每组10只。造模采用灌胃56%vol白酒(10 mL/kg),2 h后,各用药组灌胃给药,持续给药30天。末次给药16 h后,取血,收集肝脏、脾脏和胰腺,计算LI、SI和TI,生化法测定血清ALT、AST、MDA、SOD和GSH-Px含量,ELISA法检测肝脏中IL~(-1)β、IL-6和TNF-α含量,Western blot检测肝组织NF-κB和CD14表达,HE染色观察肝脏组织病理学变化。结果表明,QWJGL可降低酒精性肝损伤大鼠的LI(P0.05),提高SI和TI(P0.05),降低肝损伤大鼠血清中ALT和AST活性(P0.05),并且可以降低MDA含量(P0.05),增强SOD和GSH-Px活性(P0.05),降低TNF-α、IL~(-1)β和IL-6水平(P0.05),抑制肝组织NF-κB和CD14表达(P0.05)。综上,QWJGL对酒精性肝损伤有明显的保护作用,其保肝作用可能与抑制氧化应激、炎症反应和调控CD14、NF-κB蛋白表达有关。     

青藤碱抗大鼠肝脏缺血/再灌注损伤作用的机制探讨

目的:观察青藤碱时大鼠肝脏缺血再灌注损伤的影响,探讨其保护大鼠肝脏缺血再灌注损伤作用的机制.方法:通过建立大鼠全肝缺血再灌注损伤模型,应用硝酸酶还原法测定肝脏缺血再灌注后60min血清NO水平变化;测定再灌注60 min后肝组织内MDA和SOD含量变化;再灌注60min取肝组织完成肝组织显微结构的观察.结果:肝脏缺血再灌注损伤后血清NO水平降低;青藤碱能提高再灌注后血清NO水平,且能改善肝脏缺血再灌注损伤的微循环,减轻肝细胞内超微结构的损害程度.结论:青藤碱对大鼠肝脏缺血再灌注损伤有保护作用,其主要作用机制是清除氧自由基和改善微循环.     

油橄榄叶提取物对大鼠酒精性脂肪肝的保护作用

目的观察油橄榄叶提取物(OLE)对酒精性肝损伤的保护作用及机制。方法用递增法灌胃乙醇24周建立大鼠肝损伤模型,造模同时用OLE(250 mg·kg~(-1)、500 mg·kg~(-1)、1 000 mg·kg~(-1))进行灌胃治疗。利用生物显微技术观察肝脏组织结构的变化,检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、甘油三酯(TG)和总胆固醇(TC)水平,用放射免疫法检测肝脏肿瘤坏死因子α(TNF-α)、白细胞介素1(IL-1β)的含量,用比色法检测肝脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)活性及丙二醛(MDA)含量,用免疫组织化学法检测固醇调节元件结合蛋白-1c(SREBP-1c)的表达情况。结果与模型组比较,OLE治疗后,血清ALT、AST、TG、TC水平降低;肝脏TNF-α、IL-1β、MDA含量及SREBP-1c表达呈降低趋势;SOD、CAT、GR水平均显著升高;肝脏损伤程度明显减轻。结论 OLE对酒精性肝损伤有一定的保护作用,可能与其减少自由基损伤、减轻炎症反应、抑制SREBP-1c表达有关。     

解酒护肝饮解酒及对急慢酒精性肝损伤的保护作用

为了评价解酒护肝饮解酒效果及其对急、慢性酒精性肝损伤保护作用机制,本研究通过建立醉酒模型,确定致醉剂量;通过醉酒睡眠实验比较解酒护肝饮解酒特性;通过测定醉酒小鼠血乙醇含量的变化,研究解酒护肝饮对乙醇代谢的影响;通过建立急慢性酒精性肝损伤模型,测定AST、ALT、SOD活性,GSH、MDA水平,HE染色切片观察肝组织形态学的变化。研究发现小鼠最佳致醉剂量为11 m L/kg;与模型组比较,解酒护肝饮高(HD)、中剂量组(MD)均可延长醉酒时间、缩短醒酒时间(p<0.05),高、中剂量组可降低酒精灌胃后2 h、3 h时间点血乙醇含量(p<0.05);与模型组比较,急慢性酒精肝损伤模型各剂量组均能显著降低血清AST、ALT活性(p<0.05),急性酒精性肝损伤模型中,各剂量组肝组织SOD、GSH水平上升(p<0.05),MDA水平下降(p<0.05),而在慢性酒精性肝损伤模型肝组织中,低剂量组(LD)的SOD、GSH及MDA水平没有统计学差异;病理切片观察可见,急慢性酒精肝损伤模型高、中、低剂量组均能显著改善肝组织因乙醇而导致的肝损伤,并且高、中剂量组效果较好。本研究表明解酒护肝饮可显著延长醉酒时间,缩短醒酒时间,降低血乙醇的含量,对酒精诱导的肝损伤有较好的保护作用。     

FH/Wjd大鼠酒精性肝损伤模型探讨

目的对FH/W jd大鼠酒精性肝损伤模型进行探讨。方法 FH/W jd大鼠按体重随机分为饮水组和饮酒组,两组均自由饮食。16周后取血,检测血清ALT、AST、TBIL、TG、CHO;取肝脏,匀浆后检测TG、GSH;流式细胞仪检测肝细胞凋亡率;Western blot检测肝脏组织PPARα蛋白表达;肝脏HE染色观察组织病理学改变。结果与饮水组比较,饮酒组两种性别FH/W jd大鼠血清TBIL、TG含量显著升高,饮酒组雌性大鼠血清ALT、CHO显著降低;饮酒组两种性别大鼠肝脏TG含量显著升高,GSH含量呈现降低趋势;饮酒组两种性别大鼠肝细胞凋亡率亦呈降低趋势;饮酒组肝脏PPARα蛋白表达明显上调;饮酒组组织病理学改变以小泡性脂肪变性为主。结论长期自主摄入酒精可以造成FH/W jd大鼠肝脏损伤。     

D-gal致大鼠急性肝损伤过程中肝卵圆细胞增殖及迁延

目的用D-gal建立大鼠急性肝损伤模型,观察肝损伤后再生过程中肝卵圆细胞的增殖和迁延。方法建立大鼠急性肝损伤模型,于第1、3、7和14天分别取肝组织,分别行病理、免疫组织化学,观察卵圆细胞的分布迁移情况,并取第7天肝组织进行组织电镜观察汇管区新增生细胞超微结构。结果病理切片显示肝细胞变性坏死程度以第7天和第14天为主,出现新增生的细胞。免疫组化示随时间阳性细胞明显增多,分布于汇管区,并向小叶中心迁移,形成大量的胆小管,并有部分向坏死区迁移。透射电镜有新生内源性细胞,小于成熟的肝细胞,细胞器较少,有细胞紧密连接,以数个细胞排列成小胆管,与免疫组化一致。结论在大鼠急性肝损伤时HOC被活化、增殖,并向肝小叶中心迁移,全程参与了肝再生过程。     

SD大鼠酒精性脂肪肝模型的监测分析

目的：通过血清生化指标和病理学的监测分析来建立标准的SD大鼠酒精性脂肪肝动物模型。方法：选取40只SD大鼠,随机分为两组,模型组采用直接饮酒法,于第8、12和20周时检测大鼠血清生化指标：丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、甘油三酯（TG）,并于第8、12周时随机采集5只大鼠肝组织,20周时采集剩余所有大鼠肝组织并进行病理学分析。结果：模型组于第8、12和20周时体重增长量均低于对照组（P〈0．01）,血清ALT、AST均高于对照组（P〈0．01）,第8周和12周时TG高于对照组（P〈0．01）。病理学结果显示肝组织从8周至20周呈现出酒精性脂肪肝、重度酒精性脂肪肝伴肝炎和酒精性肝纤维化等演变过程。结论：直接饮酒法可成功地复制出酒精性脂肪肝动物模型,通过监测分析可了解酒精性脂肪肝病变的整个过程,为今后建立酒精性脂肪肝和肝纤维化动物模型提供了理论参考。     

Characterization of the protective effects of melatonin and related indoles against alpha-naphthylisothiocyanate-induced liver injury in rats

The protective effect of melatonin, 6-hydroxymelatonin and N-acetylserotonin against alpha-naphthylisothiocyanate (ANIT)-induced liver injury was investigated and compared in rats injected once with the hepatotoxicant (75 mg/kg body weight). In rats injected with ANIT alone, liver injury with cholestasis developed within 24 h, as indicated by both serum levels of alanine aminotransferase (SGPT) and aspartic acid aminotransferase (SGOT) activities and serum total bilirubin concentration. The administration of melatonin or 6-hydroxymelatonin (10 mg/kg body weight) to ANIT-injected rats reduced significantly the serum levels of both SGPT and SGOT and the serum total bilirubin concentration. For all hepatic biochemical markers, melatonin was more effective that 6-hydroxymelatonin. By comparison, the administration of N-acetylserotonin (10 mg/kg body weight) to ANIT-injected rats did not reduce the serum levels of either hepatic enzymes or the serum total bilirubin concentration. In ANIT-injected rats, hepatic lipid peroxidation (LPO) was significantly higher than in control animals and this increase was significantly reduced by either melatonin, 6-hydroxymelatonin or N-acetylserotonin. Furthermore, ANIT treatment caused a significant reduction in liver microsomal membrane fluidity and this reduction was completely reversed by the three indoles. The liver from ANIT-injected rats showed several histopathological alterations; above all there was an acute infiltration of polymorphonuclear neutrophils and an increase in the number of apparent apoptotic hepatocytes. The concurrent administration of melatonin reduced the severity of all morphological alterations, specially the neutrophil infiltration and the number of presumed apoptotic cells. On the contrary, the administration of 6-hydroxymelatonin or N-acetylserotonin did not provide any protective effect in terms of the histopathological alterations. These results indicate that melatonin protects against ANIT-induced liver injury with cholestasis in rats, and suggests that this protective effect is likely due to its antioxidant properties and above all to its capacity to inhibit liver neutrophil infiltration, a critical factor in the pathogenesis of ANIT-induced liver injury. 6-hydroxymelatonin, although able to provide partial protection against the ANIT-induced hepatic injury, probably through its antioxidant properties by mechanisms that are unclear, was unable to reduce neutrophil infiltration. Finally, N-acetylserotonin in the experimental conditions of this study, only exhibited some antioxidant protection but had no protective effect against ANIT-induced hepatic damage.     

奶油栓孔菌子实体多糖的理化性质、抗氧化活性与保肝作用

本研究旨在探讨奶油栓孔菌子实体多糖（TLFPS）的化学性质和酒精性肝损伤的保护作用。首先用水提醇沉法提取得到多糖,通过化学组成分析、紫外吸收光谱法、傅里叶红外光谱法和刚果红染色法对多糖结构进行初步表征,以DPPH、ABTS、超氧阴离子自由基的清除能力和铁离子还原能力为指标评价了多糖体外抗氧化能力,在小鼠急性肝损伤之前连续灌喂多糖8d,比较各组小鼠血清和肝的相关生化指标以及组织病理切片来确定多糖对酒精性肝损伤小鼠的保护作用。结果显示：多糖具有β-吡喃糖环结构,含有较高含量的糖醛酸和硫酸根基团,空间构型不具备三股螺旋结构。在体外抗氧化活性方面,多糖对DPPH、ABTS和超氧阴离子自由基均有良好的清除活性,铁离子还原能力也呈良好的剂量依赖性。在小鼠保肝实验中,与模型组相比,多糖能够显著延长小鼠的醉酒时间和缩短醒酒时间,降低了酒精性肝损伤小鼠的肝指数,并且显著降低血清中谷丙转氨酶（alanine aminotransferase,ALT）、谷草转氨酶（aspartate aminotransferase,AST）、甘油三酯（triglyceride,TG）、总胆固醇（total cholesterol,TC）和肝脏中丙二醛（malondialdehyde,MDA）的含量,同时明显提高了肝脏中超氧化物歧化酶（superoxide dismutase,SOD）和过氧化氢酶（catalase,CAT）的活性。结果证实奶油栓孔菌子实体多糖具有良好的抗氧化能力,可以减轻由酒精引起的急性肝细胞损伤,而且对机体的毒害作用很小。肝组织病理切片也进一步证实了奶油栓孔菌多糖的保肝活性。研究结果不仅丰富了奶油栓孔菌的药用价值,而且对多糖在功能食品领域的应用提供了药效基础。     

Ameliorative effect of Partysmart in rat model of alcoholic liver disease

Present study was designed to investigate the effect of polyherbal formulation PartySmart in experimental model of alcoholic liver disease in male Wistar strain rats. Alcohol plus fish oil were administered to animals for 8 weeks to induce liver injury. PartySmart was administered at doses of 250 and 500 mg/kg body weight. After 8 weeks, parameters such as liver weight, liver function serum markers alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) and lipid peroxidation were studied. Livers from all the groups were subjected for histological evaluation. Treatment with PartySmart at the dose of 500 mg/kg body weight showed significant reduction in the levels of serum ALT, AST and ALP with a decrease in liver weight as compared to ethanol-fed rats. A significant decrease was also observed in malondialdehyde levels following treatment with PartySmart at 500 mg/kg body weight. Histological profile of liver tissue in PartySmart-treated animals showed lesser vacuolar degeneration and intactness of hepatic architecture along with improved glycogen deposition as demonstrated by PAS staining. PartySmart ameliorated alcohol-induced liver injury by preventing cell membrane disturbances, reduction of oxidative stress by free radical scavenging and antioxidant activity and normalization of altered intracellular redox status. Thus, PartySmart can be beneficial in the treatment of alcohol-induced liver damage.     

Hepatoprotective activity of Leucas hirta against CCl4 induced hepatic damage in rats

Methanol and aqueous leaf extracts of L. hirta demonstrated hepatoprotective activity against carbon tetrachloride induced liver damage in rats. The parameters studied were serum total bilirubin, total protein, alanine transaminase, aspartate transaminase and alkaline phosphatase activities. The hepatoprotective activity was also supported by histopathological studies of liver tissue. Results of the biochemical studies of blood samples of CCl4 treated animals showed significant increase in the levels of serum markers and decrease in total protein level reflecting the liver injury caused by CCl4. Whereas blood samples from the animals treated with methanol and aqueous leaf extracts showed significant decrease in the levels of serum markers and increase in total protein indicating the protection of hepatic cells. The results revealed that methanol leaf extract followed by aqueous extract of L. hirta could afford significant protection against CCl4 induced hepatocellular injury.     

黑果枸杞汁对大鼠酒精性肝损伤的保护作用*

目的: 研究黑果枸杞汁对大鼠酒精性肝损伤的保护作用,探讨其中Toll样受体4(TLR4)/p38 丝裂原活化蛋白激酶(p38 MAPK)信号通路的调节机制。方法: 60只雄性SD大鼠随机分为空白对照组(C)、模型组(M)、低剂量黑果枸杞汁组(LLM)、中剂量黑果枸杞汁组(MLM)、高剂量黑果枸杞汁组(HLM),每组12只。M、LLM、MLM和HLM组每天以20 ml/kg(8 g/(kg·d))剂量分2次灌胃400 g/L酒精,C组于相同时间点灌胃等体积蒸馏水。每日首次酒精灌胃前4 h,黑果枸杞汁各剂量组分别以2.4、4.8、9.6 ml/(kg·d)进行灌胃,其他组于相同时间点灌胃等体积蒸馏水。实验周期4周,末次实验结束后24 h处死大鼠,取血液和肝脏,计算肝脏指数,HE染色观察肝脏组织形态,比色法检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性,免疫组化法检测肝脏TLR4、p38 MAPK及磷酸化p38 MAPK(p-p38 MAPK)蛋白质表达,酶联免疫吸附试验检测肝脏肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-10(IL-10)、白细胞介素-18(IL-18)水平。结果: 与C组比较,M组成功建立酒精性肝损伤模型。与M组比较,黑果枸杞汁各剂量组的相关指标出现改善,其中HLM组肝脏组织形态改善最为显著,其肝脏系数、血清ALT和AST、肝脏TLR4蛋白质表达、p-p38 MAPK/p38 MAPK比值、TNF-α、IL-1β和IL-18水平均显著降低(P＜0.05或P＜0.01),肝脏IL-10水平显著升高(P＜0.01)。黑果枸杞汁各剂量组组间比较,肝脏系数、血清AST、肝脏TLR4蛋白质表达、p-p38 MAPK/p38 MAPK比值、TNF-α和IL-18水平,HLM组较LLM组均显著降低(P＜0.05或P＜0.01);肝脏IL-10水平,HLM组较LLM和MLM组均显著升高(P＜0.05或P＜0.01);其余主要指标组间比较均无统计学差异(P＞0.05)。结论: 黑果枸杞汁可以通过调控TLR4/p38 MAPK信号通路,改善炎症应激,缓解大鼠酒精性肝损伤,高剂量组效果优于其他剂量组。     

The effect of dimethyl dimethoxy biphenyl dicarboxylate (DDB) against tamoxifen-induced liver injury in rats: DDB use is curative or protective

Tamoxifen citrate is an anti-estrogenic drug used for the treatment of breast cancer. It showed a degree of hepatic carcinogenesis, when it used for long term as it can decrease the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in liver rat cells leading to liver injury. In this study, a model of liver injury in female rats was done by intraperitoneal injection of tamoxifen in a dose of 45 mg/kg body weight for 7 successive days. This model produced a state of oxidative stress accompanied with liver injury as noticed by significant declines in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant elevations in TBARS (thiobarbituric acid reactive substance) and liver transaminases; sGPT (serum glutamate pyruvate transaminase) and sGOT (serum glutamate oxaloacetate transaminase) levels. The oral administration of dimethyl dimethoxy biphenyl dicarboxylate (DDB) in a dose of 200 mg/kg body weight daily for 10 successive days, resulted in alleviation of the oxidative stress status of tamoxifen-intoxicated liver injury in rats as observed by significant increments in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases; sGPT and sGOT levels. The administration of DDB before tamoxifen intoxication (as protection) is more little effective than its curative effect against tamoxifen-induced liver injury. The data obtained from this study speculated that DDB can mediate its biochemical effects through the enhancement of the antioxidant enzyme activities and reduced glutathione level as well as decreasing lipid peroxides.     

三七皂苷R1 对肝纤维化大鼠TGF-beta1/Smad3信号的影响

目的:探讨SD大鼠肝纤维化后肝组织及血清中转化生长因子-β1(Transforming Growth Factor-β1,TGF-β1)及Smad3的表达和变化,以及三七皂苷R1对肝纤维化的保护作用。方法:72只健康雄性SD大鼠分为对照组、二甲基亚硝胺(NDMA)组和三七皂苷R1组,再按不同时间点分为1、2、4周,3个亚组,每个亚组8只动物。NDMA组采用NDMA 2 m L/kg腹腔注射,三七皂苷R1组同时静脉注射三七皂苷R1,剂量为100 mg/kg体重,对照组注射等量的生理盐水。在各组的不同时间点采用RT-PCR及ELISA技术检测肝组织及血清中TGF-β1、Smad3的表达及变化。结果:1、TGF-β1、Smad3 m RNA及蛋白在各组中均有表达。2、对照组各时间点比较均无统计学意义(P>0.05)。NDMA组中,随着损伤时间的延长,TGF-β1、Smad3 m RNA及蛋白的表达逐渐上调,且各时间点与对照组比较有统计学意义(P<0.05)。而三七皂苷R1组TGF-β1、Smad3 m RNA及蛋白在各时间点均较NDMA组表达下调,有统计学意义(P<0.05)。结论:1、TGF-β1/Smad3信号参与了肝纤维化的发生和发展过程,且随损伤的逐渐加重,表达越高。2、三七皂苷R1可降低肝组织中TGF-β1/Smad3信号的表达,减轻肝细胞的纤维化,发挥保护肝组织损伤的作用。     

超声在评价大鼠酒精性脂肪肝模型中的应用

目的利用超声技术来评价大鼠酒精性脂肪肝动物模型。方法选取40只SD大鼠随机分为两组（n=20只）。模型组按每周测定的体重早晚各1次乙醇灌胃（10 g/kg）,第1周浓度为40%,第2、3周分别为45%和50%,第4周为55%灌胃直至12周;对照组给予等体积的生理盐水灌胃。造模于第4、8和12周时对两组大鼠进行超声监测,并从两组中各随机抽取3只大鼠进行肝脏病理学分析,与超声监测结果进行对比分析。结果超声与病理检查结果均提示酒精性脂肪肝造模成功,超声可以监测模型组大鼠肝脏脂肪病变从轻到重的渐变过程以及对照组大鼠无脂肪病变过程。这与肝组织的病理学诊断结果具有一致性。结论超声检测技术可以较好地进行活体评价大鼠酒精性脂肪肝动物模型。     

Effect of taurine on alcoholic liver disease in rats

To investigate the effect of taurine on alcoholic liver disease in rats, male Wistar rats were administered alcohol intragastrically for 3 months. The effect of β-alanine-mediated taurine depletion and taurine administration on the development of alcoholic liver disease was examined. It was found that taurine administration produced lower levels of aspartate aminotransferase and alkaline aminotransferase than that of the untreated group. In addition, the levels of hepatic total protein, glutathione and superoxide dismutase were higher in the taurine treated groups than those in the untreated control or the taurine depleted groups, while hepatic malondialdehyde content exhibited the negative effect. Moreover, the concentrations of hepatic hydroxyproline, serum hyaluronic acid, interleukin-2, interleukin-6, tumor necrosis factor-α and laminin were all decreased in the taurine treated groups. The pathological changes showed that the percentage of fatty degeneration and inflammation in the taurine groups were lower than that of the control, taurine depleted and automatic recovery groups. These in vivo findings demonstrate that hepatic disease caused by chronic alcohol consumption can be prevented and cured by administration of taurine.