大蒜油与大蒜素对急性乙醇性肝损伤预防作用比较

目的 比较大蒜油和大蒜素对急性乙醇性肝损伤预防作用的效果.方法 提前4h给予一次大蒜油或大蒜素后,一次性给予体积分数50%的乙醇,16h后测定血清生化指标和肝脏脂质过氧化指标,肝脏组织苏丹Ⅲ染色观察组织病理学改变.结果 提前给予一次大蒜油、大蒜素均可以有效的预防4.8g/kg乙醇摄入引起的急性肝损伤.与对照组相比,中剂量大蒜油及大蒜素分别使肝匀浆中MDA含量下降了29.9%和25.1%,使血清中的TG降低了44.5%和40.2%.病理学检查表明,模型组有大量橙黄色脂滴蓄积,太蒜油低剂量和大蒜素组小鼠肝脏脂滴明显减少、变小,大蒜油中、高剂量组仅有个别小鼠肝脏切片可见少量脂滴.结论 提前给予一次大蒜油、大蒜素均可以有效的预防4.8g/kg乙醇摄入引起的急性肝损伤,且大蒜油作用效果优于单独应用大蒜素的作用效果.     

芹菜对小鼠睾丸组织中某些生化指标的影响

芹菜属伞形花科的二年生蔬菜,含有丰富的黄酮类化合物,具有降压安神、保护血管和增强免疫等功效.泰国博差丽医师研究发现,常吃芹菜能减少男性精子的数量[1].     

氟染毒雄性大鼠睾丸组织对某些生化指标的影响北大核心CSCD

目的探讨慢性氟中毒对雄性大鼠睾丸组织某些生化指标水平的影响,为氟的生殖毒性研究提供实验依据。方法健康雄性Wistar大鼠32只,体重150~180 g,随机分为4组：对照组、低、中和高氟组[100、200和300 mg/（kg·d）NaF],灌胃染毒90 d,每天称体重。染毒结束后处死大鼠,摘取睾丸组织,称重并计算脏器系数;分光光度法检测睾丸组织匀浆中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）及一氧化氮合酶（NOS）的活性和丙二醛（MDA）、过氧化氢（H2O2）及一氧化氮（NO）的含量。结果染氟第30天大鼠体重组间比较,差异有统计学意义（P〈0.05）,其中低、中氟组高于高氟组（P〈0.05）;第0、60和90天大鼠体重组间比较,差异无统计学意义（P〉0.05）。与对照组比较,各组睾丸组织的SOD和CAT活性无显著性改变（P〉0.05）,低氟组MDA、中氟组H2O2含量均有显著性升高（P〈0.05）,低氟组NOS活性显著性降低（P〈0.01）。结论慢性氟中毒可增强睾丸组织氧化应激效应,损害大鼠生殖系统。     

地塞米松对二甲基甲酰胺致小鼠急性肝损伤的保护作用

目的 研究地塞米松(DEX)对二甲基甲酰胺(DMF)致小鼠急性肝损伤的保护作用.方法 采用DMF致小鼠急性肝损伤模型.染毒48 h后,测定血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和乳酸脱氢酶(LDH)的活力.留取肝脏组织.常规石蜡包埋切片,HE染色,光学显微镜观察肝脏组织病理变化;制备肝匀浆,测定肝中金属硫蛋白(MT)的含量.结果 与正常组比较,模型组小鼠血清中ALT、AST和LDH活力明显升高,肝脏组织出现明显的肝细胞变性坏死;先给予和后给予DEX的各剂量组小鼠血清中ALT、AST和LDH活力与模型组比较显著降低,肝脏组织病理损伤明显减轻.肝脏MT的含量明显升高.结论 DEX对DMF引起的小鼠急性肝损伤具有明显的保护作用,MT可能是其保护机制的参与因子之一.     

铀尾矿浸出液对斑马鱼组织某些生化指标的研究

铀尾矿是铀冶炼厂经过水冶处理提出铀后排出的废渣,含有少量铀及其他如镉、硫化物等有毒有害物质.在长期风化淋溶作用下,可能致使铀尾矿中大量有害物质迁移至周围河水及地下水中,对该地区的饮水安全、生态环境、污染综合防治等产生重大影响.     

丹参多酚酸联合乌司他丁治疗急性呼吸窘迫综合征的疗效及对患者生化指标的影响

摘 要 目的：探讨丹参多酚酸联合乌司他丁治疗急性呼吸窘迫综合征（ARDS）疗效及对患者生化指标的影响。方法: ARDS患者86例随机分为观察组43例与对照组43例。对照组采用乌司他丁等常规治疗,观察组在对照组基础加用丹参多酚酸注射液治疗。两组疗程均为10 d。比较两组患者治疗总有效率、治疗前后呼吸频率（RR）、心率（HR）、血气分析指标氧分压（PaO₂）、动脉血二氧化碳分压（PaCO₂）、动脉血氧饱和度（SaO₂）及血浆白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、C反应蛋白（CRP）水平变化。结果: 观察组总有效率为86.05%,明显高于对照组的67.44%（P＜0.05）。治疗后,两组患者RR、HR,PaCO₂、IL-6、TNF-α、CRP等指标均有明显降低,PaO₂、SaO₂则明显增加（P＜0.05）,且观察组各项指标均优于对照组（P＜0.05）。结论:丹参多酚酸联合乌司他丁治疗ARDS疗效显著,可明显改善患者心率、呼吸频率、血气分析及降低血清炎症因子水平,值得临床推广。     

注射用核糖核酸对小鼠免疫功能的影响

目的:研究脱氢卡维汀(YHL-DC)对四氯化碳(CCI4)致小鼠急性肝损伤的影响.方法:YHL-DC预防和治疗给药后观察其对CCl4致急性肝损伤小鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)和总胆红素(TBIL)的影响,并对肝脏进行了病理组织学及电镜观察.结果:YHL-DC预防和治疗给药均能显著降低急性肝损伤小鼠ALT、AST和TBIL的升高,有效减轻CCl4引起的小鼠肝细胞变性、坏死、爽性细胞浸润和肝细胞超微结构的破坏.结论:YHL-DC对四氯化碳致小鼠急性肝损伤具有保护作用.     

大蒜油对CCl4引起的急性化学性肝损伤的预防作用

目的 研究大蒜油对四氯化碳(carbon tetrachloride,CCl4)引起的急性化学性肝损伤是否有预防作用.方法 雄性昆明小鼠90只,随机分为阴性对照组、溶剂对照组、CCl4模型组、大蒜油低、中、高剂量组,每天灌胃1次/d,30 d后模型组和大蒜油组一次性灌胃给予CCl4 80 mg/kg,24 h后取血测定各组小鼠血清中丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)的活力,取肝脏,称重,并计算肝脏系数,同时取肝左叶进行病理组织学检查.结果 与阴性对照组相比,CCl4模型组血清ALT、AST活力明显升高,肝脏重量和肝脏系数明显增加(P＜0.01).与模型组相比,大蒜油低、中、高剂量组血清ALT、AST活力明显降低(P＜0.01),并存在剂量-效应关系;大蒜油低、中、高剂量组肝脏重量和肝脏系数明显减小(P＜0.01);同时大蒜油可有效减轻CCl4引起的细胞坏死、气球样变等肝细胞损伤.结论 大蒜油对CCl4引起的急性化学性肝损伤有明显的预防作用.     

大蒜油、大蒜素、茶多酚对四氯化碳急性肝损伤预防作用的比较

目的 比较大蒜油、大蒜素、茶多酚对四氯化碳(carbon tetrachloride,CCl4)引起的急性化学性肝损伤的预防效果.方法 提前给予大蒜油、大蒜素和茶多酚后,一次性灌胃CCl4 80 mg/kg,测定血清中丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)的活力,同时比较各组小鼠的肝脏系数和肝脏病理组织学变化.结果与阴性对照组相比,CCl4模型组肝脏重量和肝脏系数明显增加,血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)活力明显升高(P<0.01).与模型组相比,大蒜油可明显抑制CCl4引起的肝脏肿大,血清ALT、AST活力明显下降(P<0.01),并存在剂量-反应关系,同时组织病理学检查也表明,大蒜油可预防CCl4引起的肝细胞肿胀、气球样变等病理改变;大蒜素和茶多酚对血清ALT和AST活力升高有一定的抑制作用,病理组织学检查显示肝细胞病理改变有所减轻.结论大蒜油、大蒜素、茶多酚对CCl4引起的急性化学性肝损伤均有预防作用,但大蒜油效果最明显,并存在剂量-反应关系.     

Ligularia fischeri extract attenuates liver damage induced by chronic alcohol intake

Context Ligularia fischeri (Ledebour) Turcz. (Compositae) has been used as a leafy vegetable and in traditional medicine to treat hepatic disorder in East Asia.

Objective The present study explores the antioxidant activity of LF aqueous extract on EtOH-induced oxidative stress accompanied by hepatotoxicity both in vitro and in vivo.

Materials and methods In vitro study using the mouse liver NCTC-1469 cell line was conducted to estimate the cytotoxicity as well as the inhibitory effect of LF extract against alcohol-treated cell damage. In vivo study used an alcohol-fed Wister rat model orally administered EtOH (3.95?g/kg of body weight/d) with or without LF extract (100 or 200?mg/kg body weight) for 6 weeks. Serum and liver tissue were collected to evaluate hepatic injury and antioxidant-related enzyme activity.

Results The EC₅₀ value for the DPPH radical scavenging capacity of LF extract was 451.5?μg/mL, whereas the IC₅₀ value of LF extract in terms of EtOH-induced reactive oxygen species (ROS) generation was 98.3?μg/mL without cell cytotoxicity. LF extract (200?mg/kg body weight) significantly reduced the triglyceride content of serum (33%) as well as hepatic lipid peroxidation (36%), whereas SOD activity was elevated three-fold. LF extract suppressed expression of CYP2E1 and TNF-α, and attenuated alcohol-induced abnormal morphological changes.

Discussion and conclusion LF extract attenuated liver damage induced by alcoholic oxidative stress through inhibition of ROS generation, down-regulation of CYP2E1, and activation of hepatic antioxidative enzymes. Homeostasis of the antioxidative defence system in the liver by LF extract mitigated hepatic disorder following chronic alcohol intake.     

Effects of adenosine on liver cell damage induced by carbon tetrachloride

Adenosine administration delayed the fatty liver and cell necrosis induced by carbon tetrachloride without affecting the action of the hepatotoxin on protein synthesis and liver triacylglycerol release. Adenosine produced a drastic antilipolytic effect accompanied by a decrease in the incorporation of [1-14C]palmitic acid into triacylglycerols and free fatty acids of the liver. Furthermore, a decrease in the serum levels of ketone bodies was observed at early times. The nucleoside also avoided the release of intracellular enzymes and prevented the lipid peroxidation produced by carbon tetrachloride during the 4 hr of treatment. The protective action of adenosine was transient, lasting 3-4 hr, probably the time required to be metabolized. The results suggest that the antilipolytic effect of the nucleoside, the inhibition of hepatic fatty acid metabolism, and the decrease in carbon tetrachloride-induced lipoperoxidation that it produced are involved in the delayed acute hepatotoxicity induced by carbon tetrachloride.     

右美托咪定对脂多糖导致的小鼠急性肺水肿作用的研究

目的探讨右美托咪定对脂多糖(LPS)导致的小鼠急性肺水肿的作用,以明确其在治疗急性肺水肿的过程中是否存在某些作用。方法应用LPS气管滴注的方法造小鼠急性肺水肿的模型,然后给予右美托咪定,并通过相关指标判断其是否起到作用。结果与LPS组相比,LPS加右美托咪定组的小鼠血清中肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6等炎性因子含量以及小鼠肺湿干质量比都有所降低。结论临床上对合并肺脏损害的患者进行镇静时,可以考虑右美托咪定对肺水肿保护作用的影响,应用其进行相应的治疗。     

Oxidative damage of biomolecules in mouse liver induced by morphine and protected by antioxidants

This study investigates the oxidative damage of biomolecules in livers of mice treated with morphine intraperitoneally. The oxidative damage of DNA as measured by single cell electrophoresis and high-performance liquid chromatography equipped with electrochemical and UV detection, the protein carbonyl content was measured by 2,4-dinitrophenylhydrazine method, and the malondialdehyde content was measured by the HPLC method. The activities of antioxidative enzymes, superoxide dismutase, catalase and glutathione peroxidase, and the activity of alanine aminotransferase were assayed by spectrophotometer method. Glutathione and oxidized glutathione were detected by fluorescence spectrophotometer method. All the indexes of oxidative damage, such as 8-OHdG, protein carbonyl group and malondialdehyde content, and the activity of alanine aminotransferase (n=27) increased significantly compared to those of control (n=27) (P<0.01) in livers of morphine-administered alone mice, while the indexes related with the in vivo antioxidative capacity, such as the ratio of glutathione and oxidized glutathione, activities of superoxide dismutase, catalase and glutathione peroxidase significantly decreased (P<0.01). When mice were treated with morphine combined with exogenous antioxidants, glutathione and ascorbic acid, all the indexes of oxidative damage and the activity of alanine aminotransferase showed no changes as compared to those of control (P>0.05), i.e., both glutathione and ascorbic acid completely abolished the damage of morphine on the hepatocyte. These results implied that morphine caused a seriously oxidative stress in mice livers and hence caused hepatotoxicity, while exogenous antioxidants were able to prevent the oxidative damage of biomolecules and hepatotoxicity caused by morphine. Thus, blocking oxidative damage may be a useful strategy for the development of a new therapy for opiate abuse.     

Saeng-Maek-San,a medicinal herb complex,protects liver cell damage induced by alcohol

The effect of treatment with Saeng-Maek-San (SMS) Complex (SMS1 or SMS2) upon rat hepatocytes exposed to alcohol was investigated. We compared the serum biochemistry and liver histology of rats administered both alcohol and SMS to control rats treated with alcohol alone. SMS treatment resulted in a significant reduction in the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and triglycerides (TG) compared to the control rats. In contrast, expression levels of alcohol dehydrogenase (ADH) were increased. Electron microscopy indicated that administration of SMS preserved the structure of organelles, including the nucleus and mitochondria. In addition, lipid droplets and secondary lysosomes were observed in the control rats. These data suggest that SMS represents an excellent candidate for protection of rat hepatocytes from alcohol-mediated damage.     

法莫替丁致急性肝损伤

1例25岁男性患者因上腹部持续绞痛3 h口服法莫替丁片20 mg,2次/d;鼠李铋镁片2片,3次/d。2 d后患者腹痛加重,实验室检查示丙氨酸转氨酶（ALT）178 U/L。给予法莫替丁注射液20 mg和葡醛内酯注射液266 mg,2次/d静脉滴注。第2天肝功能检查示ALT 133 U/L,天冬氨酸转氨酶（AST）63 U/L,γ-L-谷氨酰转移酶（γ-GT）162 U/L;第8天ALT 414 U/L,AST 134 U/L,γ-GT714 U/L,碱性磷酸酶（ALP）161 U/L,总胆红素（TBil）15.2μmol/L,直接胆红素（DBil）9.7μmol/L。怀疑肝损害可能为法莫替丁所致。停用法莫替丁注射液,换用注射用泮托拉唑钠40 mg溶于0.9%氯化钠注射液100 ml静脉滴注,2次/d,并给予注射用还原型谷胱甘肽1.8 g和复方甘草酸苷160 mg溶于5%葡萄糖注射液250 ml静脉滴注,1次/d。换药后5 d,ALT 62 U/L,γ-GT 315 U/L,TBil 13.1μmol/L,DBil 6.2μmol/L。1周后复查,ALT 28 U/L,AST 31 U/L。     

褪黑素对大鼠急性酒精性肝损伤的作用

目的探讨褪黑素对大鼠急性酒精性肝损伤的作用及机制。方法采用乙醇灌胃法建立大鼠急性酒精性肝损伤模型,生化法检测血清ALT、AST活性和肝匀浆SOD活性、MDA含量,HE染色观察肝脏病理形态学改变,免疫组化法检测肝组织中TNF-α和IL-1β表达。结果褪黑素干预组血清ALT、AST活性明显低于模型组(分别为P<0.05,P<0.01);褪黑素干预组肝匀浆MDA水平较模型组明显下降(P<0.05),SOD活性较模型组明显升高(P<0.05);光镜下显示褪黑素干预组肝脏病理损伤有所减轻;褪黑素干预组肝组织中TNF-α和IL-1β表达较模型组明显减弱(分别为P<0.05,P<0.01)。结论褪黑素对大鼠酒精所致急性肝损伤具有改善作用,其作用机制可能与抗氧化,以及减少TNF-α和IL-1β的生成有关。