刺梨汁阻断四氯化碳肝毒性的实验研究

给予大鼠５０～１００％浓度的刺梨汁预处理，然后再按６４０ｍｇ／ｋｇ剂量给予四氯化碳（ＣＣｌ４）。实验发现，经刺梨汁预处理的大鼠血清ＧＰＴ和ＧＯＴ活性，肝组织谷胱甘肽（ＧＳＨ）和脂质过氧化物（ＭＤＡ）含量与ＣＣｌ４对照组比较有显著性差异（Ｐ＜０．０５或Ｐ＜０．０１）；肝脏组织学检查表明刺梨汁预处理大鼠肝损害明显轻于ＣＣｌ４对照组。实验结果提示，刺梨汁对ＣＣｌ４的肝损害具有一定的保护作用。     

二硫化碳对大鼠肝脏脂质过氧化作用的研究

观察了二硫化碳（ＣＳ２）腹腔注射染毒对大鼠肝脏脂质过氧化物（ＬＰＯ）含量超氧化物歧化酶（ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）活力的影响，急性染毒实验结果显示，大鼠肝ＬＰＯ含量随ＣＳ２染毒剂量增加而明显升高（ｒ＝０．８１０８，Ｐ＜０．０１），ＳＯＤ活性随剂量增加有降低趋势，ＧＳＨ－ＰＸ活性未见显著变化。亚急性实验结果显示，染毒２１ｄ染毒组ＧＳＨ－ＰＸ活力，染毒４５ｄ染毒组ＳＯＤ及ＧＳＨ－ＰＸ活力与对照组比较均显著降低（Ｐ＜０．０５），这表明，ＣＳ２是一个重要的致脂质过氧化物。     

镉对大鼠睾丸间质细胞脂质过氧化的影响

目的观察镉对离体睾丸间质细胞的毒性作用。方法测定不同ＣｄＣｌ２染毒浓度下（含镉０、１０、２０和４０μｍｏｌ／Ｌ）间质细胞的脂质过氧化水平。结果染毒２４小时后，染毒组的细胞存活率显著低于对照组（Ｐ＜０．０１），且存在剂量－效应关系；随染毒浓度的增高，丙二醛（ＭＤＡ）含量和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力显著增高（Ｐ＜０．０５），而超氧化物歧化酶（ＳＯＤ）活力则显著下降（Ｐ＜０．０１）。相关分析结果显示：ＳＯＤ与ＭＤＡ呈负相关、与ＧＳＨ－Ｐｘ呈显著负相关（ｒ＝－０．４３３９，Ｐ＜０．０５）；ＭＤＡ与ＧＳＨ－Ｐｘ呈显著正相关（ｒ＝０．４３２９，Ｐ＜０．０５），表明镉可使睾丸间质细胞的脂质过氧化作用增强、抗氧化能力减弱。结论镉对睾丸间质细胞具有直接毒性作用。     

月见草油对实验性高脂血症脂质过氧化、血浆TXA2、PGI2及ET水平的影响

用含２％月见草油的高脂饲料喂饲实验性高脂血症大鼠４周，分别对血脂、血清脂质过氧化物（ＬＰＯ）、血浆超氧化物歧化酶（ＳＯＤ）、血栓素（ＴＸＡ２）、前列腺素（ＰＧＩ２）及内皮素（ＥＴ）进行了检测，并用扫描电镜对动脉内皮进行了观察。结果发现：月见草油能降低血清总胆固醇（ＴＣ）及甘油三酯（ＴＧ）含量，提高高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）含量；月见草油能显著降低血清ＬＰＯ水平，提高血浆ＳＯＤ活力；月见草油组大鼠血浆ＰＧＩ２水平明显增高，而ＴＸＡ２／ＰＧＩ２比值及血浆ＥＴ水平明显下降；月见草油组大鼠肝脏脂肪蓄积稍轻于高脂对照组；扫描电镜观察亦发现月见草油组大鼠动脉内皮损伤明显轻于高脂对照组。结果提示月见草油具有良好的降脂、保护内皮细胞及预防动脉粥样硬化形成的作用     

大豆磷脂合剂对大鼠血清、组织脂质水平和脂质过氧化及脂肪肝的影响

大豆磷脂合剂（大豆磷脂和ＶＥ按一定比例混合）５０ｍｇ·Ｃａｐｉｔａ（－１）·ｄ（－１）饲喂实验性高脂血症和脂肪肝大鼠四周。可使大鼠血清总胆固醇（ＴＣ）、血清脂质过氧化物（ＬＰＯ）、肝脏脂质过氧化物（肝ＬＰＯ）、肝脏和主动脉壁胆固醇和甘油三酯含量（肝ＣＨ、肝ＴＧ，主动脉ＣＨ，主动脉ＴＧ）明显减少（Ｐ＜０．０１）；血清高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）水平升高（Ｐ＜０．０１）；肝脏脂肪变性程度减轻（Ｐ＜０．０１）。实验结果提示：大豆磷脂合剂具有降低血脂、促进脂肪肝恢复和延缓血清和组织脂质过氧化的生物学作用。     

沙棘果汁及硒强化沙棘果汁对高脂血症大鼠脂质及脂质过氧化作用的影响

给实验性高脂血症大鼠喂饲沙棘果汁及硒强化沙棘果汁，观察其对大鼠机体脂质代谢及脂质过氧化作用的影响．结果表明：沙棘果汁及硒强化沙棘果汁可显著降低大鼠血中ＴＣ、ＬＤＬ－Ｃ含量，提高ＨＤＬ－Ｃ水平，各实验组大鼠血清及肝脏脂质过氧化物（ＬＰＯ）水平显著低于高脂组，谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）活性以硒强化沙棘果汁组增高更为显著（Ｐ＜０．０５）．提示：沙棘果汁及硒强化沙棘果汁能有效地降低高脂大鼠血ＴＣ水平，提高ＨＤＬ－Ｃ水平，并能抑制其体内脂质过氧化作用．     

脂质过氧化与抗氧化在肾小球疾病中的研究

本研究测定了２５例原发性肾病综合症（ＰＮＳ），１５例急性肾小球肾炎（ＡＧＮ）患者和３０例健康人血清脂质过氧化物（ＬＰＯ）、全血超氧化物歧化酶（ＳＯＤ）和全血谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的含量。结果：ＰＮＳ组和ＡＧＮ组血清ＬＰＯ均显著高于对照组（Ｐ＜０．０１）；ＰＮＳ组和ＡＧＮ组全血ＳＯＤ均显著低于对照组（Ｐ＜０．０５）；ＰＮＳ组和ＡＧＮ组全血（ＧＳＨ－Ｐｘ）与对照组相比，均无显著性差异（Ｐ＞０．０５）。表明ＰＮＳ和ＡＧＮ患者脂质过氧化作用增强，抗氧化机能下降，提示ＰＮＳ和ＡＧＮ的发生与脂质过氧化和抗氧化机能失衡有关。     

尘肺患者血清β－胡萝卜素与抗氧化功能的研究

本研究测定了尘肺病人、慢性支气管炎（慢支）病人及健康成人的血清β－胡萝卜素（ＢＣ）和ＶｉｔＡ含量以及血清脂质过氧化酶（ＬＰＯ）含量，超氧化物歧化酶（ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ活性。结果发现，尘肺组血清ＢＣ含量明显低于健康组和慢支组（Ｐ＜０．０１）。而血清ＶｉｔＡ含量３个组相近（Ｐ＞０．０５）。与健康组和慢支组比较，尘肺组血ＬＰＯ含量明显升高，ＳＯＤ和ＧＳＨ－Ｐｘ活性则明显降低（Ｐ均＜０．０ｌ）。上述结果提示，尘肺病人抗氧化功能明显减弱可能与血清ＢＣ含量较低有关。     

紫草素拮抗膜脂流动性下降和脂质过氧化损伤的作用

ＳＤ大鼠按体重随机分成５组，喂饲含脂肪酸组成不同的饲料９０天，研究其对肝中脂肪酸组成和膜脂流动性的影响及紫草素阻抑ＣＣｌ４诱导的肝细胞膜脂流动性下降和脂质过氧化损伤的能力。结果表明肝脏中的脂肪酸组成与摄入饲料的脂肪酸组成呈显著的正相关（相关系数ｒ为０８５３）；不同脂肪酸组成的肝脏，其细胞膜脂流动性之间有显著差异（Ｐ＜００５），摄食含多不饱和脂肪酸（ＰＵＦＡ）较多且以含ｎ－３系列脂肪酸最多的第４组，其膜脂流动性较好，但当加入１００μｌＣＣｌ４时，各组的膜脂流动性均显著降低，且以第４组的降低最显著。而当加入１００μｌ００５ｇ／Ｌ紫草素时，则能不同程度地拮抗由于ＣＣｌ４引起的膜脂流动性的降低，在第４组其拮抗效果最好。加入前后有非常显著的差异。紫草素也可以显著拮抗由ＣＣ１４诱导的肝脏脂质过氧化损伤，拮抗的作用程度因使用的紫草素浓度及肝脏中含脂肪的饱和程度有很大差异。第４组肝脏含ＰＵＦＡ最多，也最易受到ＣＣｌ４的诱导，且随使用紫草素浓度增大，阻抑能力增加。     

牛磺酸对四氯化碳致肝细胞凋亡影响的研究

本文观察了四氯化碳亚慢性染毒后血清ＡＬＴ、肝脏ＧＳＨ、ＭＤＡ及肝脏的形态学变化，同时研究了牛磺酸对ＣＣｌ４肝毒性的干预作用。结果表明：ＣＣｌ４引起了肝脏明显的脂质过氧化及肝损伤，但ＡＬＴ与ＭＤＡ之间并不完全并行，说明ＬＰＯ并非肝损伤的一唯一原因。ＣＣｌ４组肝组织中凋亡小体明显增加，可能是机体对损伤的一种反应，ｔａｕ干预组肝ＬＰＯ减轻，凋亡小体明显减少，表明ｔａｕ对ＣＣｌ４肝毒性有一定干预作用，其机     

扇贝提取物对肝损伤小鼠抗氧化功能的影响

目的　观察扇贝提取物 (SE)对肝损伤小鼠抗氧化功能的影响。方法　一次灌胃6% CCl4 油溶液 1 0 ml/kg bw,通过谷胱甘肽过氧化物酶 (GSH- Px)、超氧化物歧化酶 (SOD)、脂质过氧化物 (LPO)等指标观察给予 0 .5、1 .5、3.0 (g/kg)扇贝提取物的作用。结果　给予不同剂量扇贝提取物降低 LPO、提高 GSH- Px及 SOD的作用不同 ,以 1 .5g/kg bw效果最好。结论　扇贝提取物可能具有保护肝脏的作用     

葡萄籽提取物的体外抗脂质过氧化作用

以大鼠肝、脑组织匀浆为材料研究葡萄籽提取物 (GSE)的抗氧化作用。组织匀浆与GSE共浴后 ,比色法测定丙二醛 (MDA)生成量。组织匀浆与GSE共浴后 ,分别以自由基诱导剂CCl4、H2 O2 和铁离子 -抗坏血酸 (Fe2 + VC)激发脂质过氧化作用 ,以MDA产生和还原型谷胱甘肽 (GSH)耗竭作为脂质过氧化作用程度指标。结果表明 ,GSE可明显降低大鼠肝、脑组织自发性MDA的生成 ,减轻CCl4、H2 O2 、Fe2 + VC所致的肝脏脂质过氧化反应 ,减轻肝组织GSH耗竭。提示GSE具有良好的抗脂质过氧化作用。     

Preventive effect of D-002, a mixture of long-chain alcohols from beeswax, on the liver damage induced with CCl4 in rats

D-002 is a mixture of higher aliphatic primary alcohols purified from beeswax with antioxidant effects. Acute hepatotoxicity induced with CCl4 in rats has been related to increased hepatic lipid peroxidation and prevented with some antioxidants. This study investigated whether D-002 could prevent the acute CCl4-induced hepatotoxicity in rats. Animals were randomly distributed into four groups: a negative control treated orally with the vehicle and three groups injected with CCl4 (1 mL/kg) and treated orally either with the vehicle (positive control) or with D-002 (25 and 100 mg/kg). Eighteen hours after CCl4 dosing, rats were anesthetized, and livers were removed for histopathological studies. Some portions were taken and homogenized for assessing malondialdehyde (MDA) concentrations. Positive, but not negative, controls showed ballooned cells, swollen hepatocytes, and lipid-included hepatocytes, as well as necrotic areas and inflammatory infiltrates. D-002 (25 and 100 mg/kg) dose-dependently and significantly (P < .01) decreased the frequency of all abnormal liver cell types and increased that of normal hepatocytes compared with the positive controls, not showing necrotic areas or inflammatory infiltrates. D-002 dose-dependently decreased hepatic MDA levels, but only in the highest dose group were these levels significantly lower than in the positive control. In conclusion, D-002 effectively prevented the histological liver disturbances and lowered MDA levels, a marker of cellular lipid peroxidation, in rats treated with CCl4. Since increased liver lipid peroxidation has been postulated as a cause of CCl4-induced liver damage in rats, the preventive effects of D-002 could be due to its antioxidant action, but such a proposal still requires further research.     

维生素E对四氯化碳肝毒性保护作用的评价

VE (at dosage of 200mg/kg) significantly depressed the liver microsomal lipid peroxidation induced by 50 mg/kg CCl4; on the other hand, VE potentiated the SGPT, or liver triglyceride, or liver microsomal cytochrome P450 during CCl4 poisoning. The interaction between VE and CCl4 should be carefully taken in to consideration, especially when using VE in preventing and curing CCl4 poisoning.     

Food restriction attenuates blood lipid peroxidation in carbon tetrachloride-intoxicated rats

OBJECTIVE: We investigated whether food restriction offers protection against the toxicity of carbon tetrachloride (CCl(4)) and, if so, at what percentage of restriction. METHODS: The effects of food restriction (75% and 50% of food intake) and food restriction followed by CCl(4) treatment on lipid peroxidation and antioxidant enzymes were studied in female Wistar rats. A single dose of CCl(4) (3 mL/kg of body weight, subcutaneous) was administered at the end of the 30-d feeding period. RESULTS: The magnitude of increase in lipid peroxidation was less after CCl(4) treatment in food-restricted animals than in animals fed ad libitum (control), whereas alanine transaminase, aspartate transaminase, and alkaline phosphatase activities in plasma were enhanced due to CCl(4) treatment. The magnitude of increase in the marker enzymes was less in food-restricted animals than in control animals. Erythrocytes from food-restricted rats were more resistant to hydrogen peroxide-induced peroxidation than were those from control rats. The activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase were higher in food-restricted animals. CONCLUSIONS: The present results suggested that food restriction can minimize drug-related increases in peroxidation and protect the system against drug toxicity, presumably by induction of antioxidant potential.     

Curcumin or saikosaponin a improves hepatic antioxidant capacity and protects against CCl4-induced liver injury in rats

Curcumin and saikosaponin a, the bioactive phytochemicals of turmeric and Bupleurum, act as antioxidants. This study investigated the effects of supplementation with curcumin and/or saikosaponin a on hepatic lipids and antioxidant status in rats with CCl(4)-induced liver injury. Male Sprague-Dawley rats were randomly divided into control, CCl(4), CCl(4) + curcumin (0.005%; CU), CCl(4) + saikosaponin a (0.004%; SS), and CCl(4) + curcumin + saikosaponin a (0.005% + 0.004%; CU+SS) groups. CCl(4) (40% in olive oil) was injected intraperitoneally at a dose of 0.75 mL/kg once a week. Curcumin and/or saikosaponin a was administered orally 1 week before CCl(4) injection for 8 weeks. The pathological results showed that liver fibrosis was ameliorated in the SS and CU+SS groups. After 8 weeks, supplementation with curcumin and/or saikosaponin a significantly decreased plasma alanine aminotransferase and aspartate aminotransferase activities, as well as plasma and hepatic cholesterol and triglyceride levels. The CU+SS group showed reversal of the impaired hepatic superoxide dismutase activity and an increase in total glutathione level. Supplementation with curcumin and/or saikosaponin a significantly improved hepatic antioxidant status and suppressed malondialdehyde formation. Therefore, supplementation with curcumin and/or saikosaponin a protects against CCl(4)-induced liver injury by attenuating hepatic lipids and lipid peroxidation and enhancing antioxidant defense. Curcumin and saikosaponin a had no additive effects on hepatoprotection except for greater improvement in the total glutathione level and antioxidant status.     

烟叶硒蛋白在实验性小鼠肝损伤中的抗氧化作用

观察了烟叶硒蛋白（Ｓｅ－Ｒｕｂｉｓｃｏ）对四氯化碳肝损伤小鼠的保护作用。结果表明了一次灌胃６％四氯化碳油溶液１０ｍｌ／ｋｇｂｗ可使小鼠肝组织严重受损，谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）、超氧化物歧化酶（ＳＯＤ）活力急剧降低，脂质过氧化产物丙二醛（ＭＤＡ）显著上升。若提前补充烟叶硒蛋白或亚硒酸钠７ｄ，则可降低ＣＣｌ＿４对肝的损伤，并呈现出剂量效应关系，同时在抗脂质过氧化方面，硒蛋白明显优于亚硒酸钠和不含硒蛋白（Ｒｕｂｉｓｃｏ）组。     

富硒乳酸菌对肝损伤小鼠红细胞脂质过氧化和免疫功能的影响

目的 :　探讨富硒乳酸菌制剂保护 CCl4诱发肝损伤小鼠红细胞脂质过氧化和免疫功能变化及作用机制。方法 :　选择 48只雌雄各半健康成年小鼠 ,随机分成对照组 (C组 ) ,CCl4组 ,CCl4-中剂量富硒乳酸菌制剂保护组 (CCl4- MSe组 ) ,CCl4-高剂量富硒乳酸菌制剂保护组 (CCl4-HSe组 ) ,通过腹腔注射 CCl4诱发肝损伤后 ,分别在第 1、2 w观察 RBC- CR1 花环率和 RBC- IC花环率及 GSH- Px、GST、SOD和 MDA的变化。结果 :　在注射 CCl4后 ,RBC- CR1 花环率均低于或显著低于对照组 ,但 CCl4- MSe、CCl4- HSe组均高于或显著高于 CCl4组 ;CCl4组 RBC- IC花环率显著升高 ,CCl4- MSe和 CCl4- HSe组未见明显上升 ,与对照组相近 ;CCl4组红细胞溶血液 GSH- Px活性与对照组差异不显著 ,但 CCl4- MSe、CCl4- HSe组均显著高于对照组和 CCl4组 ;各组间 GST活性除第 1 w CCl4- HSe组显著高于 CCl4组外无显著差异 ;SOD活性仅见第 2 w CCl4- MSe、CCl4- HSe组比 CCl4组明显升高 ;各处理组溶血液 MDA含量均明显高于对照组 ,但 CCl4- MSe和 CCl4- HSe组均低于或显著低于 CCl4组。结论 :　 CCl4诱发肝损伤小鼠红细胞脂质过氧化和免疫功能变化非常显著 ,富硒乳酸菌制剂能通过增强红细胞免疫功能和抗氧化酶活性发挥有效作用。     

Protective effect of Aronia melanocarpa fruit juice pretreatment in a model of carbon tetrachloride-induced hepatotoxicity in rats

The main active ingredients of Aronia melanocarpa fruit juice (AMFJ) are phenolic substances, mainly flavonoids from the anthocyanin subclass. AIM: The aim of the present study was to investigate the effect of AMFJ applied as pretreatment in a model of carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. MATERIAL AND METHODS: AMFJ was given orally to rats for 2 days at doses of 5, 10 and 20 ml/kg either alone or as pretreatment before the oral application of CCl4 (0.2 ml/kg, 2 days). The plasma activities of aspartate transaminase (AST) and alanine transaminase (ALT) were measured as markers of the liver cell damage. The levels of malondialdehyde (MDA), a lipid peroxidation marker, were determined in rat liver and plasma. RESULTS: Administration of CCl4 caused an elevation of plasma AST and ALT activities. It also induced an elevation of MDA levels in rat liver and plasma. AMFJ applied alone in the tested doses did not cause any significant changes in the measured enzyme activities and in MDA levels. AMFJ applied as pretreatment prevented the CCl4-induced increase of AST and ALT activities, and also prevented the elevation of plasma and liver MDA levels. CONCLUSIONS: AMFJ showed a protective effect in a model of CCl4-induced hepatotoxicity in rats. This effect might be due to the antioxidant activity of its active ingredients.     

黑米花色苷对四氯化碳亚急性肝损伤的保护作用及其机制

目的研究黑米皮花色苷(black rice anthocyanins,BRA)对CCl4亚急性肝损伤小鼠的保护作用。方法NIH小鼠60只,随机分为:对照组、CCl4模型组、黑米花色苷低、中、高剂量组(BRA-L0.40g/kgbw、BRA-M0.80g/kgbw、BRA-H1.60g/kgbw)共5组。饲养前3w内,除对照组外的其他4个组动物均腹腔注射四氯化碳(CCl4)玉米油溶液。每周2次,共3w,诱导化学性亚急性肝损伤动物模型。饲养7w后,测定各组动物血清谷丙转氨酶(ALT)和谷草转氨酶水平(AST),血清和肝脏中脂质过氧化产物丙二醛(MDA)含量、抗氧化酶活性及总抗氧化能力,用ELISA法分析BRA对各组动物血清中DNA主要氧化产物8-羟基脱氧鸟苷(8-hydroxy-2'-deoxyguanosine,8-OHdG)的影响,通过HE染色观察肝组织病理学变化。结果摄入BRA后的各剂量组,CCl4诱导的亚急性肝损伤小鼠的ALT、AST活性较模型组显著降低(P<0.05),血清和肝脏中MDA的生成量显著减少(P<0.05),SOD、GSH-Px活性明显增强(P<0.05),肝脏组织的总抗氧化能力(T-AOC)显著增强(P<0.05);摄入高剂量BRA,8-OHdG的含量显著降低(P<0.05);由CCl4引起的肝脏组织气球样变、脂肪变性,炎症浸润等病理学损伤,喂食BRA后,均可得到明显改善。结论BRA对CCl4诱导的亚急性肝损伤具有保护作用,这一作用与其抗氧化活性有关。