岩藻聚糖硫酸酯降血脂及抗氧化作用的研究

目的：　观察低分子量岩藻聚糖硫酸酯（ｌｏｗ ｍｏｌｅｃｕｌａｒ ｓｕｌｆａｔｅｄ ｆｕｃａｎ , Ｌ Ｍ Ｓ Ｆ） 对实验性高脂血症大鼠的血脂水平及血清和组织中脂质过氧化物（ Ｌ Ｐ Ｏ） 含量和 Ｓ Ｏ Ｄ 活力的影响,探讨其降血脂、抗氧化作用与抗动脉粥样硬化（ Ａ Ｓ） 的关系。方法：　利用实验性高脂血症大鼠模型观察 Ｌ Ｍ Ｓ Ｆ 的降脂作用及对血清和组织中 Ｌ Ｐ Ｏ 和 Ｓ Ｏ Ｄ 的影响。结果：　３０ 天实验结束后,高脂血症大鼠在血脂升高的同时,血清和组织中 Ｌ Ｐ Ｏ 含量上升, Ｓ Ｏ Ｄ 活力下降。 Ｌ Ｍ Ｓ Ｆ 能显著降低高脂血症大鼠血清中 Ｔ Ｇ（ Ｐ＜ ０ ．０５） 和 Ｔ Ｃ（ Ｐ＜ ０ ．０１） 含量,提高 Ｈ Ｄ Ｌ Ｃ 含量（ Ｐ＜ ０ ．０５） ; Ｌ Ｍ Ｓ Ｆ 对高脂血症大鼠具有较强的抗氧化作用,能显著降低血清和组织中 Ｌ Ｐ Ｏ 含量（ Ｐ＜ ０ ．０１） ,同时升高 Ｓ Ｏ Ｄ 活力（ Ｐ＜ ０ ．０１） 。结论：　 Ｌ Ｍ Ｓ Ｆ 显著的降血脂及抗氧化作用使其在抗动脉粥样硬化（ Ａ Ｓ） 方面有较大的应用价值。     

抗氧化剂对黄曲霉毒素染毒的转基因小鼠肝肿瘤的防护

目的研究抗氧化剂２,３叔丁基４羟基茴香醚（ＢＨＡ）对黄曲霉毒素（ＡＦＢ１）染毒的乙型肝炎病毒（ＨＢＶ）转基因小鼠肝肿瘤发生的防护作用。方法对ＡＦＢ１染毒和未染毒的４９只转基因小鼠与４８只非转基因小鼠,测定肝醌还原酶（ＱＲ）和谷胱甘肽Ｓ转移酶（ＧＳＴ）活性、肝丙二醛（ＭＤＡ）含量、肝氧自由基浓度（ＯＦＲ）。结果染毒的转基因小鼠ＢＨＡ组肝腺瘤发生率１７％,癌变率０,显著低于普通饲料组的肝腺瘤发生率（６７％）和癌变率（２２％）。与普通饲料组比较,ＢＨＡ使肝ＯＦＲ和ＭＤＡ含量显著降低;ＢＨＡ组肝ＱＲ和ＧＳＴ活性平均升高３～７倍。结论ＢＨＡ能显著诱导肝脏生物转化Ⅱ相酶活性,清除氧自由基,抑制变异肝细胞生长,可能与抑制或延缓小鼠肝癌的发生、发展进程有关     

腰/臀比值与糖、脂代谢相关性研究

测定２２６例ＮＩＤＤＭ、３８９例ＩＧＴ患者体质指数（ＢＭＩ）及腰／臀比值（ＷＨＲ），并与１５３例糖耐量正常对照组作了比较。结果显示：ＮＩＤＤＭ组、ＩＧＴ组ＢＭＩ、ＷＨＲ均显著高于对照组（Ｐ＜０．０１）；ＮＩＤＤＭ组ＷＨＲ显著高于ＩＧＴ组（Ｐ＜０．０１），两组间ＢＭＩ无显著性差异（Ｐ＞０．０５）。另外，ＮＩＤＤＭ组、ＩＧＴ组的ＦＩｎｓ、２ｈＢＧ、２ｈＩｎｓ、ＴＧ、ＳＢＰ、ＤＢＰ及高血压患病率均显著高于正常组（Ｐ＜０．０１）；ＮＩＤＤＭ组ＦＢＧ、ＦＩｎｓ、２ｈＢＧ、ＴＧ及高血压患病率显著高于ＩＧＴ组（Ｐ＜０．０１），而ＩＤ１、２ｈＩｎｓ、ＩＤ２显著低于ＩＧＴ组（Ｐ＜０．０１）。ＮＩＤＤＭ组Ｃｈ明显高于对照组（Ｐ＜０．０５），而ＩＧＴ组Ｃｈ与对照组相比无显著性差异（Ｐ＞０．０５）。相关分析结果示ＷＨＲ与ＩＤ１、ＩＤ２、Ｃｈ、ＴＧ、ＳＢＰ、ＤＢＰ，均呈正相关。提示ＷＨＲ是体脂分布对糖、脂及胰岛素代谢影响较重要的指标。     

硒多糖、亚硒酸钠对大鼠血硒浓度和肝细胞色素P_(450)单加氧酶系的影响

研究了一次和连续７天腹腔注射硒多糖、亚硒酸钠对大鼠血硒浓度及肝细胞色素Ｐ４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的影响；并比较了硒多糖与亚硒酸钠的作用。结果表明：一次腹腔注射Ｓｅ０．６ｍｇ／ｋｇ体重的硒多糖和亚硒酸钠后，血硒浓度迅速增加，在注射后２小时血硒浓度达到高峰，随后血硒浓度逐渐下降。亚硒酸钠在大鼠体内的吸收和排出均较硒多糖快。连续７天腹腔注射０．２ｍｇ／ｋｇ体重剂量硒多糖和亚硒酸钠后，硒多糖和亚硒酸钠组大鼠血硒浓度分别为对照组的２．６倍和２．１倍，其中硒多糖组的血硒含量显著高于亚硒酸钠组（Ｐ＜０．０５）；硒多糖和亚硒酸钠在体内、外均降低肝细胞色素Ｐ４５０、ｂ５的含量，抑制ＧＳＴ的活性，硒多糖的作用尤为显著，分别为对照组的５７％、７０％和６２％（Ｐ＜０．０５）。两种硒化合物对ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶无明显影响。硒多糖和亚硒酸钠均能显著增强ＧＳＨ－Ｐｘ的活性（Ｐ＜０．０５）。     

桦木尘和柞木尘对大鼠肺泡巨噬细胞分泌细胞因子的影响

为研究体外桦木尘（ＢＤ）和柞木尘（ＯＤ）对大鼠肺泡巨噬细胞（ＡＭ）分泌细胞因子的影响，从支气管肺泡灌洗液中分离３０只Ｗｉｓｔａｒ大鼠的ＡＭ，进行体外培养，分别以不同剂量的ＢＤ或ＯＤ（１００、１５０、２００、２５０μｇ／ｍｌ）诱导ＡＭ，于不同时间（４、２４、４８、７２小时），检测ＡＭ分泌ＩＬ－１、ＩＬ－２、ＩＬ－６和ＴＮＦα的活性。结果显示：ＢＤ和ＯＤ诱导ＡＭ分泌ＩＬ－１、ＩＬ－２、ＩＬ－６和ＴＮＦα，其活性均高于或明显高于对照组（Ｐ＜０．０５或Ｐ＜０．０１），而ＢＤ组与ＯＤ组相比，也有不同或明显不同（Ｐ＜０．０５或Ｐ＜０．０１）。在２００μｇ／ｍｌ的时间曲线中也显示ＢＤ组高于或明显高于ＯＤ组（Ｐ＜０．０５或Ｐ＜０．０１）。提示：ＢＤ和ＯＤ均能刺激ＡＭ分泌ＩＬ－１、ＩＬ－２、ＩＬ－６和ＴＮＦα的活性增加，而ＢＤ较ＯＤ更为明显。     

乙醇慢性摄入染毒对大鼠肝脏ADH和GST活性,GSH含量的影响

给实验动物慢性摄入乙醇平均每只每天量为８．０ｇ／ｋｇ体重，历时９０天。结果显示：（１）大鼠肝细胞浆中醇脱氢酶（ＡＤＨ）和谷胱甘肽硫转移酶（ＧＳＴ）活性，染毒组较对照组均明显减低（Ｐ＜０．０１）；（２）大鼠肝细胞浆内谷胱甘肽（ＧＳＨ）含量染毒组较对照组也明显减低（Ｐ＜０．０１）。提示ＡＤＨ和ＧＳＴ活性及ＧＳＨ含量在酒精性肝病发病中起着重要作用。     

核桃低聚肽对６０Ｃｏγ射线照射小鼠氧化损伤 保护作用的实验研究

摘要：目的　探讨核桃低聚肽（ＷＯＰｓ）对６０Ｃｏγ射线辐照小鼠氧化损伤的保护作用。方法　将９６ 只ＳＰＦ 级雌性ＢＡＬＢ／ｃ小鼠随机分为６ 组：空白对照组、模型对照组、乳清蛋白组（０．４４ｇ／ｋｇ）、ＷＯＰｓ组低、 中、高组（０．２２ｇ／ｋｇ、０．４４ｇ／ｋｇ、０．８８ｇ／ｋｇ）,连续饮水途径给予不同溶液第１４ 天,除空白对照组外, 所有小鼠全身照射３．５ Ｇｙ剂量６０Ｃｏγ 射线,分别在辐照后第３ 天和第１４ 天检测小鼠血清及肝脏ＳＯＤ、 ＧＳＨ Ｐｘ活性及ＭＤＡ 含量。结果　辐照降低了小鼠肝脏及血清ＳＯＤ、ＧＳＨ Ｐｘ含量,增高了ＭＤＡ 含量。 辐照后第３ 天,ＷＯＰｓ中组小鼠肝脏及血清ＳＯＤ 活性均高于模型对照组和乳清蛋白组（犘＜０．０５）;辐照后 第１４ 天,ＷＯＰｓ低组小鼠肝脏及血清ＳＯＤ 活性均高于模型对照组和乳清蛋白组（犘＜０．０５）。辐照后第 ３ 天,ＷＯＰｓ低组小鼠肝脏及血清ＧＨＳ Ｐｘ 活性均高于模型对照组和乳清蛋白组（犘＜０．０５）; 辐照后第 １４ 天,ＷＯＰｓ低组小鼠肝脏及血清ＧＳＨ Ｐｘ活性均高于模型对照组和乳清蛋白组（犘＜０．０５）。辐照后第 ３ 天,ＷＯＰｓ低、中组小鼠肝脏和血清ＭＤＡ 含量均低于模型对照组和乳清蛋白组（犘＜０．０５）; 辐照后 第１４ 天,ＷＯＰｓ低、中、高组小鼠肝脏及血清ＭＤＡ 含量均低于模型对照组和乳清蛋白组（犘＜０．０５）。结 论　ＷＯＰｓ对辐照所致氧化损伤具有一定的保护作用。 关键词：核桃低聚肽;辐照;氧化损伤;超氧化物歧化酶;谷胱甘肽过氧化物歧化酶;丙二醛 中图分类号：Ｒ１５１　　文献标识码：Ａ　　文章编号：１００９ ６６３９ （２０１９）０３ ０２１２ ０５     

铅对大鼠血清两二醛含量和红细胞抗氧化酶活性影响的研究

观察连续饮用含醋酸铅水５０天的大鼠血清两二醛（ＭＤＡ）含量，红细胞超氧化物歧化酶（ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性及血中还原型谷胱甘肽（ＧＳＨ）含量的变化。结果，染毒大鼠血清ＭＤＡ含量明显高于对照组（Ｐ＜００１），血中ＧＳＨ含量，红细胞ＳＯＤ和ＧＳＨ－Ｐｘ活性明显低于对照组（Ｐ＜０．０５或Ｐ＜０．０１）。提示铅致脂质过氧化与其损伤机体的抗氧化能力有关。     

绿茶及混合茶抑制二乙基亚硝胺诱发大鼠肝癌前期病变的抗氧化机理研究

用二乙基亚硝胺（ＤＥＮ）诱发Ｗｉｓｔａｒ大鼠肝癌前期病变（Ｓｏｌｔ－Ｆａｒｂｅｒ模型）。实验前６周给大鼠饮用２％绿茶水及０．５％混合茶水，于实验第８周末宰杀动物。结果发现，绿茶组及混合茶组肝ｒ－ＧＴ异常病灶数均明显低于阳性对照组（Ｐ＜０．０１）。经ＨＰＬＣ法分离肝微粒体脂质过氧化产物丙二醛（ＭＤＡ）、乙醛（ＡＣＴ）、戊醛（ＰＰ）、丙酮（ＡＣＯＮ），与阳性对照组相比，绿茶组和混合茶组的各种脂质过氧化产物均有不同程度的降低。此外，对多种抗氧化酶和Ⅱ相代谢酶活性进行检测，其中绿茶组ＳＯＤ、ＧＳＴ、ＱＲ活性明显高于阳性对照组；混合茶组ＣＡＴ、ＳＯＤ、ＧＳＴ、ＱＲ活性明显高于阳性对照组。结果表明，绿茶和混合茶对ＤＥＮ诱发大鼠肝癌的发生均有显著的预防作用。其作用机理可能和诱导抗氧化酶及某些Ⅱ相代谢酶活性，以及抑制脂质过氧化作用有关。     

缺锌对大鼠脑发育的影响

本文通过建立大鼠缺锌（ｚｉｎｃｄｅｆｉｃｉｅｎｃｙ，ＺＤ）、常锌配对（ｐａｉｒｆｅｅｄｉｎｇ，ＰＦ）模型，从微观及宏观角度，较深入地研究缺锌对学习记忆的影响。结果表明：（１）ＺＤ组的摄食量、体重增长值、饲料效价均非常显著地低于ＰＦ组。（２）ＺＤ组脑的Ｇ０／Ｇ１．期细胞高于ＰＦ组，而Ｓ＋Ｇ２／Ｍ期细胞、细胞容积、脑细胞ＤＮＡ、ＲＮＡ含量均低于ＰＦ组（Ｐ＜０．０５或Ｐ＜０．０１）。（３）ＺＤ组脑细胞内的ｃＡＭＰ高于而ＮＯ含量低于ＰＦｊＨ（Ｐ＜０．０１）。（４）ＺＤ组血清锌和海马锌含量非常显著地低于ＰＦ组。（５）ＺＤ组全脑锌含量无显著下降，然脑铜含量较高，铁含量极低，与ＰＦ组比较有非常显著的差异。（６）ＺＤ组海马ＣＡ１区的ＬＴＰ诱出率为０。串刺激前后ＰＳ峰潜伏期和幅度无明显变化，而ＰＦ组ＬＴＰ诱出率为１００％，串刺激后ＰＳ峰潜伏期缩短，峰幅度明显增高。（７）ＺＤ组海马ＣＡ，区超微结构表现椎体细胞突触内突触小泡减少。（ｓ）ＺＤ组大鼠主动回避行为习得率为２４％，非常显著地低于ＰＦ组的６４％。     

微囊藻毒素LR对SD大鼠的短期毒效应研究

目的：研究和探讨微囊藻毒素（MCLR）对动物的短期毒效应作用。方法：SD大鼠经腹腔注射不同剂量的MCLR,分别于注射的1、7d和停药后第7天（即第14天）采目力大鼠的血清和肝、肾、心等组织标本,经酶学及病理学检验,观察其损伤效应。结果：122цg/kg剂量组,注射后24h可观察到大鼠心肌细胞肌浆溶解,核变性固缩,肌原纤维局部坏死;血清中天冬氨酸转氨酶(AST)、乳酸脱氢酶（LDH）和磷酸肌酸激酶（CPK）与其他组相比显著升高;肾细胞变性,血清中肌酐（BCr）和尿素氮（BUN）亦显著升高;同时肝细胞片状出血、坏死,注射剂量为50цg/kg和25цg/kg时,仍出现肝细胞重度和轻度颗粒变性。血清中丙氨酸转氨酶（ALT）、碱性磷酸酶（LDH）和AST显著上升。对照组大鼠的肝、肾、心等脏器均正常。结论：MCLR可引起SD大鼠肝、肾、心等脏器的短期毒效应,且随着剂量的增加,损伤效应加重。     

二甲基甲酰胺与乙醇联合毒性初探

经口分别给予Wistar大鼠蒸馏水、DMF 400mg/kg、乙醇1000mg/kg及DMF400mg/kg 乙醇1000mg/kg,染毒21天。结果表明DMF组及联合染毒组大鼠血清ALT明显增高,SLDH在后者也明显升高,且两组肝组织ATP酶及SDH活性明显降低。各染毒组尿LDH活性显著上升,DMF组及联合染毒r-GT活性显著降低,此两组肾脏组织AKP、ATP、SDH活性也明显降低。上述变化联合染毒组较单独作用组明显,因此认为DMF对肝肾具有损伤作用,乙醇可加重DMF的损伤作用。     

Inhalation exposure of rats to asphalt fumes generated at paving temperatures alters pulmonary xenobiotic metabolism pathways without lung injury

Asphalt fumes are complex mixtures of various organic compounds, including polycyclic aromatic hydrocarbons (PAHs). PAHs require bioactivation by the cytochrome P-450 monooxygenase system to exert toxic/carcinogenic effects. The present study was carried out to characterize the acute pulmonary inflammatory responses and the alterations of pulmonary xenobiotic pathways in rats exposed to asphalt fumes by inhalation. Rats were exposed at various doses and time periods to air or to asphalt fumes generated at paving temperatures. To assess the acute damage and inflammatory responses, differential cell counts, acellular lactate dehydrogenase (LDH) activity, and protein content of bronchoalveolar lavage fluid were determined. Alveolar macrophage (AM) function was assessed by monitoring generation of chemiluminescence and production of tumor necrosis factor-alpha and interleukin-1. Alteration of pulmonary xenobiotic pathways was determined by monitoring the protein levels and activities of P-450 isozymes (CYP1A1 and CYP2B1), glutathioneS-transferase (GST), and NADPH:quinone oxidoreductase (QR). The results show that acute asphalt fume exposure did not cause neutrophil infiltration, alter LDH activity or protein content, or affect AM function, suggesting that short-term asphalt fume exposure did not induce acute lung damage or inflammation. However, acute asphalt fume exposure significantly increased the activity and protein level of CYP1A1 whereas it markedly reduced the activity and protein level of CYP2B1 in the lung. The induction of CYP1A1 was localized in nonciliated bronchiolar epithelial (Clara) cells, alveolar septa, and endothelial cells by immunofluorescence microscopy. Cytosolic QR activity was significantly elevated after asphalt fume exposure, whereas GST activity was not affected by the exposure. This induction of CYP1A1 and QR with the concomitant down-regulation of CYP2B1 after asphalt fume exposure could alter PAH metabolism and may lead to potential toxic effects in the lung.     

二月桂酸二丁基锡对大鼠肝脏毒性作用

目的用二月桂酸二丁基锡（DBTD）染毒大鼠，探讨DBTD对大鼠肝脏及血清中酶活性的影响。方法选踺康成年大鼠28只。随机分为0，5，10，20mg／kg4个剂量组，每组7只动物，用DBTD灌胃染毒5周后处死动物，测定血清中碱性磷酸酶（ALP）、谷丙转氨酶（GPT）、γ-谷氨酰基转移酶（GGT）、肝组织中酸性磷酸酶（ACP）、碱性磷酸酶（AKP）、乳酸脱氢酶（LDH）活性及肝脏中锡含量。结果各剂量组大鼠肝脏中锡含量，肝组织中ACP、AKP、LDH。血清中ALP、GGT、GPT活性明显高于对照组（P〈0．01，P〈0．05）。结论DBTD可在肝组织中蓄积，具有肝毒性．可影响忏审酶的活幛两阡的下皆曲能     

Soy induces phase II enzymes but does not inhibit dimethylbenz[a]anthracene-induced carcinogenesis in female rats.

Isoflavones in soy may play a role in the prevention of cancer through their capacity to affect antioxidant or protective phase II enzyme activities. This study evaluated the effects of dietary isoflavone levels on the induction of antioxidant and phase II enzyme activities and inhibition of breast carcinogenesis. Female Sprague-Dawley rats (36 d) were fed one of four purified diets with casein, or with soy containing three levels of isoflavonoids (0.03, 0.4 or 0.81 mg/g diet; low, middle and high level of isoflavones, respectively). After 2 wk, enzyme activity was determined of rats (n = 6-7) from each diet group. Liver glutathione peroxidase and glutathione reductase activities, blood glutathione levels, kidney glutathione S-transferase and colon quinone reductase (QR) activities were greater in rats consuming the high isoflavone diet compared to rats consuming the casein diet. Kidney QR and liver, kidney, small intestine, and colon UDP-glucuronosyltransferase activities were greater in rats fed the high isoflavone diet compared to rats fed the casein and low-isoflavone diets. Liver and blood oxidized glutathione were lower in rats fed the high-isoflavone diet compared to those fed the low-isoflavone diet. A subset of rats (n = 86) was fed the purified diets for 2 wk and intubated with dimethylbenz[a]anthracene or peanut oil and palpated weekly for tumors. At 13 wk, there was an inverse relationship (R(2) = 0.911, P < 0.09) between tumor incidence and increasing isoflavone intake. These data support the mechanism of soy and soy isoflavones as antioxidant and phase II enzyme inducers, but not as tumor inhibitors.     

Effect of acrylamide on chick embryonic liver glutathione S-transferases

Glutathione S-transferases (GSTs, EC 2.5.1.18), as the detoxifying enzymes, play an important protective role in embryonic tissues. The GSTs of eleventh-day chick embryonic liver were purified to electrophoretic homogeneity with an overall yield of 31%. The SDS-PAGE analysis of chick embryonic liver GSTs resolved in to three bands, CL1, CL2 and CL3, with relative molecular weights of 27.0, 26.0 and 25.0 kDa respectively. On 72 hours of treatment with acrylamide (AC) (0.1, 0.2 and 0.3 mg) the specific activities of GSTs with CDNB, pNBC, EPNP, BSP, Δ⁵5A and pNPA increased significantly. Total GPx levels were decreased with CHP in liver samples. Immunoblot analysis of AC-treated liver samples showed a dose-dependent increase in the induction of GSTs. CL1 of theta class, CL2 of Mu class and CL3 of alpha class were induced with AC treatment. The theta, mu and alpha classes induced by AC might inhibit the initiation of carcinogenesis.     

Modulatory Effects of Curcumin in Conjunction with Piperine on Benzo(A)Pyrene-Mediated DNA Adducts and Biotransformation Enzymes

The antigenotoxic effects of curcumin alone and with piperine on benzo(a)pyrene-diol (BaP) epoxide DNA adducts (BaPDE-DNA adducts), and carcinogen biotransformation enzymes was investigated in liver and lung of mice. Male Swiss albino mice received curcumin (100 mgkg^?1 body weight) and piperine (20 mgkg^?1 body weight) separately as well as in combination orally in corn oil for 7 days as pretreatments and thereafter 2 h, BaP (125 mgkg^?1 body weight) was administered orally in corn oil. A single dose of BaP to normal mice increased the activities of ethoxyresorufin o-deethylase (EROD), pentoxyresorufin o-depentylase (PROD) and levels of BaPDE-DNA adducts in both the tissues. Quinone reductase (QR) activity was also elevated in the BaP-treated group in both liver and lung when compared with normal control group. Pretreatment of curcumin and curcumin plus piperine before administration of BaP significantly decreased the activities of EROD, PROD, and the level of BaPDE-DNA adducts with consequent increase in QR activities. The study clearly indicates that curcumin, when given in combination with piperine, is more effective in modulating BaPDE-DNA adducts (liver and lung), and activity of EROD (liver).     

单磷酸类脂A预处理对大鼠肝缺血再灌注损伤的保护作用及其机制

目的研究单磷酸类脂A（MPLA）是否通过血红素氧合酶-1-一氧化碳-环磷酸鸟苷（HO-1-CO-cGMP）途径促进降钙素基因相关肽（CGRP）释放,发挥其对大鼠肝缺血再灌注损伤的保护作用。方法健康雄性SD大鼠分为对照组、假手术组、肝脏缺血再灌注组、MPLA低、中、高剂量组（肝脏缺血再灌注＋MPLA0．2、0．5、1．0mg／kg）,复制肝缺血再灌注模型,随后电子显微镜观察细胞超微结构;多功能生化分析仪测定血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、乳酸脱氢酶（LDH）和肝组织CO水平;免疫组化检测肝组织HO-1表达;放射免疫分析法测定肝组织CGRP、cGMP浓度。结果和缺血再灌注组比较,MPLA低、中、高剂量组细胞损害相对较轻;各项肝功能指标显著降低;HO-1、CO、cGMP、CGRP含量升高（P〈0．05）,且HO—1与CO、CO与cGMP、cGMP与CGRP两两者之间存在明显的正相关关系（P〈0．05）。结论MPLA通过HO—1—CO-cGMP途径促进肝脏缺血／再灌注期间CGRP的合成和释放,这可能是MPLA减轻大鼠肝缺血再灌注损伤作用机制之一。     

Low doses of diallyl disulfide, a compound derived from garlic, increase tissue activities of quinone reductase and glutathione transferase in the gastrointestinal tract of the rat.

Diallyl disulfide (DADS), a substance that is formed from the organosulfur compounds present in garlic, is known to increase tissue activities of the phase II detoxification enzymes quinone reductase (QR) and glutathione transferase (GT) in animals. In previous experiments, however, high doses of DADS were employed and only a limited range of tissues were examined. In the present studies, increased activities of QR and GT were recorded in the forestomach, glandular stomach, duodenum, jejunum, ileum, cecum, colon, liver, kidneys, spleen, heart, lungs, and urinary bladder of rats given DADS over a wide range of dose levels. Large variations in response were recorded among the different organs, with forestomach, duodenum, and jejunum being the most sensitive to enzyme induction by DADS. In these organs, significant increases in QR activity were observed at a dose of only 0.3 mg/kg/day. Such a dose level is close to that which may be achieved through human consumption of garlic, suggesting that induction of phase II enzymes may contribute to the protection that is afforded by this vegetable against cancer of the gastrointestinal tract in humans.