灯盏花素对大鼠糖尿病模型肾组织TGF-β1与CTGF表达影响的实验研究

目的　探讨灯盏花素对大鼠糖尿病模型肾组织转化生长因子 β1(TGF β1)与结缔组织生长因子 (CTGF)表达的影响。方法　建立STZ诱导的单侧肾切除糖尿病模型 ,随机分 :对照组、模型组、灯盏花素给药组 (2 0mg·kg-1·d-1,灌胃 )。观察 8wk后大鼠体重、肾重、肾重 /体重、2 4h尿白蛋白排泄率 (AER)、肾小球面积 (AG)和容量 (VG)及系膜区面积 (AM)的变化 ,并检测肾组织与尿MDA含量及肾组织SOD、CAT、GSH PX活性 ,通过免疫组化检测肾小球TGF β1与CTGF蛋白表达。结果　灯盏花素给药对大鼠糖尿病模型血糖、体重无明显影响 ,可明显抑制肾重、肾重 /体重、AER、AG、VG 及AM 的增加 (P <0 0 5 ) ;对肾组织及尿MDA含量的增加有明显抑制作用 (P <0 0 5 ) ,并明显提高肾组织SOD、CAT及GSH PX活性 (P <0 0 5 ,P <0 0 1)。免疫组化半定量分析显示 ,与对照组相比糖尿病大鼠肾小球TGF β1及CTGF表达明显增加 (P <0 0 1) ,灯盏花素给药对其有明显抑制作用 (P <0 0 5 )。结论　灯盏花素对大鼠糖尿病模型肾脏有明显保护作用 ,其机制部分与抑制肾组织TGF β1与CTGF过高表达有关     

灯盏花素对糖尿病大鼠肾组织巨噬细胞浸润的影响

目的探讨灯盏花素对糖尿病大鼠肾组织巨噬细胞浸润的影响。方法建立STZ诱导的单侧肾切除糖尿病模型,随机分:对照组、模型组、灯盏花素给药组与MMF给药组。8wk末检测尿白蛋白排泄率(AER)、肾组织蛋白激酶C(PKC)活性,应用免疫组化方法检测肾组织ED1及单核细胞趋化蛋白1(MCP1)与细胞间黏附因子1(ICAM1)表达。结果灯盏花素或MMF给药组大鼠肾重、肾重/体重、AER明显低于模型组(P<0.05)。模型组肾组织细胞浆、细胞膜及细胞总PKC活性明显高于对照组(P<0.01),灯盏花素给药组肾组织PKC活性明显低于模型组(P<0.05),MMF给药组肾组织PKC活性与模型组相比无差异。模型组肾小球ED1阳性细胞数及MCP1、ICAM1表达明显高于对照组(P<0.01),灯盏花素或MMF给药可明显缓解这些变化(P<0.05)。结论灯盏花素对糖尿病大鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织巨噬细胞浸润有关。     

灯盏花素的抗氧化作用及拮抗硒对大鼠肝脏毒性的研究

目的　探讨灯盏花素对人类允许的最高摄入量 (UL upperlimitofintake)硒所致毒性的拮抗作用。 方法　采用体外化学发光法测定灯盏花素清除亚硒酸钠 (Na2 SeO3)产生的活性氧自由基 (ROS)的能力、动物模型研究灯盏花素对大鼠肝脏丙二醛 (MDA)含量、抗氧化酶活性及组织病理学损伤的影响。结果　体外实验表明灯盏花素能有效清除由Na2 SeO3产生的ROS。动物实验中补UL硒及灯盏花素组大鼠肝脏MDA含量低于仅补UL硒组 ;超氧化物歧化酶(SOD)、过氧化氢酶 (CAT)、谷胱甘肽过氧化物酶 (GSH Px)活性高于仅补UL硒组 ;肝组织切片显示受损伤程度与仅补UL硒组相比减轻。结论　灯盏花素能有效拮抗UL硒所致的毒性 ,其机制与灯盏花素清除硒产生的ROS的作用有关     

灯盏花素对胰岛素抵抗大鼠肝脏的保护作用

目的探讨灯盏花素对胰岛素抵抗(IR)大鼠肝脏的保护作用。方法采用高脂高糖饲料饲养12周建立IR大鼠模型,成模后随机均分为灯盏花素高剂量组(HD组)、灯盏花素低剂量组(LD组)、模型组(MO组),各组以相应的药物干预2周。另设正常组(NO组),普通饲料喂养,不给药物干预。通过测定大鼠血清空腹胰岛素(FINS)和空腹血糖值(FBG)来计算胰岛素敏感指数(ISI);检测肝脏组织中丙二醛(MDA)、超氧化物岐化酶(SOD)的活性以观察药物对大鼠肝脏氧化和抗氧化的作用;运用苏木精-伊红(HE)染色制片检测大鼠肝脏组织病理学改变;油红O染色法观察肝脏组织脂肪沉积和脂肪浸润。结果与NO组相比,MO组大鼠ISI明显降低(P<0.01);肝脏中MDA含量明显升高,SOD活性明显下降(P<0.01);HE形态显示,与NO组相比,MO组大鼠肝细胞明显脂肪变性,经过灯盏花素治疗后,与MO组相比,HD组及LD组大鼠肝细胞脂肪变性明显好转;油红O染色结果显示,MO组大鼠肝脏组织脂肪沉积明显,强度大(P<0.01);与MO组相比,HD组和LD组大鼠肝脏脂肪沉积明显好转,HD组大鼠SOD活性较MO组明显升高(P<0.01),MDA的含量较MO组明显下降(P<0.01)。结论灯盏花素可改善IR,对IR大鼠肝脏具有保护作用,其机制可能与改善IR和抗氧化有关。     

还原型谷胱甘肽对大鼠肝纤维化肝内抗氧化体系的影响

目的 探讨还原型谷胱甘肽（GSH）对大鼠肝纤维化肝内抗氧化体系的影响.方法 将36只雄性SD大鼠随机分为三组：正常组、模型组、GSH组,每组各12只.除正常组外,大鼠造模采用腹部皮下注射四氯化碳法制备大鼠肝纤维化模型,GSH组在造模的同时进行GSH治疗,各组于第14周测定大鼠肝脏中过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、维生素E（VitE）和丙二醛（MDA）.结果 模型组大鼠肝组织中CAT、SOD、VitE明显低于正常组（P＜0.01）,而MDA明显升高（P＜0.01）;GSH组与模型组比较,各组的SOD、CAT、VitE均明显升高,而MDA明显下降,差异均有统计学意义（P＜0.01）.结论 GSH能有效降低大鼠肝纤维化肝内脂质过氧化.     

黄芩素对急性肝损伤模型小鼠的保护作用及其机制

目的探讨黄芩素对四氯化碳（CCl4）诱导小鼠急性肝损伤的保护作用及其机制。方法建立CCl4诱导小鼠急性肝损伤模型,在预防性给药与治疗性给药两种给药方式中,检测小鼠血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）活性、肝匀浆丙二醛（MDA）含量及超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH Px）、过氧化氢酶（CAT）活性。结果黄芩素能降低模型小鼠肝脏指数,血清ALT、AST活性,肝匀浆MDA含量,并提高小鼠肝匀浆SOD、GSH PX、CAT活性。结论黄芩素对CCl4诱导肝损伤的保护作用,可能与其抗氧化作用机制有关。     

木芙蓉叶提取物对糖尿病大鼠抗氧化能力的影响

目的：研究木芙蓉叶提取物对2型糖尿病大鼠血糖及抗氧化能力的影响。方法采用高糖高脂饲料联合小剂量链脲佐菌素制备2型糖尿病大鼠模型,给予二甲双胍及木芙蓉叶提取物灌胃治疗,连续给药4周。给药2周后,检测血清 SOD含量;给药4周后,检测血清SOD、GSH－PX和肝脏SOD、GSH含量。结果给药2周后,木芙蓉叶提取物高剂量组的血清SOD含量比糖尿病模型组显著提高;给药四周后,木芙蓉叶提取物高、低剂量组的血清SOD、GSH－PX和肝脏GSH含量比糖尿病模型组显著提高,木芙蓉叶提取物低剂量组和二甲双胍组的肝脏SOD含量比糖尿病模型组显著提高。结论木芙蓉叶提取物能提高2型糖尿病大鼠的抗氧化能力,这可能是其降糖作用的机制之一。     

抗痹颗粒对糖尿病周围神经病变大鼠的疗效和氧化应激的影响

目的 探讨抗痹颗粒对糖尿病周围神经病变（DPN）大鼠的疗效和氧化应激指标的影响。方法 取SD大鼠喂食高能饲料结合腹腔注射链脲佐菌素（STZ）制备DPN大鼠模型。模型大鼠随机分为3组：模型组、抗痹颗粒高剂量组[3.24 g/（kg·d）]、抗痹颗粒低剂量组[0.81 g/（kg·d）],每组10只。另取10只作为正常组。正常组和模型组给予生理盐水灌胃,抗痹颗粒给药组按剂量灌胃给药,1次/d,连续给药8周,实验总计9周。在实验的0、1、5、9周测量大鼠的体质量、血糖水平。在实验第9周,处死大鼠,切取部分坐骨神经组织测超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽（GSH）、过氧化氢酶（CAT）活性水平。结果 与正常组相比,模型组体质量、血糖明显增加（P <0.05）,SOD、CAT活性明显降低,MDA含量升高,GSH含量降低;与模型组相比,给药组体质量、血糖明显降低（P <0.01）,SOD、CAT活性明显升高,MDA含量减少,GSH含量升高。结论抗痹颗粒能够降低糖尿病周围神经病变大鼠的氧化应激反应。     

灯盏花素对大鼠脑创伤的保护作用

目的:观察灯盏花素对大鼠脑创伤后脑水肿、血脑屏障通透性和氧自由基的影响。方法:84只大鼠随机分为假手术组,模型组及低(25 mg/kg×2)、高(50 mg/kg×2)剂量灯盏花素组。采用液压颅脑损伤模型,脑创伤的同时尾静脉注射灯盏花素,8 h后重复给药一次。检测各组大鼠脑创伤后24 h脑组织含水量,伊文思蓝、超氧化物歧化酶(SOD)和丙二醛(MDA)的含量。结果:模型组大鼠脑创伤后脑组织含水量,伊文思蓝、MDA和SOD含量与假手术组有显著性差别。大鼠脑创伤后注射低剂量和高剂量灯盏花素均可显著降低脑组织含水量、伊文思蓝含量和MDA含量,显著增加SOD含量(P＜0．05)。结论:灯盏花素可减轻大鼠脑创伤后脑水肿,其对大鼠脑创伤的保护作用与降低血脑屏障通透性、抑制氧自由基反应有关。     

解毒化淤Ⅱ方中药配方颗粒剂对肝衰竭大鼠肝线粒体月旨质过氧化的影响

目的研究解毒化淤Ⅱ方的中药配方颗粒对暴发性肝衰竭大鼠肝线粒体内脂质过氧化作用的影响.方法采用皮下注射硫代乙酰胺(TAA)法复制暴发性肝衰竭大鼠模型.取Wistar大鼠84只,随机分为空白组、模型组、解毒化淤Ⅱ方中药配方颗粒剂(低、中、高剂量组)、安宫牛黄丸组、乳果糖组,造模前3d开始灌胃给药,2次·d-1,间隔12h,共给药11次;造模完成12h后,测定各组大鼠肝线粒体内丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、还原型谷胱甘肽(GSH)、一氧化氮(NO)及肝脏的坏死面积.结果解毒化淤Ⅱ方中药配方颗粒剂能显著减少肝脏坏死面积,抑制肝线粒体内脂质过氧化终产物MDA的生成,恢复SOD、CAT的活力,提高GSH、NO的含量,并呈量效关系,与模型组比较差异有统计学意义(P＜0.05或P＜0.01);肝脏的坏死面积与肝线粒体内MDA呈正相关关系,与SOD、CAT、GSH、NO呈负相关关系.结论解毒化淤Ⅱ方中药配方颗粒剂对暴发性肝衰竭肝细胞具有较强的保护作用,其作用机制可能是通过拮抗脂质过氧化来实现.     

地黄寡糖对二型糖尿病大鼠糖脂代谢及肝脏超微结构的影响

目的 观察地黄寡糖对2型糖尿病大鼠糖脂代谢的影响及肝脏的保护作用。方法 取♂SD大鼠用高脂高糖饲料喂养8周后,腹腔注射链脲佐菌素25 mg·kg^-1制备糖尿病大鼠模型,造模成功后随机分组为：糖尿病模型组、地黄寡糖高剂量组、地黄寡糖中剂量组、地黄寡糖低剂量组、二甲双胍组,每组10只;另取8只用普通大鼠饲料喂养8周后,腹腔注射等体积柠檬酸-柠檬酸钠缓冲液,作正常对照组。在第0,2,4,8周末各测定一次空腹血糖(FBG);第8周末测定血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、和空腹血清胰岛素(FINS);实验结束处死大鼠,取肝组织检测谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平;HE染色后光镜观察肝脏病理变化;透射电镜观察肝脏超微结构的改变。结果 与糖尿病模型组比较,地黄寡糖中、高剂量组FBG、TG、TC、LDL-C、FINS水平均明显降低,HDL-C升高(P<0.05);糖尿病大鼠肝组织氧化应激水平增高,地黄寡糖中、高剂量组糖尿病大鼠SOD、GSH-Px活性均显著增加,MDA水平显著下降;HE染色显示,各地黄寡糖治疗组大鼠肝细胞脂肪变性明显减少,肝细胞排列基本规则。透射电镜结果显示,地黄寡糖高剂量组大部分线粒体结构清晰内质网完整。结论 地黄寡糖可降低糖尿病大鼠血糖、血脂,减轻肝细胞脂肪变性,从而达到保护肝脏的作用,其作用机制可能与其增强肝组织抗氧化作用,减缓糖尿病对肝组织的损伤有关。     

Prevention of early liver injury by breviscapine in streptozotocin-induced diabetic rats

The aim of this study was to investigate the protective effect of breviscapine extracted from the Chinese herb Erigeron breviscapus on liver injury in diabetic rats induced by streptozotocin. Treatment with breviscapine significantly reduced liver weight, liver lipid level, fatty liver and liver fibrosis score in diabetic rats. Treatment with breviscapine also significantly decreased lipid peroxidation malondiadehyde levels and increased the activities of antioxidative enzymes such as superoxide dismutase, catalase and glutathione peroxidase in diabetic liver. Immunohistochemical observations revealed that macrophage (ED-1-positive cells) infiltration in diabetic liver was inhibited by treatment with breviscapine. Western blot analysis showed that the expression of transforming growth factor-beta1 in diabetic liver was lowered by breviscapine treatment. In conclusion, our results indicate that breviscapine has potential as a treatment for diabetic liver injury through attenuating liver lipid accumulation and oxidative stress.     

糖肾方对 2 型糖尿病大鼠肝脏氧化应激水平及病理改变的影响

目的 观察糖肾方对 2 型糖尿病大鼠肝脏氧化应激水平及病理改变的影响, 并探讨其可能的机制。方法 采用高脂饲料喂养和小剂量链脲佐菌素(STZ)腹腔内注射方法, 建立 2 型糖尿病合并非酒精性脂肪肝动物模型。将造模成功的大鼠随机分为正常组、 模型组、 糖肾方组和二甲双胍组, 比较各组大鼠血清丙氨酸转氨酶(ALT)、 天冬氨酸转氨酶(AST)、 三酰甘油 （TG）、 总胆固醇 （CHO） 和低密度脂蛋白胆固醇 （LDL-C） 水平, 肝组织超氧化物歧化酶(SOD)、 过氧化氢酶(CAT)、 维生素 E （VE）、 一氧化氮 （NO） 和一氧化氮合酶 （NOS） 水平, 并在光镜下观察各组大鼠肝组织病理形态学改变。结果 与模型组相比, 二甲双胍组和糖肾方组大鼠表现状态较好, 毛色较光泽, 粪便成形; 二甲双胍组和糖肾方组大鼠的肝脏质量和肝脏质量指数较模型组明显下降, 2 组大鼠血清 ALT、 AST、 TG、 CHO、 LDL-C 水平显著降低。与模型组相比, 糖肾方组大鼠肝组织匀浆中 SOD、 CAT、 VE 水平明显升高, NO、 NOS 水平减低; 二甲双胍组大鼠肝组织匀浆中 SOD、 CAT 水平明显升高, NO、 NOS 水平减低。HE 染色显示二甲双胍组和糖肾方组较模型组大鼠肝细胞脂肪变性明显减少, 肝细胞排列基本规则。结论糖肾方可改善 2 型糖尿病大鼠肝功能, 降低血脂水平, 减轻肝脏脂质沉积, 其作用机制可能与其清除脂质过氧化物, 改善肝组织氧化应激水平有关。     

Effects of acute alcohol consumption and vitamin E co-treatment on oxidative stress parameters in rats tongue

The aim of this study was to evaluate the effects of acute alcohol consumption and vitamin E co-treatment upon oxidative stress parameters in rats tongue. Thirty-eight, Wistar rats were separated into five groups (alcohol, alcohol/vitamin E, control, Tween, vitamin E). Alcohol and alcohol vitamin E groups had the standard diet, and 40% alcohol on drinking water. Other groups were fed with the same standard diet and water ad libitum. Vitamin E was given by gavage to vitamin E and alcohol/vitamin E rats twice a week. Alcohol and control groups were subjected to saline gavage and Tween group to 5% Tween 80 solution, the vitamin E vehicle. At day 14, the animals were anesthetized and specimens were obtained from tongue. Lipid peroxidation (TBARS), protein oxidative damage, catalase (CAT) and superoxide dismutase (SOD) activities were quantified. Alcohol group decreased TBARS in relation to control group and alcohol vitamin-treated animals decreased TBARS when compared to Tween and vitamin E groups. SOD activity was lower and CAT activity was higher in animals treated with both alcohol and vitamin E. These results suggest that short-term alcohol consumption decreases lipid peroxidation levels. Alternatively, alcohol/vitamin E group increased CAT, showing the toxicity of this association.     

长叶胡颓子降血糖、血脂及抗脂质过氧化作用的研究

目的研究长叶胡颓子果实降血糖、血脂及抗脂质过氧化作用并探讨其药理作用机制.方法以高胆固醇高脂饲料诱发高脂模型大鼠,四氧嘧啶致糖尿病小鼠,应用长叶胡颓子果实水煎液进行实验观察.检测空腹血糖(FBG)、血清胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、胰岛素(INS)、C肽(C-P)及血清脂质过氧化产物丙二醛(MDA)、活性氧(ROS)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)水平.结果长叶胡颓子果实具有抑制高脂血症大鼠TC、TG、LDL-C的升高,降低ROS、MDA,增强SOD、CAT、GSH-PX活力的作用(P＜0.05),可使糖疗病小鼠FBG降低(P＜0.05),对血浆INS和C-P无影响,但胰岛素敏感指数(ISI)明显高于实验对照组(P＜0.05).结论长叶胡颓子果实具有降血糖、血脂和抗脂质过氧化作用,对心血管系统疾病、糖尿病有预防保健作用.     

Combined effects of vitamin C, vitamin E, and sodium selenate supplementation on absolute ethanol-induced injury in various organs of rats

In this study, the effect of combination of vitamin C (ascorbic acid), vitamin E (alpha -tocopherol), and selenium (sodium selenate) on ethanol-induced liver and intestine injury in rats was investigated. The ethanol-induced injury was produced by the administration of 1 ml of absolute ethanol to each rats. Animals received vitamin C (250 mg/kg), vitamin E (250 mg/kg), and sodium selenate (Se) (0.5 mg/kg) for 3 days; 1 h after the final antioxidant administration, they were sacrificed. Lipid peroxidation and glutathione levels, catalase (CAT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GP(x)) activities were determined in liver and intestine tissues. Myeloperoxidase (MPO), aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) were determined in liver tissue. Also, CAT activity, urea, creatinine, uric acid, and total lipid levels were determined in serum samples. In the ethanol group, serum urea, creatinine, uric acid, and total lipid levels; liver and intestine LDH; liver MPO, AST, ALP, ALT, and GGT activities; and liver and intestine LPO levels increased, whereas serum CAT activity, liver and intestine GSH levels, and CAT, SOD, and GP(x) activities decreased. On the other hand, treatment with vitamin C, vitamin E, and Se reversed these effects. As a result of these findings, we can say that the combination of vitamin C, vitamin E, and selenium has a protective effect on ethanol-induced changes in lipid peroxidation, glutathione levels, and antioxidant enzyme activities in liver and intestine tissues, and in some serum parameters of rats.     

Endosulfan-induced cardiotoxicity and free radical metabolism in rats: the protective effect of vitamin E

Endosulfan is widely used in insect control and it is absorbed by both humans and animals through ingestion, inhalation and percutaneously. The aim of this work was to study antioxidant enzyme system which include superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) and malondialdehyde (MDA), the end product of lipid peroxidation and ultrastructural changes that might occur in the heart tissue of adult male Wistar rats as a result of endosulfan intoxication. Vitamin E (200 mg/kg, twice a week), endosulfan (2 mg/kg, per day, once a day in corn oil) and vitamin E (200 mg/kg, twice a week)+endosulfan (2 mg/kg, per day, once a day in corn oil) combination were given to rats (n = 10/group) orally via gavage for 6 weeks. SOD, GPx, CAT activities and MDA level increased in the endosulfan-treated group heart tissue compared to control group (P < 0.01, P < 0.01, P < 0.05 and P < 0.01, respectively). SOD, GPx activities and MDA level decreased in the vitamin E + endosulfan-treated group compared to endosulfan-treated group (P < 0.05, P < 0.05 and P < 0.05, respectively). Decrease of CAT activity was not significant statistically in the vitamin E + endosulfan-treated group compared to endosulfan-treated group. CAT activity increased in the vitamin E + endosulfan treated group compared to control group (P < 0.05). Increase of SOD, GPx activities and MDA levels were not significant statistically in the vitamin E + endosulfan-treated group compared to control group. In electron microscopic investigations while cytoplasmic edema and swelling and vacuolization of mitochondria of myocardial cells in endosulfan-treated group was observing, only a weak swelling of mitochondria of myocardial cells in vitamin E + endosulfan-treated group was observed. We conclude that vitamin E significantly reduce endosulfan-induced cardiotoxicity in rats.     

Effect of oral vitamin E administration on acute gastric mucosal lesion progression in rats treated with compound 48/80, a mast cell degranulator

The effect of oral vitamin E administration on acute gastric mucosal lesion progression was examined in rats treated once with compound 48/80 (C48/80) (0.75 mg/kg, i.p.) in comparison with that of subcutaneously administered superoxide dismutase (SOD) plus catalase (CAT). Vitamin E (50, 100 or 250 mg/kg) administered at 0.5 h after C48/80 treatment reduced progressive gastric mucosal lesions at 3 h after the treatment dose-dependently, like SOD plus CAT administered at the same time point. The gastric mucosa of C48/80-treated rats had decreased Se-glutathione peroxidase activity and vitamin E, ascorbic acid, and hexosamine contents and increased myeloperoxidase and xanthine oxidase activities and thiobarbituric acid reactive substances content at 3 h after the treatment. Administered vitamin E attenuated all these changes found at 3 h after C48/80 treatment dose-dependently, like administered SOD plus CAT. C48/80-treated rats administered with vitamin E (100 or 250 mg/kg) had higher gastric mucosal vitamin E content than C48/80-untreated rats. Neither administered vitamin E nor SOD plus CAT had any effect on the increases in serum serotonin and histamine concentrations and the decrease in gastric mucosal blood flow found at 3 h after C48/80 treatment. In the gastric mucosa of C48/80-untreated rats administered with vitamin E, thiobarbituric acid reactive substances content decreased with an increase in vitamin E content. These results indicate that orally administered vitamin E prevents acute gastric mucosal lesion progression in C48/80-treated rats possibly by suppressing oxidative stress, neutrophil infiltration, and mucus depletion in the gastric mucosa like administered SOD plus CAT.     

Methiocarb-induced oxidative damage following subacute exposure and the protective effects of vitamin E and taurine in rats

Methiocarb, is used worldwide in agriculture and health programs. Besides its advantages in the agriculture, it causes several toxic effects. In this study, we aimed to investigate subacute effects of methiocarb on lipid peroxidation, reduced glutathione (GSH), antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) and histopathological changes in rat tissues. Moreover, we examined the possible protective effects of vitamin E and taurine on methiocarb-induced oxidative damage in rat tissues. Rats were randomly divided into six groups as follows; I-control group; II-methiocarb group; III-vitamin E group; IV-vitamin E + methiocarb group; V-taurine group and VI-taurine + methiocarb group. Methiocarb significantly increased lipid peroxidation in liver and kidney when compared to control groups. Levels of GSH and activities of SOD, CAT and GSH-Px were found to be decreased, while GSH-Rd remained unchanged in rat liver and kidney treated with methiocarb. Pretreatment of vitamin E and taurine resulted in a significant decrease on lipid peroxidation, alleviating effects on GSH and antioxidant enzymes. The degenerative histological changes were less in liver than kidney of rats treated with methiocarb. Pretreatment of vitamin E and taurine showed a protective effect on the histological changes in kidney comparing to the liver of rats treated with methiocarb.