桦木酸体内抗肿瘤作用的初步研究

目的研究桦木酸对H22、S180小鼠肿瘤细胞药效学作用及对肿瘤细胞膜Ca^2＋、Mg^2＋-ATP酶活性的影响。方法通过限量实验确定桦木酸的给药剂量。动物随机分为6组,分别为桦木酸500、250、125mg／kg剂量组,阳性对照组给予环磷酰胺（20mg／kg）,模型对照组分别给予相同体积的生理盐水和配药溶剂,灌胃给药。观察生命延长时间与瘤重抑制率;紫外分光光度法测定Ca^2＋、Mg^2＋-ATP酶活性,结果桦木酸使S180荷瘤小鼠肿瘤细胞膜Ca^2＋、Mg^2＋-ATP酶活性提高（P〈0．05）。结论桦木酸抗肿瘤作用机制与其上调肿瘤细胞膜p53蛋白的表达,改变肿瘤细胞膜Ca^2＋、Mg^2＋-ATP酶活性有关。     

地高辛抗血清阻断内洋地黄素对心肌缺血/再灌注损伤的影响

目的：探讨地高辛抗血清对大鼠实验性心肌缺血／再灌注损伤（MI／R）的心肌氧化应激的影响。方法：采用左冠状动脉前降支结扎30min,复灌45min建立在体大鼠MI／R模型。SD大鼠随机分成假手术组、缺血／再灌注模型组、生理盐水组、维拉帕米组、小、中、大剂量地高辛抗血清组：于再灌注45min后检测左室心尖部缺血区心肌中内洋地黄素含量、心肌细胞膜Na^＋,K^＋-ATP酶和SOD活性以及MDA含量,光镜下观察心肌组织形态学变化。结果：MI／R组和生理盐水组大鼠心肌组织内洋地黄素水平明显升高,细胞膜Na^＋,K^＋-ATP酶活性明显下降,心肌组织SOD活性降低,MDA水平升高。治疗组包括维拉帕米组均能减轻心肌组织结构损伤,降低MDA水平,部分恢复SOD活性;但只有地高辛抗血清能降低心肌组织内洋地黄素水平,恢复心肌细胞膜Na^＋,K^＋-ATP酶活性。结论：地高辛抗血清通过拮抗内洋地黄素,恢复心肌细胞膜Na^＋,K^＋-ATP酶活性,从而减轻缺血／再灌注时的氧自由基损伤。     

D-半乳糖诱导大鼠脑损伤的糖基化机制

目的D-半乳糖（D-galactose）诱导大鼠体内不同糖基化水平,研究其脑损伤发生的机理。方法采用不同剂量D-半乳糖[150、75、37．5mg／（kg·d）]分别腹腔注射（ip）处理大鼠8周,诱导糖基化状态和脑损伤。采用硫代巴比妥酸（TBA）比色法测定糖化血红蛋白,硝基四氮唑蓝（NBT）比色法测定血清果糖胺;按文献方法分别测定血红细胞醛糖还原酶活性和晚期糖基化终末产物（AGEs）含量及脑组织中AGEs含量,羟胺法和比色法分别测定SOD和GSH-Px活性,硫代巴比妥酸法测定MDA含量;以Fura-2／AM作为钙荧光指示剂,双波长荧光分光光度法检测脑海马神经细胞胞质[Ca^2＋]i的变化;透射电镜观察脑海马神经细胞线粒体的变化。结果D-半乳糖处理8周后,大鼠血红细胞醛糖还原酶活性升高,糖化产物形成增多;脑组织中AGEs及脑细胞胞质[Ca^2＋]i含量明显升高,SOD及GSH-Px活性下降,MDA含量升高（P〈0．01,P〈0．05）,海马神经细胞线粒体出现病理性改变。结论D-半乳糖通过诱导体内蛋白糖基化和脑组织AGEs大量生成,降低抗氧化能力及胞质[Ca^2＋]i超负荷等,导致脑细胞损伤。     

富硒大豆多肽对高脂致大鼠脂肪肝和抗氧化功能的影响

目的：探讨富硒大豆多肽改善高脂所致脂肪肝大鼠肝抗氧化功能的影响及机制。方法：将40只Wistar大鼠分成4组（n=10）,分别饲喂标准饲料＋水（NC）、标准饲料＋富硒大豆多肽液（SeN）、高脂饲料＋水（HC）、高脂饲料＋富硒大豆多肽液（SeH）,10周后处死,用苏丹Ⅲ染色肝脏组织切片观察脂肪变性程度,免疫组织化学方法测定肝组织葡萄糖调节蛋白78（GRP78）表达情况,并分析其肝功能、血脂及血清和肝匀浆中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）含量的变化情况。结果：HC组在血清TC、TG水平、肝脏脂肪化程度、GRP78表达情况都明显高于NC、SeN、SeH组（P〈0.01）。SeH组血清和肝组织中MDA含量较HC组降低（P〈0.01）,GSH-Px、SOD活性升高。NC和SeN两组各项指标之间无明显差异。结论：富硒大豆多肽能有效提高脂肪肝大鼠肝内抗氧化酶活性,抑制脂质过氧化反应,降低肝组织内GRP78表达。     

大豆异黄酮干预对围绝经期女性综合征及性激素水平的影响研究

目的：分析大豆异黄酮对改善围绝经期女性综合征及性激素水平等方面的影响,为科学规范指导围绝经期女性营养保健提供科学依据。方法：选取80名围绝经期女性患者随机分为大豆异黄酮组和安慰剂组,于研究前、干预后3个月、6个月进行血清激素、抗氧化指标、肿瘤标志物检测及更年期自我综合征评定、疲劳量评定、焦虑和抑郁评分。结果：干预6个月后,大豆异黄酮组雌二醇（E2）水平、谷胱甘肽过氧化酶（GSH）含量与基线值的平均变化均显著高于安慰剂组（P<0.01）;大豆异黄酮组促黄体生成素（LH）水平、丙二醛（MDA）含量、更年期综合征评分、疲劳评分、焦虑评分、抑郁评分与基线值的平均变化均显著低于安慰剂组（P<0.01）。结论：大豆异黄酮对围绝经期女性改善围绝经期症状、维持激素水平是有效、安全的,适宜剂量的大豆异黄酮可作为围绝经期女性的营养保健手段。     

脱氢表雄酮对大鼠脂类代谢和抗氧化作用的影响

目的：研究灌胃脱氢表雄酮（DHEA）对大鼠脂类代谢和抗氧化作用的影响。方法：选用健康雄性SD大鼠40只,随机分为4组（n=10）。对照组灌胃给予灭菌生理盐水,实验组灌胃给予20mg／kg、10mg／kg、5mg／kg体重的DHEA受试溶液,灌胃量均为1．5ml。每天一次,连续35d。实验结束后采血测定血糖（BG）、甘油三酯（TG）、总胆固醇（TO）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）,血清和肝脏超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。结果：DHEA显著降低大鼠血糖、TG、HDL-c及血清和肝脏MDA含量,显著升高血清LDL-c含量和肝脏SOD活性,而对大鼠体重、血清TC含量和SOD活性没有显著影响。结论：DHEA具有降低大鼠血脂和增强抗氧化能力的作用。     

益坤宁对围绝经期大鼠卵巢bcl-2和bax表达的影响

目的:研究中药益坤宁(Yikunning,YKN)对围绝经期大鼠卵巢bcl-2和bax基因表达的影响,探讨益坤宁治疗围绝经期综合征的作用机制。方法:选用自然衰老的围绝经期雌性大鼠,随机分为3组(n=10):围绝经期对照组、利维爱(Livial)对照组和益坤宁组,另选10只青年雌性大鼠作为青年对照组。连续灌胃处理4周后,采用逆转录-聚合酶链反应(RT-PCR)检测大鼠卵巢中凋亡相关基因bcl-2和baxmRNA表达,采用蛋白印迹(Westernblot)检测大鼠卵巢中Bcl-2和Bax蛋白表达。结果:益坤宁组大鼠卵巢中Bcl-2、BaxmRNA及其蛋白表达高于围绝经期对照组,差异有统计学意义(P0.01);益坤宁组大鼠卵巢中Bcl-2/BaxmRNA比值和蛋白比值高于围绝经期对照组,差异有统计学意义(P0.05或P0.01)。结论:中药益坤宁通过上调围绝经期大鼠卵巢中凋亡相关基因bcl-2和bax的表达,上调Bcl-2/BaxmRNA比值和蛋白比值,从而延缓卵巢衰老,这可能是其治疗围绝经期综合征的分子机制之一。     

维生素E对老年大鼠卵巢颗粒细胞保护作用机制的探讨

目的：通过观察维生素E（VE）对老年雌性大鼠卵巢凋亡相关蛋白Bcl-2、Bax的影响及对其抗氧化能力的影响,探讨VE延缓卵巢衰老的作用和机制。方法：采用自然衰老雌性大鼠,给予不同剂量外源性VE,用免疫组化方法观察卵巢颗粒细胞凋亡调控蛋白Bcl-2、Bax的表达,用Western Blot法检测卵巢Bcl-2、Bax蛋白含量,用生化法测定血清总超氧化物歧化酶（SOD）活力和丙二醛（MDA）含量。结果：与成年对照组相比,老年对照组Bcl-2表达明显降低、Bax表达明显升高（P〈0．01）,血清中SOD活力下降、MDA含量显著升高（P〈0．01）。与老年对照组相比,VE纽Bcl-2表达升高,Bax表达降低（P〈0．05）,MDA含量显著减少（P〈0．01）。结论：VE可调控凋亡相关蛋白Bcl-2、Bax的表达和对抗自由基对颗粒细胞的损伤,对卵巢颗粒细胞具有一定的保护作用。     

外源一氧化氮供体硝普钠对干旱胁迫下小麦幼苗叶中ATP酶活性和膜脂过氧化的影响

研究外源一氧化氮（NO）供体硝普钠（sNP）对干旱胁迫下小麦幼苗叶片ATP酶活性和膜脂过氧化影响的结果表明,15％聚乙二醇．6000（PEG-6000）模拟的干旱胁迫下小麦幼苗叶中H^＋-ATP酶和Ca^2＋．ATP酶活性显著升高后迅速下降,硫代巴比妥酸反应产物（TBARs）和质量膜透性增加;0．1mm01．L^-1 SNP可提高干旱胁迫下小麦幼苗叶中超氧化物歧化酶（SOD）、过氧化物酶（POD）和过氧化氢酶（cAT）活性,降低超氧阴离子（O2^-）和过氧化氢（H2O2）水平,缓解膜脂过氧化,稳定生物膜的结构和功能,H^＋-ATP酶和Ca^2＋-ATP酶也可以保持更高的活性。     

有氧运动和褪黑素对2型糖尿病大鼠抗氧化运动功能的影响

目的：探讨有氧运动和褪黑素对糖尿病大鼠抗氧化功能的影响。方法：成年sD大鼠50只随机分为5组（n=10）：正常对照组（N）、糖尿病组（D）、糖尿病运动组（D＋E）、糖尿病褪黑素组（D＋M）、糖尿病运动和褪黑素组（D＋E＋M）,观察大鼠血清丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH．Px）、血糖和血脂的变化。结果：与N组相比,D组大鼠血清SOD、cSH-PX水平、高密度脂蛋白胆固醇（HDL-C）含量下降,MDA水平、血糖、胆固醇（TC）、血清甘油三酯（TG）和低密度脂蛋白胆固醇（LDL-C）含量明显上升（P〈0．05,P〈0．01）。D＋E组和D＋M组大鼠与D组比较血清中SOD、GSH-Px活性、HDL-C含量显著升高,MDA水平、血糖、TC、TG和LDL-C含量显著降低（P〈0．05,P〈0．01）,有氧运动和褪黑素同时干预可使糖尿病大鼠血清中SOD、GSH-Px活性、HDL-C含量进一步升高,MDA水平、血糖、TC、TG和LDL-C含量进一步降低（P〈0．05,P〈0．01）。结论：有氧运动扣褪黑素均能对糖尿病大鼠氧化应激有明显的抑制作用,且两者联合干预的效果更加显著,其可能机制与糖尿病大鼠的糖脂代谢紊乱状态改善有关。     

硫化氢对1型糖尿病大鼠肾脏的保护作用

目的：观察硫化氢（H₂S）对1型糖尿病大鼠肾脏的保护作用及其机制。方法：32只雄性SD大鼠随机分为4组：正常对照（NC）组、糖尿病（DM）组、糖尿病治疗（NaHS+DM）组和NaHS对照（NaHS）组（n=8）。DM组和NaHS+DM组大鼠采用链脲佐菌素（STZ）55 mg/kg腹腔注射诱导1型糖尿病模型。造模成功后,NaHS+DM组和NaHS组采用腹腔注射NaHS溶液56 μmol/kg干预治疗。8周后,测定大鼠24 h尿蛋白含量、肾重指数、空腹血糖、尿素氮、肌酐等指标;HE染色观察肾脏组织形态学变化;测定肾脏组织脂质过氧化物丙二醛（MDA）含量、超氧化物歧化酶（SOD）和Caspase-3的活性;Western blot检测肾脏组织Bcl-2和Bax蛋白表达。结果：与NC组相比,NaHS组各项指标均无显著差异,DM组,24 h尿蛋白含量、肾重指数、空腹血糖、尿素氮和肌酐水平均明显升高;HE染色结果显示肾小球基底膜增厚、系膜基质增多;MDA含量、Caspase-3活性和Bax蛋白表达明显增高;SOD活性和Bcl-2蛋白表达显著降低。与DM组相比,NaHS+DM组肾功能损伤明显减轻,肾脏组织形态学变化明显改善,MDA含量、Caspase-3活性和Bax蛋白表达明显下降,SOD活性和Bcl-2蛋白表达显著增高。结论：H₂S对1型糖尿病大鼠肾脏具有保护作用,其机制可能与抑制氧化应激和细胞凋亡有关。     

莪术油注射液对慢性低氧大鼠学习与记忆的影响

本文旨在探讨莪术油注射液对慢性低氧大鼠学习与记忆的影响及其可能机制.将Sprague.Dawley大鼠随机分为对照组、慢性低氧组、5 mg/kg体重莪术油组、10 mg/kg体重莪术油组、20 mg/kg体重莪术油组,每组14只.慢性低氧处理采用低氧舱内吸入大约10%O2、5%CO2,饲养10 h/d,持续饲养28 d.莪术油组大鼠低氧处理前腹腔注射相应浓度的莪术油注射液.实验结束次日,通过Morris水迷宫测试各组动物学习和记忆成绩的变化;测定各组大鼠血清和海马组织丙二醛(malonaldehyde,MDA)含量和超氧化物歧化酶(superoxide dismutase,SOD)活性以及海马组织Ca2 浓度([Ca2 i]);通过免疫组织化学和Western blot检测磷酸化Ca2 /钙调蛋白依赖性蛋白激酶Ⅱ(phosphorylated Ca2 /calmodulin-dependent pro-tein kinase Ⅱ,p-CaMKII)在海马组织和胞膜上的表达.结果显示,与对照组相比,慢性低氧组大鼠隐蔽平台的逃避潜伏期明显延长(P<0.05),血清和海马组织MDA含量明显增高,SOD活性显著降低(P<0.05,P<0.01),海马组织[Ca2 ]i明显增高(P<0.01),海马P-CaMKII表达量显著降低(P<0.01).与慢性低氧组比较,莪术油各组发生以下变化:10、20 mg/kg体重莪术油组大鼠隐蔽平台的逃避潜伏期显著缩短(P<0.05):5、10、20 mg/kg体重莪术油组大鼠血清和海马组织MDA含量均显著降低(P相似文献   

紫檀芪调节Keap-1/Nrf2/HO-1信号通路对非酒精性脂肪肝大鼠氧化应激和细胞凋亡的影响

摘要 目的：研究紫檀芪调节Kelch样ECH关联蛋白1（Keap-1）/核因子E2相关因子2（Nrf2）/血红素加氧酶-1（HO-1）信号通路对非酒精性脂肪肝（NAFLD）大鼠氧化应激和细胞凋亡的影响。方法：将60只SD大鼠随机分为对照组、模型组、紫檀芪低剂量组（30 mg/kg）、紫檀芪高剂量组（60 mg/kg）、紫檀芪（60 mg/kg）+N-（4-（2,3-二氢-1-（2''-甲基苯甲酰）-1H-吲哚-5-基）-5-甲基-2-噻唑基）-1,3-苯并二氧唑-5-乙酰胺（ML385）（30 mg/kg）组，每组12只。模型组与药物干预组大鼠以高脂饲料饲养诱导NAFLD模型，对照组大鼠以普通饲料饲养，各组连续喂养12周。以紫檀芪和ML385分组处理14 d后（对照组以等剂量生理盐水处理），检测各组大鼠脂代谢指标[三酰甘油（TG）、总胆固醇（TC）及游离脂肪酸（FFA）水平]、肝指数、肝功能指标[谷丙转氨酶（ALT）及谷草转氨酶（AST）]水平、血清白细胞介素（IL）-17、IL-6、IL-10、氧化应激指标[丙二醛（MDA）、超氧化物歧化酶（SOD）及过氧化氢酶（CAT）]水平；原位末端标记法（TUNEL）染色检测各组大鼠肝细胞凋亡率；蛋白免疫印迹法检测各组大鼠肝组织凋亡相关蛋白及Keap-1/Nrf2/HO-1通路相关蛋白表达。结果：与对照组相比，模型组大鼠血清IL-10、SOD及CAT水平、肝组织Nrf2、HO-1、Bcl-2表达水平显著降低（P＜0.05），TG、TC及FFA水平、肝指数、ALT及AST水平、血清IL-17、IL-6、MDA水平、肝细胞凋亡率、肝组织Keap-1及Bax表达水平显著升高（P＜0.05）。与模型组相比，紫檀芪低、高剂量组大鼠血清IL-10、SOD及CAT水平、肝组织Nrf2、HO-1、Bcl-2表达水平均升高（P＜0.05），TG、TC及FFA水平、肝指数、ALT及AST水平、血清IL-17、IL-6、MDA水平、肝细胞凋亡率、肝组织Keap-1、Bax表达水平均降低（P＜0.05）；与紫檀芪低剂量组相比，紫檀芪高剂量组大鼠血清IL-10、SOD及CAT水平、肝组织Nrf2、HO-1、Bcl-2表达水平升高（P＜0.05），TG、TC及FFA水平、肝指数、ALT及AST水平、血清IL-17、IL-6、MDA水平、肝细胞凋亡率、肝组织Keap-1及Bax表达水平降低（P＜0.05）；与紫檀芪高剂量组相比，紫檀芪+ML385组大鼠血清IL-10、SOD及CAT水平、肝组织Nrf2、HO-1、Bcl-2表达水平降低（P＜0.05），TG、TC及FFA水平、肝指数、ALT及AST水平、血清IL-17、IL-6、MDA水平、肝细胞凋亡率、肝组织Bax表达水平升高（P＜0.05）。结论：紫檀芪可能通过激活Keap-1/Nrf2/HO-1信号通路，改善NAFLD大鼠脂代谢水平，调节炎症反应及氧化应激，减轻肝组织脂肪变性及细胞凋亡。     

Effects of vitamin E on microsomal Ca(2+) -ATPase activity and calcium levels in streptozotocin-induced diabetic rat kidney

Vitamin E treatment has been found to be beneficial in preventing or reducing diabetic nephropathy. Increased tissue calcium and abnormal microsomal Ca(2+)-ATPase activity have been suggested as contributing factors in the development of diabetic nephropathy. This study was undertaken to test the hypothesis that vitamin E reduces lipid peroxidation and can prevent the abnormalities in microsomal Ca(2+)-ATPase activity and calcium levels in kidney of streptozotocin (STZ)-induced diabetic rats. Male rats were rendered diabetic by a single STZ injection (55 mg x kg(-1) i.p.). After diabetes was verified, diabetic and age-matched control rats were untreated or treated with vitamin E (400-500 IU kg(-1) x day(-1), orally) for 10 weeks. Ca(2+)-ATPase activity and lipid peroxidation (MDA) were determined spectrophotometrically. Blood glucose levels increased approximately five-fold (> 500 mg x dl(-1)) in untreated-diabetic rats but decreased to 340+/-27 mg x dl(-1) in the vitamin E treated-diabetic group. Kidney MDA levels did not significantly change in the diabetic state. However, vitamin E treatment markedly inhibited MDA levels in both control and diabetic animals. Ca(2+)-ATPase activity was 0.483+/-0.008 U l(-1) in the control group and significantly increased to 0.754+/-0.010 U l(-1) in the STZ-diabetic group (p < 0.001). Vitamin E treatment completely prevented the diabetes-induced increase in Ca(2+)-ATPase activity (0.307+/-0.025 U l(-1), p < 0.001) and also reduced the enzyme activity in normal control rats. STZ-diabetes resulted in approximately two-fold increase in total calcium content of kidney. Vitamin E treatment led to a significant reduction in kidney calcium levels of both control and diabetic animals (p < 0.001). Thus, vitamin E treatment can lower blood glucose and lipid peroxidation, which in turn prevents the abnormalities in kidney calcium metabolism of diabetic rats. This study describes a potential biochemical mechanism by which vitamin E supplementation may delay or inhibit the development of cellular damage and nephropathy in diabetes.     

B型钠尿肽对急性心肌缺血损伤发挥保护作用的机制

本研究旨在研究B型钠尿肽(brain natriuretic peptide, BNP)对异丙肾上腺素(isoproterenol, ISO)诱导的急性心肌缺血(acute myocardial ischemia, AMI)相关损伤的保护作用。将大鼠随机分作5组:对照组、ISO处理组、ISO+普萘洛尔(5 mg/kg)处理组、ISO+BNP (5 mg/kg)和ISO+BNP (10 mg/kg)处理组。再将4个给药组中的大鼠连续2 d皮下注射ISO。通过心电图(ECG)记录ST段数据;ELISA检测血清中肌酸激酶(CK)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6 (IL-6)和IL-1β的表达水平;接着使用Western blotting对Bax-2、Bcl-2、PI3K、Akt、GSK-3β、MDA5和SOD1蛋白表达水平进行检测,并测定PI3K、Akt和GSK-3β的磷酸化。实验结果显示,BNP (5 mg/kg, 10 mg/kg)可降低血清中MDA和CK的表达水平以及SOD和LDH的蛋白活性;经BNP预处理显著降低了促炎因子IL-1β、IL-6和TNF-α的表达水平;同时BNP也降低了ST段抬高。此外,BNP改善了ISO诱导的大鼠中SOD1、MDA5、Bax-2、Bcl-2、p-PI3K、p-Akt和p-GSK-3β的表达。综上所述,通过调节PI3K/Akt/GSK-3β信号传导途径,BNP保护大鼠免受AMI损伤。     

Carnosine and taurine treatments decreased oxidative stress and tissue damage induced by d-galactose in rat liver

d-galactose (GAL) causes aging-related changes and oxidative stress in the organism. We investigated the effect of carnosine (CAR) or taurine (TAU), having antioxidant effects, on hepatic injury and oxidative stress in GAL-treated rats. Rats received GAL (300 mg/kg; s.c.; 5 days/week) alone or together with CAR (250 mg/kg/daily; i.p.; 5 days/week) or TAU (2.5 % w/w; in rat chow) for 2 months. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and hepatic malondialdehyde (MDA), protein carbonyl (PC) and glutathione (GSH) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-0050x), and glutathione transferase (GST) activities were determined. Hepatic expressions of B cell lymphoma-2 (Bcl-2), Bax and Ki-67 were evaluated. Serum ALT, AST, hepatic MDA, and PC levels were observed to increase in GAL-treated rats. Hepatic Bax expression, but not Bcl-2, increased, Ki-67 expression decreased. GAL treatment caused decreases in GSH levels, SOD and GSH-Px activities in the liver. Hepatic mRNA expressions of SOD, but not GSH-Px, also diminished. CAR or TAU treatments caused significant decreases in serum ALT and AST activities. These treatments decreased apoptosis and increased proliferation and ameliorated histopathological findings in the livers of GAL-treated rats. Both CAR and TAU reduced MDA and PC levels and elevated GSH levels, SOD and GSH-Px (non significant in TAU?+?GAL group) activities. These treatments did not alter hepatic mRNA expressions of SOD and GSH-Px enzymes. Our results indicate that CAR and TAU restored liver prooxidant status together with histopathological amelioration in GAL-induced liver damage.     

筒鞘蛇菰提取物蛇菰多糖对D-半乳糖诱导大鼠肝损伤的保护作用及其机制

目的:探讨筒鞘蛇菰提取物蛇菰多糖(BIH)对D-半乳糖(D-gal)致大鼠肝损伤的保护作用及机制.方法:雄性SD大鼠60只,随机分为正常组(Con)、模型组(D-gal)、蛇菰多糖低剂量组(D-gal+50 mg/kg BIH,BIH-L)、蛇菰多糖中剂量组(D-gal+100 mg/kg BIH,BIH-M)、蛇菰多...     

In vivo treatment with stobadine prevents lipid peroxidation,protein glycation and calcium overload but does not ameliorate Ca2+ -ATPase activity in heart and liver of streptozotocin-diabetic rats: comparison with vitamin E

Hyperglycemia leads to excess production of reactive oxygen species (ROS), lipid peroxidation and protein glycation that may impair cellular calcium homeostasis and results in calcium sequestration and dysfunction in diabetic tissues. Stobadine (ST) is a pyridoindole antioxidant has been postulated as a new cardio- and neuroprotectant. This study was undertaken to test the hypothesis that the treatment with ST inhibits calcium accumulation, reduces lipid peroxidation and protein glycation and can change Ca2+,Mg2+-ATPase activity in diabetic animals. The effects of vitamin E treatment were also evaluated and compared with the effects of combined treatment with ST. Diabetes was induced by streptozotocin (STZ, 55 mg/kg i.p.). Some of diabetic rats and their age-matched controls were treated orally with a low dose of ST (24.7 mg/kg/day), vitamin E (400-500 IU/kg/day) or ST plus vitamin E for 10 weeks. ST and vitamin E separately produced, in a similar degree, reduction in diabetes-induced hyperglycemia. Each antioxidant alone significantly lowered the levels of plasma lipid peroxidation, cardiac and hepatic protein glycation in diabetic rats but vitamin E treatment was found to be more effective than ST treatment alone. Diabetes-induced increase in plasma triacylglycerol levels was not significantly altered by vitamin E treatment but markedly reduced by ST alone. The treatment with each antioxidant completely prevented calcium accumulation in diabetic heart and liver. Microsomal Ca2+,Mg2+-ATPase activity significantly decreased in both tissues of untreated diabetic rats. ST alone significantly increased microsomal Ca2+,Mg2+-ATPase activity in the heart of normal rats. However, neither treatment with ST nor vitamin E alone, nor their combination did change cardiac Ca2+,Mg2+-ATPase activity in diabetic heart. In normal rats, neither antioxidant had a significant effect on hepatic Ca2+,Mg2+-ATPase activity. Hepatic Ca2+,Mg2+-ATPase activity of diabetic rats was not changed by single treatment with ST, while vitamin E alone completely prevented diabetes-induced inhibition in microsomal Ca2+,Mg2+-ATPase activity in liver. Combined treatment with ST and vitamin E provided more benefits in the reduction of hyperglycemia and lipid peroxidation in diabetic animals. This study describes potential mechanisms on cellular effects of ST in the presence of diabetes-induced hyperglycemia that may delay or inhibit the development of diabetic complications. The use of ST together with vitamin E can better control hyperglycemia-induced oxidative stress.