葛根提取物抗糖尿病大鼠氧化应激的实验研究

目的:探讨葛根提取物防治糖尿病血管病变的机制.方法:采用链脲霉素腹腔注射制备糖尿病大鼠模型,以氨基胍作为阳性药物对照,以葛根总提取物和总黄酮为受试药物,测定各实验组大鼠血糖、超氧化物歧化酶、丙二醛、一氧化氮及一氧化氮合酶,观察葛根提取物对糖尿病大鼠的作用与影响.结果:与正常对照组相比,模型组血糖、血浆超氧化物歧化酶和丙二醛有显著差异(P＜0.05,P＜0.01);葛根总提取物、葛根总黄酮可降低糖尿病大鼠血糖,与模型组比较有显著差异(P＜0.05);氨基胍、葛根总提取物和葛根总黄酮可提高糖尿病大鼠血浆超氧化物歧化酶的活性,减少丙二醛的产生,与模型组比较有显著差异(P＜0.05,P＜0.01).结论:葛根提取物具有抗氧化应激的作用,可防治糖尿病血管病变的发生.     

筋脉通对大鼠坐骨神经传导速度及红细胞抗氧化作用的影响

目的观察中药复方筋脉通对糖尿病大鼠坐骨神经传导速度及抗氧化作用的影响.方法采用链脲菌素(STZ)致大鼠糖尿病模型,给予筋脉通灌胃22.5g*kg-1,qd,并以氨基胍(AG)对照,疗程8周.观察该制剂对糖尿病大鼠坐骨神经传导速度和超氧化物歧化酶(SOD)活性、丙二醛(MDA)的影响.结果经筋脉通治疗后,糖尿病大鼠坐骨神经传导速度增快,和AG对照组、糖尿病组比较差异有显著性(P＜0.05～0.01).红细胞SOD活性与糖尿病组比较明显升高(P＜0.01),血浆MDA含量明显降低(P＜0.01).对血糖有降低作用.结论筋脉通能够提高STZ糖尿病大鼠SOD活性,降低MDA水平,增快神经传导速度,对改善糖尿病神经病变有一定的疗效.     

四味地黄乙醇提取物治疗糖尿病心肌病与氨基胍药效比较

目的:研究四味地黄2种醇提取物对STZ诱导糖尿病大鼠心肌病及血管病变的药效,与AGEs选择性阻断剂氨基胍比较。方法:腹腔一次注射60 mg.kg-1链脲佐菌素(STZ)建立糖尿病大鼠模型,4周后随机分组,5～8周分别灌胃:100 mg.kg-1氨基胍(AMG),10 g.kg-1复方地黄70%乙醇提取物,或10 g.kg-1 95%乙醇提取物。8周后,测定肠系膜动脉内皮依赖性舒张、血流动力学及心脏重量指数,血清中血糖、胆固醇(CHO),心肌组织中过氧化氢酶(CAT)、一氧化氮(NO)、一氧化氮合酶(NOS)、羟脯氨酸(HYP)。结果:STZ诱导的糖尿病大鼠血管内皮功能受损,血管内皮依赖性舒张减弱;血流动力学参数反映心功能明显下降,心肌肥大。血清中血糖与CHO含量较正常组显著升高。心肌组织中iNOS及tNOS分别较正常组大鼠升高+59.7%及+50.0%(P<0.01,P<0.01),CAT(U.mg prot-1)而活性降低-14.6%(P<0.05),HYP(μg.mg prot-1)含量显著增高+26.6%(P<0.01)。氨基胍和2种乙醇提取物,均明显改善糖尿病的血管与心脏的并发症,但无明显的降糖作用。...     

灯盏花素对糖尿病大鼠肾脏氧化应激的影响

目的　在链脲菌素诱导的糖尿病大鼠模型上 ,灯盏花素与化学合成药氨基胍相比较来探讨灯盏花素对糖尿病大鼠肾脏的保护作用及与氧化应激的关系。方法　用链脲菌素诱导糖尿病大鼠模型后 ,将糖尿病大鼠分为 :糖尿病组、灯盏花素组 (0 1g·kg-1)和氨基胍组 (饮水含 1g·L-1的氨基胍 )。在给药 15～ 17wk后进行与氧化应激相关的各项实验观察。结果　① 15～ 17wk的糖尿病大鼠与正常对照组相比 :肾指数显著增加 ,肾脏的抗氧化能力显著降低且氧化应激增强。②灯盏花素组与糖尿病组相比 :肾指数显著降低 ,总抗氧化能力和肾脏超氧化物歧化酶活性显著提高 ,脂质过氧化产物丙二醛显著降低。③氨基胍组与糖尿病组相比 :肾脏超氧化物歧化酶活性显著提高 ,肾脏的脂质过氧化产物丙二醛显著性降低 ,总抗氧化能力差异无显著性。结论　糖尿病大鼠与正常大鼠相比肾脏抗氧化能力降低且氧化应激增强 ,灯盏花素可显著提高糖尿病大鼠肾脏的抗氧化能力和降低氧化应激     

复方地黄醇提物对糖尿病大鼠早期视网膜病及肾病并发症的干预作用*

目的:研究复方地黄2种醇提取物对链脲佐菌素(STZ)诱导糖尿病大鼠的早期视网膜病变及糖尿病肾病的干预作用。方法:腹腔注射STZ 60 mg.kg-1建立糖尿病大鼠模型,4周后随机分组,5~8周3个治疗组分别每日给予氨基胍(100 mg.kg-1),复方地黄70%乙醇提取物(10 g.kg-1)及复方地黄95%乙醇提取物(10 g.kg-1)。8周后测定各组动物血清中血糖(G lu)、肌酐(Cr)和尿素氮(BUN)的含量,并测定肾组织中过氧化氢酶(CAT)活性、诱导型一氧化氮合成酶(iNOS)活性、一氧化氮(NO)和羟脯氨酸(HYP)含量;用RT-PCR测定视网膜PreproET-1和MMP-9 mRNA的表达。结果:与正常对照组比较,模型组大鼠血清Cr及BUN的含量以及肾脏组织iNOS活性、NO和HYP含量均显著升高,肾脏组织CAT活性显著降低,视网膜Prepro ET-1 mRNA表达量显著升高,MMP-9 mR-NA表达量显著降低。复方地黄70%和95%乙醇提取物组的血糖虽然无明显降低,但上述异常指标均明显逆转,与阳性对照组氨基胍接近。结论:复方地黄70%和95%乙醇提取物均能改善STZ诱导的糖尿病大鼠早期视网膜病变及糖尿病肾病发生,药效与AGEs受体拮抗剂氨基胍相当。     

银杏叶提取物对实验性2型糖尿病大鼠肾脏的保护作用

目的:探讨银杏叶提取物(EGB)对早期糖尿病肾病的影响。方法:选3~4月龄雄性Wistar大鼠,随机分为糖尿病组、银杏叶组和正常对照组。应用链脲佐菌素(STZ)制备大鼠糖尿病模型。银杏叶组腹腔注射银杏叶提取物注射液,用药10周后,测定肾组织匀浆丙二醛、一氧化氮、超氧化物歧化酶、一氧化氮合酶的活性。结果:与糖尿病组相比,银杏叶组大鼠肾组织内SOD活性明显升高,NOS活性、NO含量明显下降;糖尿病肾组织光镜及透射电镜观察到肾脏出现明显的病理改变;银杏叶组大鼠肾脏病理改变较轻。结论:银杏叶总黄酮可改善血管内皮细胞源性NO合成和释放,能有效清除体内自由基和提高抗氧化能力。     

桑枝提取物对糖尿病大鼠的作用研究

目的研究桑枝提取物对糖尿病大鼠血糖及氧化应激的影响。方法采用四氧嘧啶复制糖尿病大鼠模型,灌胃给药4周后测定空腹血糖（FPG）、血清超氧化物歧化酶（SOD）活性、血清及肝脏中丙二醛（MDA）水平。结果桑枝提取物能够明显降低糖尿病大鼠血糖、提高血清SOD活性、降低MDA的含量,与对照组相比,差异有统计学意义（P〈0.05）。结论桑枝提取物可降低糖尿病大鼠血糖并能够提高其抗氧化能力。     

氨基胍对糖尿病大鼠视网膜一氧化氮和一氧化氮合酶的影响

目的:探讨氨基胍对糖尿病大鼠视网膜一氧化氮和一氧化氮合酶的影响.方法:选择健康成年Wistar大鼠36只,体重180～220g,随机分成正常组、模型组、治疗组,模型组和治疗组大鼠尾静脉注射四氧嘧啶(50mg/kg)造成糖尿病模型,治疗组腹腔注射氨基胍(80mg/kg.d)治疗10周,各组分别测血糖、视网膜NO、iNOS、总NO.结果:治疗组iNOS含量明显低于模型组,而NO、总NO含量比模型组高.结论:氨基胍对糖尿病大鼠视网膜病变具有良好的保护作用,这可能与其可抑制非酶蛋白质糖基化和iNOS活性等有关.     

氨基胍、牛蒡对糖尿病大鼠肾脏组织非酶糖化和细胞凋亡的影响

目的 探讨非酶糖化与糖尿病肾病(DN)的关系,以及非酶糖化抑制剂氨基胍和具有非酶糖化抑制作用的牛蒡干预治疗对DN的治疗作用.方法 雄性Wistar大鼠40只,随机分为4组,正常对照组、糖尿病组、糖尿病氨基胍(100mg·kg-1·d-1)治疗组(氨基胍组)、糖尿病牛蒡(150mg·kg-1·d-1)治疗组(牛蒡组),除正常对照组外,其他3组腹腔注射链脲佐菌素诱发糖尿病.16周后,处死大鼠,分离肾脏,测定组织非酶糖化,取部分肾脏皮质电镜观察细胞凋亡的形态学变化.结果 治疗16周结束时,糖尿病各组大鼠体质量低于正常对照组(P<0.01),糖尿病各组间体质量比较差异无统计学意义(P>0.05);血糖水平均高于正常对照组(P＜0.01);氨基胍组和牛蒡组血糖与治疗前比较,差异无统计学意义(P>0.05);糖尿病组大鼠肾组织肾皮质糖化终产物(AGEs)含量高于正常对照组(P<0.01),氨基胍组和牛蒡组AGEs含量低于糖尿病组(P<0.01),氨基胍组和牛蒡组比较差异无统计学意义(P>0.05).透射电镜下见糖尿病组肾脏肾小管上皮细胞呈典型的凋亡形态学改变,氨基胍组和牛蒡组大鼠肾组织细胞凋亡改变明显减轻.糖尿病组肾小球基底膜增厚,系膜区域扩大.结论 非酶糖化抑制剂氨基胍、牛蒡通过抑制非酶糖化、抑制细胞凋亡,明显改善糖尿病大鼠肾脏结构与功能,延缓DN的发展.     

沙棘总黄酮对糖尿病心脏病大鼠AGEs的影响

目的：研究沙棘总黄酮对糖尿痛心脏病大鼠AGEs的影响。方法：采用腹腔注射链脲佐菌素的方法造成大白鼠糖尿痛心脏病模型。将大白鼠随机分4组，对照组、模型糖尿病组、糖尿病加氨基胍组、糖尿病加沙棘总黄酮组，给药12周后处死取血、心脏，测定血糖，血清及心脏中的AGEs含量。结果：血糖、血清及心脏中AGEs含量，模型组与用药组差异显著。结论：沙棘总黄酮对糖尿痛心脏病大鼠AGEs具有明显抑制作用。     

贝那普利和维生素E对糖尿病肾病大鼠氧化应激的影响

目的:观察贝那普利及维生素E对糖尿病肾病(DN)大鼠肾脏一氧化氮合成酶(NOS)活性、一氧化氮(NO),超氧化物歧化酶(SOD)、丙二醛(MDA)含量及血清总抗氧化能力的影响,探讨两者在DN中的可能作用机制。方法:注射链佐脲菌素制作DN模型,分为4组,A组:正常对照组;B组:糖尿病肾痛模型组;C组:贝那普利治疗组;D组:贝那普利 维生素E治疗组。于第12周检测24h尿蛋白定量(TP)、血清胱蛋白酶抑制剂C(Cys C)、糖化血红蛋白(HbAlc),血清总抗氧化能力,肾组织NOS、NO、SOD、MDA含量。结果:与A组相比,B组TP、CysC、HbAlc、肾组织血糖、MDA明显升高(P<0.01),而血清总抗氧化能力,肾组织NO、NOS、SOD明显降低(P<0.01)。与B组相比,C组TP、CysC、HbAlc、肾组织血糖显著降低(P<0.01),MDA亦下降(P<0.05),而总抗氧化能力增强(P<0.05),SOD升高(P<0.01)。与C组相比,D组TP、肾组织血糖下降更加显著(P<0.01),MDA下降(P<0.05),而NO、NOS、SOD明显升高(P<0.05或P<0.01),总抗氧化能力增强(P<0.05)。结论:贝那普利能降低TP、HbAlc、肾组织血糖、MDA,增加NO、NOS、SOD,维生素E可增加血清总抗氧化能力,清除自由基而有肾保护作用。两者对治疗DN氧化应激有协同作用。     

Cardioprotective effect of Urena lobataleaves extract on diabetic rats

OBJECTIVE To know cardioprotective effect of U.lobataleaves extract on diabetic rat.METHODS This study uses control group post test only with male sprague dawley rats.Diabetic rats was induced by high fructose diet(HFD)and single dose streptozotocin 25mg·kg-1 bw intra peritoneal.The rat was administrated orally with water extract of U.lobataleaves in concentrations of 250,500 and 1000mg·kg-1 bw for 4 weeks.After scarifying,heart organ were collected and then superoxyde dismutase(SOD)heart level,malondialdehyda(MDA)and tumor necrosis factor-alpha(TNF-α)were examined.The data was analyzed using ANOVA test continued with LSD test(P<0.05).RESULTS The oral administration of U.lobataleaves extract 250,500,and 1000mg·kg-1 bw were able to increase SOD heart level about 40%,50% and 70% respectively compared to diabetic group(P<0.05),while the MDA heart level was decreased by 60%,90% and 110%(P<0.05)respectively.The supplementation of water extract from U.lobatain dose of 250,500 and 1000mg·kg-1 bw were also decrease TNF-αheart level approximately 20%,40% and 60% compared to control group(P<0.05).In diabetic groups,SOD heart level was decreased compared to normal group(P<0.05)while the MDA and TNF-αwere increased(P<0.05).CONCLUSION U.lobataleaves extract acts as cardioprotector on diabetic rats by increasing of SOD heart level,decreasing of MDA heart level and TNF-α.This effect may be related to active compounds that act as an antioxidant and anti-inflammatory in U.lobata extract.     

Potency of Urena lobataleaves extract on the inhibition of vasculopathy on diabetic rats

OBJECTIVE To know the potency of Urena lobataleaves extract on the vasculopathy inhibition of diabetic rats.METHODS This study used control group post test only with male Sprague dawley rats.Diabetic rats were induced by high fructose diet(HFD)and single dose streptozotocin 25mg·kg-1 bw intra peritoneal.The rat was administrated orally with water extract of U.lobataleaves in dose of 250,500and1000mg·kg-1 bw for 4 weeks.After scarifying,blood sample were collected and then superoxyde dismutase(SOD)serum level,malondialdehyda(MDA),tumor necrosis factor-alpha(TNF-α)and circulating endothelial cells(CECs)were examined.The data was analyzed using ANOVA test continued with LSD test(P<0.05).RESULTS The oral administration of U.lobataleaves extract 250,500 and 1000mg·kg-1 bw were able to increase SOD serum level about 40%,70% and 100%respectively compared to diabetic group(P<0.05),while the MDA serum level was decreased by 20%,40%and 50%(P<0.05)respectively.The supplementation of water extract from U.lobatain dose of 250,500 and 1000mg·kg-1 bw also decrease TNF-αserum level approximately 40%,60% and 80% compared to control group(P<0.05),whereas the CECs level was decreased by 30%,50% and 70%(P<0.05)respectively.In diabetic groups,SOD serum level was decreased compared to normal group(P<0.05)while the MDA,TNF-αand CECs were increased(P<0.05).CONCLUSION U.lobata leaves extract could inhibit vasculopathy on diabetic rats by increasing of SOD serum level,decreasing of MDA serum level,TNF-αand CECs.This potency may be related to active substances which act as an anti-inflammatory and antioxidant in U.lobata extract.     

吡格列酮对糖尿病大鼠肾脏的保护作用及其机制探讨

目的观察吡格列酮对糖尿病大鼠肾脏的保护作用并探讨其机制。方法采用链脲佐菌素(STZ)诱导糖尿病模型。24只大鼠随机分为正常对照组(NC组)、糖尿病组(DM组)、吡格列酮干预组(3mg·kg-1·d-1,DT组),每组8只。12周末,测定各组相关生化指标。运用比色法检测肾皮质中丙二醛(MDA)的含量、铜锌超氧化物歧化酶(Cu-ZnSOD)及过氧化氢酶(CAT)的活性。同时留取肾标本作电镜观察。结果与NC组相比,DM组和DT组血糖、胆固醇、甘油三酯、血清胰岛素、C肽、尿素氮、血肌酐、肾重/体重和24h尿蛋白定量差异有统计学意义。DM组与NC组比较,肾皮质Cu-ZnSOD、CAT活性明显降低(P<0.01),MDA含量明显增加(P<0.01)。DT组与DM组比较,血糖、胆固醇、甘油三酯、血清胰岛素、C肽、尿素氮、血肌酐差异无统计学意义(P>0.05),肾重/体重和24h尿蛋白定量明显降低(P<0.05);肾皮质CAT和Cu-ZnSOD活性增加(P<0.05),肾皮质MDA含量降低(P<0.05)。结论吡格列酮对糖尿病大鼠肾脏有保护作用且此作用不依赖其降糖、降脂机制,可能与吡格列酮的抗氧化机制有关。     

Potency of Urena lobataleaves extract on the inhibition of hepatic complication on diabetic rats

OBJECTIVE To investigate the potency of Urena lobata leaves extract on the inhibition of hepatic complication on diabetic rats.METHODS This study uses control group post test only with male Sprague dawley rats.Diabetic rats was induced by high fructose diet(HFD)and single dose streptozotocin 25mg·kg-1 bw intra peritoneal.The rat was administrated orally with water extract of U.lobataleaves in concentrations of 250,500 and 1000mg·kg-1 bw for 4 weeks.After scarifying,liver organ and blood were collected and then superoxyde dismutase(SOD)hepar level,malondialdehyda(MDA),tumor necrosis factor-alpha(TNF-α),serum glutamic oxaloacetic transaminase(SGOT)and serum glutamic piruvic transaminase(SGPT)were examined.The data was analyzed using ANOVA test continued with LSD test(P<0,05).RESULTS The oral administration of U.lobataleaves extract 250,500 and 1000mg·kg-1 bw were able to increase SOD hepar level about 90%,100% and 120%respectively compared to diabetic group(P<0.05),while the MDA hepar level was decreased by 40%,50% and 70% respectively(P<0.05),whereas the TNF-αhepar level was decreased by 30%,50% and 70%respectively(P<0.05).The supplementation of water extract from U.lobatain dose of 250,500 and 1000mg·kg-1 bw decrease SGOT level approximately10%,30% and 50% compared to control group(P<0.05),while the SGPT level was decreased by 10%,20% and 40%respectively(P<0.05).In diabetic groups,SOD heparlevel was decreased compared to normal group(P<0.05)whereas the MDA and TNF-αwere increased(P<0.05).Meanwhile SGOT level and SGPT were increased in diabetic group(P<0.05).CONCLUSION U.lobataleaves extract could inhibit hepatic complication on diabetic rats by increasing of SOD hepar level,decreasing of MDA hepar level,TNF-α,SGOT and SGPT.This effect may be related to active compounds that act as an antioxidant and anti-inflammatory in U.lobata extract.     

Effect of Urena lobataleaves extract on the inhibition of nephropathy diabetic complication

OBJECTIVE To investigate the effect of Urena lobataleaves extract on the inhibition of nephropathy diabetic complication.METHODS This study uses control group post test only with male Sprague dawley rats.Diabetic rats was induced by high fructose diet(HFD)and single dose streptozotocin 25mg·kg-1 bw intra peritoneal.The rat was administrated orally with water extract of U.lobataleaves in concentrations of 250,500 and 1000mg·kg-1 bw for 4 weeks.After scarifying,kidney organ were collected and then superoxyde dismutase(SOD)kidney level,malondialdehyda(MDA)and tumor necrosis factor-alpha(TNF-α)were examined.The data was analyzed using ANOVA test continued with LSD test(P<0.05).RESULTS The oral administration of U.lobataleaves extract 250,500 and 1000mg·kg-1 bw were able to increase SOD kidney level about 30%,60% and 90% respectively compared to diabetic group(P<0.05),while the MDA kidney level was decreased by 30%,60% and 70%(P<0.05)respectively.The supplementation of water extract from U.lobatain dose of 250,500 and 1000mg·kg-1 bw were also decrease TNF-αkidney level approximately 30%,40% and 60% compared to control group(P<0.05).In diabetic groups,SOD kidney level was decreased compared to normal group(P<0.05)while the MDA and TNF-αwere increased(P<0.05).CONCLUSION U.lobata leaves extract could inhibit nephropathy diabetic complication by increasing of SOD kidney level,decreasing of MDA kidney level,and TNF-α.This effect may be related to active compounds that act as an antioxidant and anti-inflammatory in U.lobata extract.     

氧化应激在糖尿病肾病中的意义及吡格列酮干预研究

目的观察糖尿病大鼠肾脏组织中氧化应激水平,探讨氧化应激在糖尿病肾病中的作用及吡格列酮干预效果。方法采用链脲佐菌素(STZ)诱导糖尿病模型。24只大鼠随机分为正常对照组(NC组)、糖尿病组(DM组)、吡格列酮干预组(3mg·kg-1.d-1,DT组),每组8只。12周末,测定各组相关生化指标。运用比色法检测肾皮质中丙二醛(MDA)的含量、铜锌超氧化物歧化酶(Cu-ZnSOD)及过氧化氢酶(CAT)的活性。结果与NC组相比,DM组和DT组血糖、胆固醇、甘油三酯、尿素氮、血肌酐、肾质量/体质量和尿蛋白定量(24h)值差异有统计学意义。DM组与NC组比较,肾皮质Cu-ZnSOD、CAT活性明显降低(P<0.01),MDA含量明显增加(P<0.01)。DT组与DM组比较,血糖、胆固醇、甘油三酯、尿素氮、血肌酐值差异无统计学意义(P>0.05),肾质量/体质量和尿蛋白定量(24h)明显降低(P<0.05);肾皮质CAT和Cu-ZnSOD活性增加(P<0.05),肾皮质MDA含量降低(P<0.05)。结论糖尿病大鼠肾脏组织中氧化应激水平升高,在糖尿病肾病发病机制中起重要作用。吡格列酮可能通过抗氧化作用改善糖尿病大鼠肾脏损害。     

糖尿病并发症相关性氧化应激的实验研究

目的链脲佐菌素(STZ)诱导大鼠1型糖尿病模型的基础上,探讨糖尿病氧化应激指标的变化。方法采用一次性腹腔注射STZ的方法,监测不同时点大鼠的空腹血糖、体质量及血浆中的丙二醛(MDA)和超氧化物歧化酶(SOD)等指标,并对结果进行统计学处理。结果大鼠注射STZ 72h后血糖值达到成模标准,并逐渐出现糖尿病表现,观察7周,始终满足成模标准,未见转复。DM组大鼠肾脏及肝脏肥大指数较CON组显著增加。氧化应激相关指标测定表明,较对照组相比,实验组大鼠血浆中脂质过氧化产物MDA水平显著升高,而SOD水平显著下降。结论本实验Ⅰ型糖尿病模型大鼠造模成功且模型稳定,氧化应激指标改变。     

褪黑素对实验性糖尿病肾脏氧化应激的影响

［摘要］目的观察褪黑素对糖尿病大鼠肾脏氧化应激和过氧亚硝基阴离子（ONOO–）特异性标志物硝基酪氨酸（NT）表达的影响。方法实验动物分为糖尿病肾病组（DN组）、糖尿病褪黑素处理组（DM组）、正常对照组（NC组），8周后比较各组体重、血糖、血胆固醇、三酰甘油及肾脏丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH Px）含量，免疫组化观察各组大鼠肾组织中NT的表达。结果和DN组比较，DM组大鼠血胆固醇、三酰甘油及肾脏MDA水平显著降低（P＜0.05），抗氧化酶SOD、GSH Px活性升高（P＜0.05），NT表达明显降低。结论褪黑素可显著提高糖尿病大鼠肾脏的抗氧化能力和降低氧化应激，对糖尿病大鼠肾脏具有保护作用。