Dose-dependent effect in the inhibition of oxidative stress and anticlastogenic potential of ginger in STZ induced diabetic rats

Ginger is an important medicinal herb has numerous bioactive components and is used in the management, control and/or treatment of diseases including diabetes mellitus. The present study was undertaken to see the dose–response effect of ginger and evaluate the possible protective effects of dietary ginger on oxidative stress and genotoxicity induced by streptozotocin (STZ) diabetic rats. Inbred male Wistar/NIN rats of 8–9 weeks old were treated with 30 mg/kg of STZ. Rats were divided into different groups of control, diabetic non-treated, and diabetic treated with ginger powder at 0.5%, 1% and 5% respectively. After feeding for a month, blood and tissues were collected to see the effect of ginger on antioxidant status, DNA damage and bone marrow genotoxicity. In this study ginger exerted a protective effect against STZ-induced diabetes by modulating antioxidant enzymes and glutathione and down regulating lipid and protein oxidation and inhibition in genotoxicity in a dose–response manner.     

Alterations in antioxidant enzyme activities and oxidative damage in alcoholic rat tissues: Protective role of Thespesia populnea

Recent advances in our understanding of the pathogenesis of alcohol-induced hepato-renal injury and the development of new approaches to its treatment have been reported in various works. This study involves alcohol-induced oxidative stress linked to the metabolism of ethanol involving both mitochondrial and peroxisomal fractions of liver and kidney. Alcohol treatment resulted in the depletion of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), Glutathione-S-Transferase (GST) activities, and reduced glutathione (GSH) content, higher level of malondialdehyde (MDA) and lower levels of protein carbonyls (PC) causing malfunction of hepatic and renal tissues, when compared to control rats. Thespesia populnea (TP) leaf extracts, administered to chronic alcohol ingested rats, were envisaged to possess significant antioxidant defence properties and help in the recovery of tissues from alcohol-induced oxidative damage. The results showed that degenerative changes in hepatic and renal cells of alcoholic groups were minimized by the administration of TP leaf extracts as also revealed by histopathological examination. The current findings indicate that treatment with TP extracts reduces alcohol-induced oxidative stress, thereby protecting the hepatic and renal tissue from alcohol-induced damage.     

血管紧张素转移酶2(ACE2)在糖尿病致大鼠肝脏氧化应激损伤中的作用及机制分析

目的：探讨血管紧张素转移酶2(ACE2)在糖尿病致大鼠肝脏氧化应激损伤中的作用和可能机制。方法：24只健康雄性SD大鼠,随机选取8只作为正常对照组,剩余16只按60mg/kg(以体质量计)一次性腹腔注射STZ溶液制备糖尿病肝脏氧化应激损伤模型,成模后大鼠随机分为2组：糖尿病组和胰岛素治疗组(优泌林 3.7×10-8mol/d),30d后宰杀,取血液和肝脏组织等进行各指标测定：1)测定血清中AGEs含量;2)测定肝脏组织中过氧化氢(H2O2)、丙二醛(MDA)的含量及过氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力;3) 肝脏组织中血管紧张素Ⅱ(AngⅡ)、血管紧张素1-7(Ang1-7)的含量,ACE和ACE2酶活力的测定。结果：1)正常对照组大鼠空腹血糖均值为(5.39±0.30)mmol/L,糖尿病组大鼠空腹血糖均值持续维持在(28.24±2.51)mmol/L(远高于高水平高血糖状态指标值16.6mmol/L),胰岛素治疗后大鼠空腹血糖水平明显下降至(11.18±1.26)mmol/L,显著高于正常对照组(P＜0.05),但同时显著低于糖尿病组(P＜0.05),且治疗后期已经低于10.0mmol/L并逐渐接近正常对照组。糖尿病组大鼠血清中的AGEs的含量显著高于正常对照组和胰岛素治疗组(P＜0.05)。2) 与正常对照组和胰岛素治疗组相比,糖尿病组大鼠肝脏组织中的MDA和H2O2极显著增多(P＜0.01),SOD和GSH-Px的活力极显著降低(P＜0.01); AngⅡ的含量显著增多(P＜0.01),Ang1-7含量显著降低(P＜0.01),ACE的酶活力显著升高(P＜0.01),而ACE2的酶活力显著降低(P＜0.01)。 结论： 糖尿病时大鼠肝脏组织局部AngⅡ显著升高,ACE2活力下降,肝脏组织处于氧化应激状态。胰岛素治疗后,ACE2活力增高,致AngⅡ降解,AngⅡ含量显著降低,肝脏的氧化应激减缓,提示ACE2对糖尿病大鼠肝脏氧化应激损伤有一定的保护作用,其机理可能与对AngⅡ降解作用增强有关。     

虾青素对D-半乳糖致衰老大鼠肾脏和心脏组织氧化损伤的修复作用

通过建立D-半乳糖致衰老模型,研究虾青素对衰老大鼠肾脏和心脏组织氧化损伤的修复作用。实验设空白组、模型组、虾青素低、中、高（5、10、15 mg/kg）剂量组和二甲双胍（MET）阳性对照组。检测肾脏和心脏系数,肾脏和心脏组织中过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活力和丙二醛（MDA）含量等指标,观测苏木精-伊红染色（HE）病理组织切片。结果表明,与模型组相比,虾青素能改善D-半乳糖造成的肾脏和心脏系数下降,减少肾脏和心脏组织中MDA含量,并显著提高抗氧化物酶（SOD、CAT、GSH-Px）活力。其中,高剂量组（15 mg/kg）大鼠肾脏和心脏中MDA含量显著降低了70.48%和38.02%（p<0.01）,对于SOD、CAT和GSH-Px活力,肾脏中分别提高了37.22%、43.73%和52.01%（p<0.01）,心脏中分别提高了85.47%、52.08%和64.77%（p<0.01）。病理切片显示虾青素能有效缓解肾脏和心脏组织的氧化损伤。以上结果全面揭示虾青素能通过减轻氧化应激来抑制衰老大鼠肾脏和心脏组织的损伤,其机制可能与抗氧化有关。     

咖啡酸苯乙酯对糖尿病大鼠胰脏的保护作用

研究了咖啡酸苯乙酯(caffeic acid phenethylester,CAPE)对2型糖尿病大鼠胰脏的保护作用及其作用机制。将30只雄性SD大鼠随机分为3组,即空白组,损伤组,保护组。以高脂高糖饲料喂养联用链脲佐菌素(Streptozocin,STZ)诱导建立2型糖尿病大鼠模型,保护组给予CAPE保护,建模成功后,测定其胰脏中丙二醛(Malondialdehyde,MDA)、蛋白羰基化(Protein carbonylation,PCO)、一氧化氮(Nitric oxide,NO)、谷胱甘肽(Glutathione,GSH)的含量及超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶(Catalase,CAT)的活性。实验结果显示,损伤组中MDA、PCO、NO含量明显升高,分别为空白组的2.52倍、1.64倍以及2.78倍,而保护组MDA、PCO、NO的含量较损伤组减少,仅为损伤组的47%、69%以及47%。说明糖尿病能够导致胰脏的氧化应激,破坏其结构与功能,给予CAPE保护可以使MDA、PCO、NO的含量降低,减少对胰脏的破坏;机体中SOD、CAT、GSH等抗氧化物质活性因机体应对氧化应激产生的过量自由基而降低,CAPE可增强SOD、CAT、GSH的活性,加快清除体内自由基的速度,对糖尿病胰脏有一定的保护作用。     

Compare Activities on Regulating Lipid-Metabolism and Reducing Oxidative Stress of Diabetic Rats of Tremella Aurantialba Broth's Extract (TBE) with Its Mycelia Polysaccharides (TMP)

ABSTRACT:  Abnormal lipid-metabolism and elevated oxidative stress are the familiar complications of diabetic mellitus. Regulated lipid-metabolism and decreased oxidative stress have become the key indices to cure diabetic complications. The activities of broth extract (TBE) and mycelia polysaccharides (TMP) of Tremella aurantialba , which is one of the best-known multipurpose medicinal fungi in China, were studied using alloxan-induced diabetic rats. TBE contains saponins, while TMP contains polysaccharides. Both TBE and TMP could reduce the blood glucose levels of diabetic rats; TBE had stronger abilities to reduce the levels of total cholesterol and total triglyceride in serum, those of malondialdehyde, and enhance the activities of superoxide dismutase and glutathione reductase in different tissues of diabetic rats ( P  < 0.01). TBE had slightly stronger abilities to enhance the total antioxidant capability, catalase, and glutathione peroxidase in different tissues of diabetic rats, but no significant difference was found between TBE and TMP groups. All these results indicated that TBE was more capable of regulating lipid-metabolism and decreasing oxidative stress.     

Protective role of Punica granatum (pomegranate) peel and seed oil extracts on diethylnitrosamine and phenobarbital-induced hepatic injury in male rats

The present study is an attempt to reveal the protective role of Punica granatum peel and seed oil extracts against diethylnitrosamine (DEN) and phenobarbital (PB) induced hepatic injury in rats. DEN administration increased the levels of malondialdehyde (MDA), DNA fragmentation, caspase-3 and glutathione reductase (GSR) activities, while the level of reduced glutathione (GSH) and the activities of superoxide dismutase (SOD), glutathione S-transferase (GST) and total glutathione peroxidase (t-GPx) were decreased compared with the control. Treatment with peel and seed oil extracts pre, during and post DEN administration improved liver functions, decreased the levels of MDA, DNA fragmentation, caspase-3 and GSR activities with an elevation in levels of GSH, SOD, GST and t-GPx activities. This indicates that these extracts reduced the oxidative stress and apoptosis induced by DEN. Also the effect of administration of PE and SOE separately for a long time (23 weeks) on healthy rats was studied.     

β-Casomorphin-7 cause decreasing in oxidative stress and inhibiting NF-κB-iNOS-NO signal pathway in pancreas of diabetes rats

β-Casomorphin-7 (β-CM-7) is a milk biological active peptide. The present study is aimed to investigate the protective effects of β-CM-7, against oxidative stress in pancreas of streptozotocin-induced diabetic rats by assaying malondialdehyde (MDA), nitric oxide (NO) level, the activity of enzymatic antioxidants such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), and NF-κB, inducible nitric oxide synthase (iNOS) gene expression. A significant increase in the level of oxidative stress was observed in pancreas of the diabetic rats when compared to control rats. After 15 d oral administration of β-CM-7 (7.5 × 10(-8) mol/d), the pancreas MDA level was markedly reduced. Oral administration of β-CM-7 to diabetic rats showed an obviously increase in the activity of catalase in pancreas, oral administration of β-CM-7 to the diabetic group of rats also showed a reduction of NF-κB and iNOS gene expression in pancreas. The elevated pancreas NO level was markedly reduced by the oral administration of β-CM-7. Thus, the results of the present study suggest that β-CM-7 may cause protective effects such as pronounced decreasing in oxidative stress and inhibiting NF-κB-iNOS-NO signal pathway in pancreas of diabetes rats.     

韩国产芝麻酱油对AAPH诱发LLC-PK1细胞氧化应激的保护作用

以芝麻酿造酱油乙醇提取物(ethanol extract sesame sauce,SSE)为研究对象,探讨其对1 mmol/L 2,2’-偶氮二异丁基脒二盐酸盐(2,2’-azobis(2-methylpropionamidine)dihydrochloride,AAPH)引发的LLC-PK1猪肾近曲小管上皮细胞氧化应激损伤的保护作用。方法:LLC-PK1细胞与不同质量浓度(10~100μg/m L)的SSE预先共同培养24 h后,用含AAPH的DMEM培养液继续培养4 h建立细胞损伤模型。细胞存活率用四甲基偶氮唑蓝法检测,细胞内丙二醛(malondialdehyde,MDA)含量和总活性氧簇(reactive oxygen species,ROS)水平分别以硫代巴比妥酸比色法和2’,7’-二氢二氯荧光黄双乙酸钠探针法测定。细胞内过氧化氢酶(catalase,CAT)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化酶(glutathione peroxidase,GSH-Px)、谷胱甘肽巯基转移酶(glutathione S-transferase,GST)、γ-谷氨酰半胱氨酸合成酶(γ-glutamylcysteine synthetase,γ-GCS)活力和谷胱甘肽(glutathione,GSH)含量按试剂盒说明书以比色法测定。结果表明,SSE预处理可以提高受损细胞存活率,降低细胞内总ROS水平和MDA含量。同时,SSE还能提高受损细胞内抗氧化酶(CAT、SOD、GSH-Px)及γ-GCS活力并提高细胞内GSH含量。实时荧光定量聚合酶链式反应分析也提示SSE能上调细胞内抗氧化物酶(CAT、SOD和GSH-Px)的m RNA表达量。此外,SSE可以通过提高细胞内源性抗氧化系统能力来降低细胞内MDA和ROS水平,并由此缓解AAPH对LLC-PK1细胞所造成的氧化应激损伤。     

葡萄籽原花青素对顺铂所致大鼠肾脏氧化损伤和线粒体损伤的防护作用

本文研究了葡萄籽原花青素(GSPE)对顺铂(CDDP)所致大鼠肾脏氧化应激损伤和线粒体损伤的防护作用。实验大鼠分为正常对照组、CDDP模型组、GSPE(400 mg/kg)组、CDDP+GSPE(200 mg/kg)组和CDDP+GSPE(400 mg/kg)组。各组分别以蒸馏水和相应剂量GSPE对大鼠连续灌胃15 d。灌胃10 d后CDDP组和CDDP+GSPE组一次性腹腔注射CDDP(8.0 mg/kg),其余注射等量生理盐水。检测血清尿素氮(BUN)和肌酐(Cr E)、肾脏指数、肾皮质抗氧化和碳水化合物代谢酶指标,光镜观察肾组织结构。GSPE预处理的大鼠在注射CDDP后与模型组相比肾脏指数、BUN、Cr E含量显著降低,肾皮质还原型谷胱甘肽(GSH)、丙二醛(MDA)含量、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和苹果酸脱氢酶(MDH)、己糖激酶(HK)活力的变化明显改善。病理切片显示,GSPE预处理可减轻顺铂引起的肾小球萎缩等病理损伤。提示GSPE对CDDP所致大鼠氧化应激损伤和线粒体损伤具有明显的防护作用。     

ANTIOXIDANT POTENTIAL OF ORAL FEEDING OF CYNODON DACTYLON EXTRACT ON DIABETES-INDUCED OXIDATIVE STRESS

The present study is an extension of our previous research work and it deals with the scientific evaluation of antioxidant potential of the aqueous extract of Cynodon dactylon on diabetes-induced oxidative stress of diabetic rats. The most effective dose of 500 mg/kg of extract was given orally to diabetic rats for 30 days. Different oxidative stress parameters were analyzed in various tissues of control and treated diabetic rats. The observed elevated level of LPO comes down significantly ( P <  0.05), and decreased activities of antioxidant enzymes such as CAT, SOD, GPx and GST got increased ( P <  0.05) significantly in diabetic rats on extract treatment. The flavonoids present in the aqueous extract of this plant might be responsible for its marked antioxidant efficacy at tissue level in STZ-induced diabetic rats.

PRACTICAL APPLICATIONS

The Cynodon dactylon has been shown to possess varied medicinal properties. The aqueous extract of the rhizome is used as anti-inflammatory, diuretic, antiemetic, antidiabetic and blood-purifying agent. Recently, it has been reported by our research group that the extract of C. dactylon has hypoglycemic as well as antidiabetic potential. The present communication is an endeavor in the direction of evaluating its in vivo antioxidant effect in STZ-induced diabetic rats so that it can be used as a value-added agent for managing diabetes as well as oxidative stress associated with it.     

佛手山药多糖对2型糖尿病大鼠糖脂代谢及氧化应激的影响

目的:探讨佛手山药多糖对实验性2型糖尿病大鼠糖脂代谢及体内氧化应激的影响。方法:SD大鼠高脂饲料喂养,结合小剂量腹腔注射链脲佐菌素40 mg/kg建立糖尿病大鼠模型,成模大鼠随机分为模型组、阳性对照组(二甲双胍150 mg/(kg·d))和佛手山药多糖组(400 mg/(kg·d)),并设正常组。观察给药期间各组体质量及血糖变化,给药6周后摘眼球取血,检测甘油三酯(triacylglyceride,TG)、胆固醇(total cholesterol,TC)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)、高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)、丙二醛(malonaldehyde,MDA)、一氧化氮(NO)含量及超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶(catalase,CAT)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活力,并解剖称取新鲜肝脏,测定肝糖原含量。结果:与模型组比较,佛手山药多糖能有效缓解糖尿病大鼠的症状,能明显降低实验性2型糖尿病大鼠空腹血糖水平(P0.05),对TC和LDL-C含量有极显著的降低作用(P0.01),对TG含量有显著降低作用(P0.05),能显著增加SOD和CAT的活力,而对肝糖原,HDL-C、MDA、NO含量及GSH-Px的活力无显著影响。结论:佛手山药多糖对实验性2型糖尿病大鼠有降低血糖作用,对血脂代谢紊乱有一定的调节作用,其降糖和降脂的具体机制可能与提高机体SOD、CAT活性相关。     

云南苦茶提取物抗氧化应激保护镉致糖尿病肾病小鼠的作用

此研究旨在评估云南苦茶提取物1,3,4,9-四甲基尿酸(1,3,4,9-tetramethyl uric acid, TC)对糖尿病肾病小鼠的氧化应激的调节潜力。实验采用喂养高脂高糖饲料,腹腔注射氯化镉(CdCl_2)12周建立糖尿病肾病动物模型,灌胃TC 28 d,评估其血清生化指标的变化;通过观察肾丙二醛(MDA)、脂质过氧化产物(LOOH)、蛋白羰基化(PCO)含量等氧化及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、还原性谷胱甘肽(GSH)等非酶抗氧化剂活性的变化,研究镉对肾脏的氧化损伤程度及四甲基尿酸的作用效果。实验结果显示,损伤组血清中的TG、ALT、LDL-C水平上调明显,分别为空白组的1.88倍、2.39倍、以及2.86倍;组织中的氧化指标MDA、PCO、NO显著升高,分别为空白组的1.51、3.88以及2.03倍;抗氧化指标CAT、SOD、GSH在损伤组有明显的下调,仅为空白组的68.75%、77.59%、80.95%;给予TC保护药后,血清指标水平较损伤组减少,仅为损伤组的68.09%、49.09%、45.65%;其氧化指标含量较损伤组减少,仅为损伤组的82.14%、74.19%、64.94%;抗氧化水平与损伤组相比明显升高,分别为损伤组的1.41、1.20及1.12倍。说明镉致糖尿病肾病(Diabetic Nephropathy, DN)小鼠机体内的氧化和抗氧化之间的平衡,进而导致氧化压力的增加;TC通过提高抗氧化酶的活性,增强抗氧化系统的抗氧化能力,通过抗氧化应激反应和抗炎作用共同保护肾脏。     

富硒蛹虫草多糖对鱼藤酮诱导伤害果蝇的保护功效

目的：探讨蛹虫草多糖和富硒蛹虫草多糖在鱼藤酮诱导的果蝇伤害模型中缓解氧化压力和神经毒保护功效。方法：采用鱼藤酮诱导伤害模型,评估饲喂含多糖与不含培养基果蝇的氧化指标和神经伤害。分别测定丙二醛(MDA)、蛋白质羧基化(PC)、谷胱甘肽(GSH和GSSG)、超氧化物歧化酶(SOD)和谷胱甘肽过-S-转移酶(GST)指标;同时测定逆重力爬行、乙酰胆碱酯酶(Ache)和丁酰胆碱酯酶(Bche)活力,对多糖的神经保护作用进行评估。结果：蛹虫草多糖和富硒蛹虫草多糖对降低果蝇体内氧化压力和神经伤害效果显著,相同质量浓度条件下富硒多糖保护效果好于普通蛹虫草多糖,其中1%富硒蛹虫草多糖溶液添加组逆重力爬行能力可回复到对照组的85%,部分氧化压力指标和酶活力也基本恢复至对照组水平。     

Hepatoprotective effects of lycopene against carbon tetrachloride-induced acute liver injury in rats

Lycopene, the major carotenoid in tomatoes, is a known antioxidant that may lower oxidative stress biomarkers by a mechanism that is not fully elucidated. The intoxication of rats with carbon tetrachloride (CCl₄) resulted in significant histological hepatic degradation accompanied by a marked increase in reactive oxygen species (ROS) and in the number of apoptotic cells. The induced oxidative stress in turn results in a significant elevation of lipid peroxidation and H₂O₂ generation, together with a decrease in the concentration of reduced glutathione (GSH) and a significant reduction in activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S transferase (GST). CCl₄-intoxicated rats, pre-treated with lycopene, showed strongly reduced cell damage and ROS generation. The level of markers for hepatic integrity in lycopene pre-treated rats was close to the controls in the absence of CCl₄ treatment, indicating the protective effect of lycopene pre-treatment. In the same way, lycopene pre-treated rats significantly increased SOD, CAT, GPx, GST activities and GSH level. In addition, we measured an increased lipoxygenase (LOX) activity in CCl₄-intoxicated rats. This activity was reduced in lycopene pre-treated rats to values close to those observed in the controls, suggesting a potential pharmacological application of this dietary carotenoid.     

红毛藻多糖对H2O2诱导的Caco-2细胞氧化损伤的保护作用

目的：研究红毛藻多糖（Bangia fusco-purpurea polysaccharide,BFP）对H2O2诱导的人结肠腺癌（Caco-2）细胞氧化应激损伤的保护作用。方法：构建过氧化氢（H2O2）诱导的Caco-2细胞氧化损伤模型,通过形态学观察和测定细胞裂解液中的抗氧化物水平及相关酶活力,评价BFP对Caco-2细胞氧化损伤的保护作用。结果：BFP可明显提高H2O2诱导氧化损伤的Caco-2细胞活力,降低细胞内活性氧生成水平,提高细胞内超氧化物歧化酶和过氧化氢酶活力以及还原型谷胱甘肽水平,减少丙二醛生成,并通过抑制Caspase-3和Caspase-9活性来改善氧化应激损伤引起的细胞凋亡。结论：BFP对H2O2诱导氧化应激损伤的Caco-2细胞具有保护作用,可通过增强细胞内源性抗氧化酶活力、提高非酶类抗氧化物水平和抑制细胞凋亡明显缓解H2O2诱导的Caco-2细胞氧化应激损伤。     

毛水苏多糖对糖尿病小鼠肾脏的保护作用

目的:探究毛水苏多糖（polysaccharides from Stachysbaicalensis, SBP）对糖尿病小鼠肾脏的保护作用。方法:采用高糖饲料喂养结合腹腔注射链脲佐菌素（STZ）诱导建立Ⅱ型糖尿病模型，连续灌胃28 d后，考察毛水苏多糖对糖尿病小鼠的体重、空腹血糖水平、肾脏指数、肾功能指标血肌酐（Scr）、尿素氮（BUN）、尿蛋白以及肾脏组织抗氧化指标超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）、丙二醛（MDA）活力与含量的影响，并进行肾脏组织病理学检测，采用qRT-PCR法测定肾脏组织中VCAM-1、IL-1β及IL-6的mRNA水平。结果:毛水苏多糖可明显减轻糖尿病症状，体重异常情况明显改善，空腹血糖值与肾脏指数明显降低。给药组小鼠肾功能指标Scr、BUN、尿蛋白含量显著降低（P<0.05），肾脏组织抗氧化指标SOD、GSH-Px、CAT含量与活力显著升高（P<0.05），抑制MDA的产生，对抑制肾脏肿胀和修复组织损伤具有良好的效果，有效降低肾脏组织中VCAM-1、IL-1β及IL-6的mRNA水平。结论:毛水苏多糖对于STZ诱导的糖尿病小鼠的肾脏保护作用可能与增强体内抗氧化能力、抑制机体的过氧化损伤、减少脂质过氧化合成以及调节炎症因子有关。     

四甲基尿酸对镉致小鼠肾脏损伤的保护作用

本文主要研究了镉对小鼠肾脏的损伤程度及不同剂量条件下的四甲基尿酸对肾脏的保护作用效果。实验中采用对小鼠腹腔注射氯化镉建立氧化损伤肾脏组织模型。雄性昆明小鼠50只,随机分为空白组、损伤组、及低、中、高不同剂量保护组,共五组,每组十只。空白组和模型组灌胃等体积生理盐水,保护组依次用10 mg/kg、20 mg/kg、40 mg/kg的四甲基尿酸混悬液进行灌胃,连续处理14 d后,颈椎脱臼法处死,取出肾脏组织,检测肾脏内脂质过氧化(MDA)、蛋白羰基化(PCO)、一氧化氮(NO)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、以及谷胱甘肽(GSH)的含量,观察肾病理变化。结果表明,与空白组相比,模型组肾脏组织中MDA、PCO、NO含量显著升高(p0.01),分别为空白组的1.89倍、3.32倍、1.64倍,而SOD、CAT、GSH活性显著降低(p0.01),分别为空白组的76.25%、77.12%、45.61%。与模型组相比,保护组均不同程度降低了肾脏组织中MDA、PCO、NO含量,提高了SOD、CAT、以及GSH活性,降低肾脏损伤的程度,病理切片显示,中剂量四甲基尿酸保护肾脏损伤效果最佳。由结果可知,四甲基尿酸对镉致小鼠肾脏损伤程度起到一定的保护作用,能有效降低肾脏氧化损伤程度并维持酶与抗氧化酶的平衡状态,其机制可能与抗氧化有关。     

Myricetin modulates streptozotocin–cadmium induced oxidative stress in long term experimental diabetic nephrotoxic rats

Oxidative stress plays a pivotal role in the development of diabetic nephropathy. The present study was aimed to evaluate the modulatory potential of myricetin on streptozotocin (STZ)–cadmium (Cd) induced oxidative stress in diabetic nephrotoxic rats. Diabetic nephrotoxicity was induced by single intraperitoneal injection of STZ at a dose of (40 mg/kg body weight (b/w)) and Cd as cadmium chloride (CdCl₂) (100 p.p.m.). Myricetin was administered to diabetic nephrotoxic rats by intraperitoneally at 1.0 mg/kg b/w for a period of 12 weeks to assess its effects on fasting plasma glucose, plasma insulin, total haemoglobin, glycosylated haemoglobin, lipid peroxidation products viz., thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), protein carbonyl content (PCO) and non-enzymatic antioxidants namely vitamins C and E and reduced glutathione (GSH) and also enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR). Improvement of antioxidant status in myricetin supplemented diabetic nephrotoxic rats revealed its cellular protective effect. Histopathology of liver and kidney confirmed the protective effects of myricetin in diabetic nephrotoxic rats. The outcome of this study concludes that myricetin could be therapeutic flavonol for regulating oxidative mechanism in STZ–Cd induced diabetic nephrotoxic rats.     

Asiatic acid prevents lipid peroxidation and improves antioxidant status in rats with streptozotocin-induced diabetes

Oxidative stress is a common pathogenesis of diabetes mellitus and asiatic acid (AA) plays an important role in ameliorating those difficulties. The present study was designed the protective effects of AA on altered lipid peroxidation products, enzymic and nonenzymic antioxidants in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in experimental rats by single dose STZ (40 mg/kg b.w.) injection. Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, lipid hydroperoxides, aspartate aminotransferase, alanine aminotransferase, bilirubin, creatine kinase, urea, uric acid, creatinine and decreased levels of plasma insulin. The activities of enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase and the levels of non-enzymatic antioxidants such as vitamin C, vitamin E and reduced glutathione were decreased in diabetic rats. Oral treatment with AA (20 mg/kg b.w.) showed near normalized levels of plasma glucose, insulin, lipid peroxidation products, enzymatic and nonenzymatic markers in diabetic rats. The results demonstrate that AA possesses potent antioxidant effect comparable with glibenclamide in improving antihyperglycemia and attenuating antioxidant status in diabetic rats.