帕宁方对帕金森病大鼠行为及氧化应激反应的影响

目的:观察帕宁方对帕金森病(PD)大鼠行为和氧化应激反应的影响.方法:运用6-羟基多巴胺(6-OHDA)立体定向脑内注射复制PD大鼠模型.将PD模型大鼠随机分为模型组、阳性对照组(美多巴0.125 g·kg-1)与帕宁方高、中、低剂量组(按生药量计为84,42,21 g·kg-1),另设同期正常组、假手术组.观察各组治疗前后大鼠旋转圈数,测定大鼠中脑黑质纹状体活性氧(ROS)、丙二醛(MDA)、谷胱甘肽(GSH)含量,谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)的活性.结果:与模型组比较,帕宁方高、中、低剂量组大鼠旋转圈数为(237.26±19.23),(246.71±37.06),(278.81±20.09)圈,活性氧含量为( 231.02±10.11),( 235.87±12.76),(247.93±11.30) U·mg-1,MDA含量为(4.56±1.25),(4.70±1.17),(4.63±1.06) nmol·mg-1,均明显减少;GSH含量明显增多,为(6.20±0.81),(6.24±0.76),(6.18±0.90 )mg·g-1;GSH-Px活性为(2.68±0.27),(2.59±0.34),(2.31±0.22) nU·g-1,SOD活性为(188.40±5.86),( 170.87±9.80),(165.62±6.54)nU·mg-1,均明显增高,差异均有统计学意义(P＜0.05).结论:帕宁方能明显改善PD大鼠旋转行为,减轻其黑质纹状体氧化应激损伤.     

涤痰汤对帕金森病大鼠行为学和氧化应激反应的影响

目的观察涤痰汤对帕金森病（PD）大鼠行为学和氧化应激反应的影响。方法运用6-羟基多巴胺立体定向注射复制PD大鼠模型。将PD模型大鼠随机分为模型组与化痰组;另设正常组和假手术组,分别给予相应处理,共14d。观察各组治疗前后大鼠旋转圈数,测定大鼠中脑黑质纹状体活性氧、丙二醛、谷胱甘肽含量,谷胱甘肽过氧化物酶、超氧化物歧化酶的活性。结果与模型组比较,化痰组大鼠旋转圈数、活性氧及丙二醛含量明显减少,谷胱甘肽含量明显增多,谷胱甘肽过氧化物酶及超氧化物歧化酶活性明显增高,差异均有统计学意义（P〈0.05）;化痰组各氧化应激指标与正常组和假手术组之间的差异有统计学意义（P〈0.05）。结论涤痰汤能明显改善PD大鼠旋转行为,减轻其黑质纹状体氧化应激损伤。     

龟羚帕安丸对帕金森病大鼠模型氧化应激反应的影响

目的：探究龟羚帕安丸对帕金森病大鼠模型氧化应激反应的影响。方法：用6一羟基多巴胺（6一OHDA）建立帕金森病（PD）大鼠模型,随机分为模型组,美多巴组,龟羚帕安丸大剂量组、中剂量组、小剂量组。分别每日管饲同体积的生理盐水,关多巴10mg·（kg·d）-1,龟羚帕安丸4．0g·（kg·d）-1、2．0g·（kg·d）-1、1．0g·（kg·d）-1。另设假手术组,常规饲养,每日管饲同体积的生理盐水。每日1次,共30d。观察血浆中超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽（GSH）实验后的变化。结果：与假手术组比较,模型组SOD的活性、GSH含量明显减少,MDA含量明显增多,差异具有统计学意义（P〈0．05）;与模型组比较,药物组SOD的活性、GSH含量明显增多,MDA含量明显减少,两组之间的差异具有统计学意义（P〈0．05）;龟羚帕安丸大剂量组SOD值显著高于美多巴组（P〈0．05）,龟羚帕安丸大剂量组GSH、MDA与美多巴组比较,差异无统计学意义（P〉0．05）。结论：龟羚帕安丸可增加帕金森大鼠模型血浆中增加SOD的活性和GSH的含量,减少MDA的含量,减轻氧化应激对神经细胞的损伤,可能是其治疗帕金森病的作用机制之一。     

中西药合用对帕金森病大鼠氧化应激反应的影响

目的：阐明中西药合用对氧化应激反应的影响。方法：采用6-OHDA注射于脑右侧黑质造成偏侧PD模型，并用中药 左旋多巴进行治疗，同时设立正常对照组、假手术组，观察中西药合用对氧化应激反应的影响。结果：中西药合用可使活性氧、MDA的含量降低，GSH、GSH—Px、SOD含量升高。结论：中西药合用可以提高机体的抗氧化能力，清除自由基，使机体免受自由基的损伤。     

拜颤停复方对帕金森病小鼠模型氧化应激反应的影响

目的:通过研究拜颤停复方(BCT)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)致小鼠帕金森病(PD)模型神经行为学、纹状体多巴胺(DA)含量、氧化应激反应的影响,探讨BCT对PD模型神经保护作用的可能作用机制。方法:雄性C57BL/6小鼠,MPTP-HC1(30 mg·kg-1·d-1,ip,0.9%生理盐水溶解)5 d,造成PD小鼠模型;设立正常组、模型组、多巴丝肼组(62.50 mg·kg-1·d-1)及BCT高、中、低剂量组(363.00,181.50,95.75 mg·kg-1·d-1),各给药组均用0.5%羧甲基纤维素钠(CMC-Na)溶解;BCT高、中、低剂量组ig给药治疗20 d后,进行爬杆实验和自主活动实验以观察小鼠行为学的变化;采用UPLC-MS-MS三重四级杆串联质谱技术检测小鼠纹状体多巴胺(DA)的含量;化学比色法检测小鼠黑质(SN)部位超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)及单胺氧化酶B(MAO-B)。结果:与正常组比较,模型组小鼠爬杆时间显著延长(P0.05),自主活动次数显著减少(P0.05),纹状体DA含量、SOD及GSH-Px水平显著降低(P0.01),MDA及MAO-B水平显著升高(P0.01)。与模型组比较,经过BCT治疗,PD小鼠的神经行为学得到显著改善(P0.05),纹状体DA含量,SOD及GSH-Px水平显著升高(P0.01,P0.05),MDA及MAO-B水平显著降低(P0.01)。结论:BCT可以通过提高机体的抗氧化和清除自由基能力,明显改善PD小鼠的神经行为学变化及纹状体DA的含量,是其对PD模型神经保护作用的可能机制。     

不同时间电针对急性脑出血大鼠氧化应激反应的影响

目的观察不同时间点针刺治疗对急性脑出血大鼠氧化应激反应的影响。方法Wistar雄性大鼠随机分为7组,正常组、模型组（模型1组、模型2组、模型3组、模型4组）、3h电针组和72h电针组,采用胶原酶Ⅶ诱发大鼠尾壳核脑出血模型。3h电针组和72h电针组分别于造模后3h、72h时开始针刺,每日1次,共针刺5次。检测血红素氧合酶-1（Heme0xygenase-1,HO-1）和血红素氧合酶-2（Heme0xygenase-2,HO—2）。结果造模后脑组织内见大量脑出血,神经纤维缠结、断裂：3h电针组脑组织仍可见泡沫细胞浸润及出血：72h电针组脑组织内坏死灶明显缩小、小胶质细胞浸润、极少量出血。正常大鼠脑组织均有HO—1和HO—2表达,脑出血大鼠HO-1表达明显增高,并与时问变化有-定联系。3h电针组、72h电针组HO-1均降低,两组之间比较差异无统计学意义（P〉0．05）。造模后5d大鼠脑组织内未出现HO-2表达,造模后8d出现表达,3h电针组、72h电针组均出现HO—2表达,72h电针组较3h电针组高,差异有统计学意义（P〈0．05）。结论电针可以改善急性脑出血后脑组织出血状况,降低脑出血后氧化应激反应,对急性脑出血后神经元损伤有-定的修复作用。脑出血后72h电针比3h电针疗效好,提示急性期脑出血早期应该慎重选择电针治疗。     

虎杖白藜芦醇及其脂质体剂型对帕金森病模型大鼠黑质细胞保护作用的研究

目的:氧化应激是帕金森病发病机制中的重要病理因素,是导致黑质多巴胺能神经元死亡的主要原因之一.白藜芦醇具有广泛的药理学作用和较强的抗氧化特性.本研究探讨从中药虎杖提取的白藜芦醇及其脂质体制剂对帕金森病模型大鼠黑质细胞的保护效应,为临床帕金森病治疗药物的开发提供实验依据.方法:实验用Wistar大鼠50只,随机分为正常组、假手术组、模型组、白藜芦醇干预组、白藜芦醇脂质体干预组,以6-羟基多巴胺单侧纹状体微量注射法制备帕金森病大鼠模型.白藜芦醇干预组及白藜芦醇脂质体干预组在造模成功后,以白藜芦醇、白藜芦醇脂质体灌胃,20 mg·kg-1,1次/d,连续14 d.观察各组大鼠的旋转行为学改变,采用HE染色、Nissl染色、酪氨酸羟化酶(TH)免疫组化方法统计黑质细胞总数、神经元总数、多巴胺能神经元数量,采用TUNEL法检测黑质细胞凋亡,以分光光度法检测黑质区总ROS活力和总抗氧化能力.结果:帕金森病模型大鼠在阿普吗啡诱导后,出现明显的行为学异常表现,黑质区细胞总数、神经元总数及多巴胺能神经元数量明显减少,凋亡细胞数量增加,组织总ROS活力显著增强,总抗氧化能力明显降低.白藜芦醇及白藜芦醇脂质体均能明显改善模型大鼠行为学异常,增加黑质区细胞总数、神经元总数、多巴胺能神经元数量,降低细胞凋亡率,提高组织总抗氧化能力,降低组织总ROS活力.在组织学指标的改善方面,白藜芦醇脂质体的效应较白藜芦醇单体更强.结论:中药虎杖来源的白藜芦醇及白藜芦醇脂质体对帕金森病模型大鼠黑质细胞具有明显的保护作用,这种保护作用可能与抗氧化活性有关.白藜芦醇脂质体较白藜芦醇单体在组织学指标改善上作用更强,可能与脂质体制剂提高了白藜芦醇的生物利用度有关.白藜芦醇脂质体可能是更有效的口服给药方式.     

黄连降糖片对2型糖尿病模型大鼠氧化应激反应的影响

目的:探讨不同剂量黄连降糖片对链脲佐菌素(STE)诱导的2型糖尿病模型大鼠氧化应激反应的影响及其量效关系。方法:将SPF级SD雄性大鼠120只随机分为正常组(n=10)和造模组(n=110),将造模组高脂高糖饲料喂养加小剂量链脲佐菌素腹腔注射建立SD大鼠2型糖尿病模型后随机分为模型组、黄连降糖片组(1～9片)及阳性组,每组10只。运用蒸馏水、黄连降糖片及盐酸二甲双胍分别干预4周后检测各组大鼠血清谷胱甘肽过氧化物酶(GSH-Px)活性、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量。结果:与模型组相比,黄连降糖片2～9片组大鼠空腹血糖(FBG)降低(P0.05),血清GSH-Px、SOD活性增强(P0.05),MDA含量降低(P0.05),与阳性组相比,黄连降糖片3～9片组大鼠血清GSH-Px活性增强(P0.05),5～9片组大鼠血清SOD活性升高(P0.05),6～9片组大鼠血清MDA含量降低(P0.05),且在2～8片范围内随着药物剂量的增加,降糖幅度增加,调节氧化应激的作用增强。结论:黄连降糖片的降糖机制可能与抑制2型糖尿病模型大鼠氧化应激反应有关,且在一定剂量范围内存在量效关系。     

绿茶多酚联合针刺治疗对鱼藤酮致帕金森病大鼠保护作用的研究

目的:拟采用鱼藤酮注射制备PD动物模型,探讨绿茶多酚联合针灸治疗能否对多巴胺神经元有保护和修复作用以及并其作用机制。方法:将Witstar大鼠随机分为对照组(10只)、鱼藤酮组(20只)和绿茶多酚加针刺治疗组(20只)。对照组背部皮下注射葵花油1mL/kg,鱼藤酮组和绿茶多酚加针刺治疗组的大鼠每日按照2.0 mg/kg背部皮下注射鱼藤酮,进行PD模型的建立,绿茶多酚加针刺治疗组在造模成功后开始在大鼠饮水中加入GTPs,并且针刺双侧阳陵泉及舞蹈震颤区。免疫组织化学法观察黑质多巴胺能神经元计数,比色法观察谷胱甘肽(GSH)和丙二醛(MDA)反映氧化应激水平。结果:免疫组化染色显示,与对照组比较,鱼藤酮组TH阳性细胞数明显低于对照组。经过绿茶多酚+针刺治疗,TH阳性细胞数有明显增加,氧化应激水平明显升高(P0.05)。结论:GTPs在保护神经细胞、抑制氧化应激、抗兴奋性毒性、抑制细胞凋亡等方面有一定作用,针灸治疗PD无明显副作用,二者联合可以作为治疗PD较理想方法。     

茶多酚对大鼠血管平滑肌细胞增殖的影响

目的　探讨茶多酚对离体大鼠胸主动脉血管平滑肌细胞增殖的影响。方法　体外培养大鼠主动脉血管平滑肌细胞 ,应用不同剂量的茶多酚作用 2 4 h后 ,采用 MTS/ PES法确定血管平滑肌细胞的增殖状态。应用流式细胞术测定细胞周期。结果　与对照组相比 ,茶多酚对血管平滑肌细胞增殖具有明显的抑制作用 (P<0 .0 0 1)。流式细胞术检测结果表明 ,茶多酚可以使血管平滑肌细胞大部分处于 G0 / G1 期 ,与对照组相比有明显差异 (P<0 .0 5 ) ,并且可以诱导其凋亡。结论　茶多酚可明显抑制离体大鼠血管平滑肌细胞的增殖。     

郁乐疏合剂治疗帕金森病伴发抑郁的临床疗效

目的:观察郁乐疏合剂治疗帕金森病伴发抑郁的临床疗效。方法:将帕金森病合并抑郁症患者68例随机分为治疗组35例和对照组33例,对照组给予常规抗帕金森病药物治疗,治疗组在对照组治疗的基础上口服郁乐疏合剂3个月。评价2组患者治疗前后统一帕金森病评分量表(UPDRS)、汉密顿抑郁量表(HAMD)以及帕金森病的非运动性症状问卷(NMSQest)评分,同时观察2组疗效并监测用药安全性。结果:2组患者治疗前UPDRS、HAMD及NMSQest评分比较差异无统计学意义(P0.05),用药6周后2组评分均有所下降,治疗组HAMD评分下降明显,与对照组比较差异有统计学意义(P0.05);治疗12周后,治疗组评分和治疗前以及对照组之间比较差异均有统计学意义(P0.05),对照组3种评分和治疗前比较差异无统计学意义(P0.05)。治疗组对于抑郁及非运动症状的总有效率分别为60.0%(21/35)和57.1%(20/35),均明显高于对照组的9.1%和9.1%,差异有统计学意义(P0.05)。结论:郁乐疏合剂能改善帕金森病伴发抑郁患者非运动症状,疗效较好且安全。     

针刀干预对帕金森病模型大鼠纹状体内去甲肾上腺素及5-羟色胺含量的影响

目的观察帕金森病模型大鼠纹状体内去甲肾上腺素(NA)、5-羟色胺(5-HT)的含量以及针刀干预后的变化,探讨针刀治疗帕金森病的作用机制。方法成年健康雄性SD大鼠76只,随机分为2组,实验组60只,空白组16只。实验组60只采用右侧纹状体双靶点注射6-羟多巴胺(6-OHDA)造模,造模结束后用阿朴吗啡(APO)诱导法进行模型评价,并通过行为学检测,实验组共有48只大鼠造模成功,随机分为模型组、药物组和针刀组,每组16只。空白组和模型组正常抓取刺激,不进行干预治疗;药物组予美多芭片悬浊液治疗,每日1次,连续4周;针刀组进行松解干预,每周2次,连续4周。治疗结束1周后进行行为学评价,通过苏木精-伊红(HE)染色图片观察大鼠纹状体的病理学变化,通过高效液相色谱法观察大鼠纹状体NA、5-HT的含量。结果行为学评价结果显示,空白组大鼠未见旋转,模型组大鼠出现旋转,干预后药物组及针刀组大鼠旋转圈数明显减少(P0.01),且治疗前后比较差异有统计学意义(P0.01)。与空白组比较,模型组大鼠纹状体内NA、5-HT含量减少(P0.05);与模型组比较,药物组和针刀组大鼠纹状体中NA、5-HT含量显著增高(P0.05)。结论针刀对帕金森病模型大鼠的治疗作用可能与其松解颈部肌肉,改善局部血液循环,增加NA、5-HT的含量,从而减轻帕金森病的症状有关。     

Influence of the Green Tea Leaf Extract on Neurotoxicity of Aluminium Chloride in Rats

Aluminium may have an important role in the aetiology/pathogenesis/precipitation of Alzheimer's disease. Because green tea (Camellia sinensis L.) reportedly has health‐promoting effects in the central nervous system, we evaluated the effects of green tea leaf extract (GTLE) on aluminium chloride (AlCl₃) neurotoxicity in rats. All solutions were injected into the cornu ammonis region 1 hippocampal region. We measured the performance of active avoidance (AA) tasks, various enzyme activities and total glutathione content (TGC) in the forebrain cortex (FbC), striatum, basal forebrain (BFb), hippocampus, brain stem and cerebellum. AlCl₃ markedly reduced AA performance and activities of cytochrome c oxidase (COX) and acetylcholinesterase (AChE) in all regions. It decreased TGC in the FbC, striatum, BFb, hippocampus, brain stem and cerebellum, and increased superoxide dismutase activity in the FbC, cerebellum and BFb. GTLE pretreatment completely reversed the damaging effects of AlCl₃ on AA and superoxide dismutase activity, markedly corrected COX and AChE activities, and moderately improved TGC. GTLE alone increased COX and AChE activities in almost all regions. GTLE reduces AlCl₃ neurotoxicity probably via antioxidative effects and improves mitochondrial and cholinergic synaptic functions through the actions of (?)‐epigallocatechin gallate and (?)‐epicatechin, compounds most abundantly found in GTLE. Our results suggest that green tea might be beneficial in Alzheimer's disease. Copyright © 2013 John Wiley & Sons, Ltd.     

绿茶多酚对血管性认知功能障碍影响的相关机制探讨

目的研究两种剂量的绿茶多酚对慢性脑低灌注后病理生理变化的影响,以探讨绿茶多酚改善血管性认知功能障碍的相关机制。方法健康雄性Wistar大鼠随机分为假手术组、双侧颈总动脉结扎（2VO）＋生理盐水组、2VO＋GTP100组[绿茶多酚100 mg/（kg.d）]、2VO＋GTP400组[绿茶多酚400 mg/（kg.d）]。采用大鼠2VO制备慢性脑低灌注模型,结扎后从第4周开始给药,给药4周后通过Morris水迷宫观察大鼠的空间学习及记忆功能,采用生化方法检测大鼠海马组织的MDA含量、超氧化物歧化酶（SOD）和乙酰胆碱酯酶（AchE）的活性,并采用实时定量PCR方法检测海马组织Nrf2mRNA的表达。结果绿茶多酚缩短慢性脑低灌注大鼠的逃逸潜伏期,使大鼠在平台区的停留时间延长。绿茶多酚减少海马组织的MDA含量,增强SOD活性,但对AchE的活性没有显著影响,400 mg/（kg.d）剂量的绿茶多酚增强海马组织Nrf2mRNA的表达。结论绿茶多酚改善慢性脑低灌注后的认知功能损害,减轻海马组织的脂质过氧化反应及抗氧化能力,尤其是400 mg/（kg.d）的剂量,但对胆碱能系统没有显著影响。     

Effects of the Total Alkaloidal Extract of Murraya koenigii Leaf on Oxidative Stress and Cholinergic Transmission in Aged Mice

Alzheimer's disease (AD) is characterized by signs of major oxidative stress and the loss of cholinergic cells. The present study was designed to investigate the role of the total alkaloidal extract from Murraya koenigii (MKA) leaves on age related oxidative stress and the cholinergic pathway in aged mice. Ascorbic acid (100 mg/kg, p.o.) was used as a standard drug. The MKA improved the level of protective antioxidants such as glutathione peroxidase (GPx), reduced glutathione (GSH), glutathione reductase (GRD), superoxide dismutase (SOD) and catalase (CAT) in brain homogenate at higher doses (20 and 40 mg/kg, p.o.). Moreover, a dose dependent decline was noted in lipid peroxidation (LPO) and the nitric oxide assay (NO) at all doses of MKA (10, 20 and 40 mg/kg, p.o.). Interestingly, significant progress was noted with the supplementation of MKA by an improvement of the acetylcholine (ACh) levels and a reduction in the acetylcholinesterase (AChE) activity in aged mouse brain. In addition, a significant elevation of serum albumin (ALBU), alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST) and total protein as well as a decline in creatinine, total cholesterol, urea nitrogen and glucose levels with MKA also ameliorated the hepatic and renal functions in normal ageing process. The results showed the possible utility of Murraya koenigii leaves in neuroprotection against neurodegenerative disorders such as Alzheimer's disease. Copyright © 2012 John Wiley & Sons, Ltd.     

Neuroprotective Effects of San-Jia-Fu-Mai Decoction: Studies on the in vitro and in vivo Models of Parkinson's Disease

Objective: The objective of this study was to investigate whether 70% aqueous ethanol extract of San-Jia-Fu-Mai decoction extract(SJFMDE) could protect against 1-methyl-4-phenylpyridinium(MPP+)-induced oxidative stress in PC12 cells and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced motor function deficits in mice. Materials and Methods: The cell viability, the levels of intracellular reactive oxygen species(ROS), malondialdehyde(MDA), and glutathione(GSH) in the MPP+-treated PC12 cells were measured. Motor function deficits and dopamine(DA) level in the brain striatum and tyrosine hydroxylase(TH)-positive cells in substantia nigra pars compacta(SNc) of the MPTP-treated mice were determined. Results: The results showed that SJFMDE could reduce cell death and the levels of ROS and MDA while increase the level of GSH in the MPP+-treated PC12 cells. In addition, in vivo studies showed that oral administration of SJFMDE(3, 6, and 12 g/kg) significantly improved the motor function deficits induced by MPTP and enhanced the DA level in the striatum and TH-positive neuronal cells in SNc of the MPTP-treated mice. Conclusions: Our results revealed that SJFMDE possessed neuroprotective effects against neurotoxicity induced by MPP + and motor function deficits induced by MPTP via suppressing oxidative stress and increasing the levels of DA and TH, indicating that SJFMDE might be a promising Chinese medicine formula for the treatment of Parkinson's disease.     

茶多酚对长期饮酒所致心肌胰岛素抵抗的影响及机制研究

目的:观察茶多酚对长期饮酒动物心肌胰岛素敏感性的影响,并探讨其作用机制。方法:Wistar大鼠随机分为正常组、酒精组、茶多酚组,每组10只。酒精组和茶多酚组每只大鼠每天灌胃给予酒精5 g/kg,茶多酚组每只大鼠每天腹腔注射茶多酚30 mg/kg,干预时间为16周。通过离体心肌对葡萄糖的摄取观察心肌胰岛素敏感性,ELISA法检测心肌组织中脂联素含量,同时对心肌氧化应激产物8-iso-PGF2α水平,抗氧化酶GSH-Px、CAT、SOD的活性进行检测。结果:长期饮酒可致心肌胰岛素敏感性降低。与酒精组比较,茶多酚可显著改善心肌胰岛素敏感性(P<0.01),增加心肌组织脂联素水平(P<0.01);茶多酚在降低心肌8-iso-PGF2α水平(P<0.01)的同时,增加多种抗氧化酶活性(P<0.05或P<0.01)。结论:茶多酚可改善长期饮酒所致心肌胰岛素抵抗,该作用与增加脂联素水平及抗氧化应激反应密切相关。     

Effect of aqueous extracts of black and green teas in arsenic‐induced toxicity in rabbits

Arsenic causes oxidative stress in the body. Its administration (3 mg/kg/day) for 14 days in rabbits resulted in a significant reduction of whole blood glutathione (GSH), and elevation of thiobarbituric acid reactive substances (TBARS) and the index of nitrite/nitrate (NOx) levels. These are the markers of oxidative stress. Both black tea (BT) and green tea (GT) (Camellia sinensis), when administered to the arsenic‐treated rabbits for 14 days, caused a significant elevation of the depleted GSH level to 53.12% and 57.47%, respectively. On the contrary, in the placebo group the level was 26.59%. The BT and GT reduced the elevated TBARS level to 43.27% and 62.28%, respectively, whereas the corresponding level in the placebo groups was 21.24%. The NOx levels were also reduced to 63.62%, 67.67% and 58.94% in BT, GT and the placebo groups, respectively. When arsenic and black tea were given concurrently to another group the results were even more pronounced. The polyphenol components of black and green tea were 27.69% and 29.71% of the dry weight of the total extracts, respectively. These results indicated that arsenic‐induced toxicities in rabbits were significantly reversed by the black and green tea polyphenols. The greater activity of green tea than that of black tea correlates with the slightly higher content of polyphenols in green tea. Copyright © 2009 John Wiley & Sons, Ltd.