自由基在视神经损伤后的毒性作用及氨基胍对其影响

目的观察氨基胍（aminoguaniding,AG）在兔视神经损伤后对视网膜超氧化物歧化酶（SOD）、丙二醛（MDA）含量的影响,研究对视网膜神经节细胞（retinalganglioncell,RGC）的保护性作用机制。方法健康成年大耳白兔66只,随机分为正常对照组、损伤对照组和损伤治疗组,损伤组按损伤后ld、3d、7d、14d、21d分5组,每组6只。损伤组采用同一反向动脉夹夹闭视神经法制作动物模型。伤后2min耳缘静脉注射2％AG溶液（损伤治疗组）及等量0．9％氯化钠溶液（损伤对照组）,测定视网膜组织中SOD、MDA的含量。结果正常视网膜组织中含有一定量的MDA、SOD,视神经损伤后MDA含量逐渐升高,而SOD活力逐渐下降,至伤后14d时达到高峰,同一时间点损伤对照组和损伤治疗组比较差异有统计学意义（P〈0．05）。结论兔视神经损伤后,AG通过对抗自由基的途径减少视神经损伤诱导的RGC凋亡。     

黄体酮对视神经损伤大鼠视网膜神经节细胞微管相关蛋白-1B的影响

目的：观察并探讨黄体酮对视神经损伤早期视网膜神经节细胞微管相关蛋白-1B的影响,以期为黄体酮在视神经保护方面的作用提供实验依据。方法60只大鼠随机分为3组,每组20只。正常对照组不做任何处理,损伤1组制作右眼视神经夹伤模型,给予0)．9％氯化钠溶液腹腔注射,损伤2组制作右眼视神经夹伤模型,给予黄体酮腹腔注射。分别于损伤后1、3、7、14、28 d将3组大鼠右眼球摘除,取视网膜组织, HE染色光学显微镜观察视网膜形态学变化,并计数视网膜神经节细胞存活数量,免疫组织化学染色观察视网膜组织中MAP-1B在视网膜神经节细胞的表达情况。结果视神经损伤后损伤1组视网膜神经纤维层明显水肿,视网膜神经节细胞数目迅速减少,经黄体酮治疗的损伤2组视网膜形态改变轻微,视网膜神经纤维层轻度水肿,视网膜神经节细胞数目减少缓慢。损伤2组各时间段视网膜MAP-1B平均光密度值较损伤1组高,差异有统计学意义（ P ＜0．05）。结论黄体酮可以通过增加细胞骨架蛋白MAP-1B减轻视神经损伤早期视网膜神经节细胞的损害,对视神经及视网膜有保护作用。     

神经生长因子对大鼠脑血肿周围细胞凋亡的影响

目的：观察脑出血后血肿周围神经细胞凋亡和Caspase-3的表达，以及NGF（神经生长因子）对上述情况的影响。方法：自体血注入法制备大鼠脑出血模型，经TUNEL染色和Caspase-3免疫组化染色，照片观察并计数阳性细胞数，结果用SPSS 11．5软件统计分析。结果：假手术组无TUNEL细胞表达，Caspase-3少量表达；脑出血组6h血肿周边组织出现TUNEL阳性细胞，72h达高峰，Caspase-3在脑出血后6h表达开始增高，24h达到高峰，脑出血后血肿周围TUNEL阳性细胞与Caspase-3的表达呈正相关（r=0．371，P〈0．05）；应用NGF干预后，自12h起各时间点TUNEL细胞和Caspase-3表达均较脑出血组减少（P〈0．05），以各自高峰时间最为显著（p〈0．05），但未能改变TUNEL细胞和Caspase-3表达的高峰时间。结论：（1）脑出血后血肿周围细胞凋亡与Caspase-3表达有关。（2）NGF能够有效地抑制脑出血后的神经细胞凋亡。     

神经生长因子β对兔实验性青光眼视网膜神经节细胞的保护作用

目的 探讨神经生长因子β（NGF-β）对青光眼性视网膜神经节细胞（RGCs）损害的保护作用。方法 建立家兔青光眼模型,并动态观察眼压。于术后14d、21d随机选择一眼玻璃体腔注射NGF-β 1μg和细胞色素C 0．1mg（实验组）,对侧眼仅注射细胞色素C 0．1mg作对照（对照组）,共10只兔。术后28d处死实验兔摘取眼球及视神经作组织学观察,并用核苷酸末端转移酶介导的dUTP缺口末端标记法（TUNEL）检测RGCs凋亡状况。结果 组织学检查显示术后28d时视神经神经纤维丢失程度实验组有8例轻于对照组,1例相似,1例较对照组为重。对照组视神经节细胞层凋亡阳性率13．46％,明显高于实验组的10．60％（P〈0．01）。结论 NGF-β对青光眼性视网膜神经节细胞损害具有一定的保护作用。     

大黄酸对脑出血大鼠神经损伤和细胞凋亡的影响

目的探讨大黄酸对脑出血（ICH）大鼠神经损伤和细胞凋亡的影响。方法在成年Sprague-Dawley大鼠尾状核注入collagenaseⅣ（0．05U／0．5uL）诱导ICH,假手术大鼠在相同位置注入相同剂量的氯化钠注射液。大鼠术后分别在3h．6h、12h腹腔注射大黄酸注射液（70mg／kg）或相同剂量的氯化钠注射液。Western blot法测定半胱氨酸天冬氨酸蛋白酶-3（caspase-3）活性,TUNEL标记凋亡细胞,阿朴吗啡诱导的旋转行为评价神经功能缺损。结果大鼠脑出血后3h和6h给予大黄酸注射液明显抑制casepase-3的激活（P〈0．001）,减少TUNEL阳性细胞数（P〈0．05）,减少阿朴吗啡诱导的旋转次数（P〈0．05）;脑出血后12h给药无效。结论脑出血后早期给予大黄酸,可能通过阻断凋亡通路起到神经保护作用。     

前列地尔与神经节苷脂钠联合治疗视神经损伤的临床观察

目的探讨前列地尔联合神经节苷脂钠对视神经损伤的临床疗效。方法自2004年1月至2008年3月外伤性视神经病变72例,其中40例（治疗组）应用前列地尔联合神经节苷脂钠治疗;30例（对照组）应用复方樟柳碱联合维生素B1、维生素B12治疗。结果治疗组总有效率92．5％,对照组总有效率65．63％;两组比较差异有显著性P〈0．05。结论前列地尔联合神经节苷脂钠促进视神经损伤后神经再生及功能恢复。     

三七皂苷对大鼠持续性高眼压视网膜神经节细胞保护的实验研究

目的 探讨三七皂苷（PNS）对大鼠持续性高眼压下视网膜神经节细胞损伤的保护作用及机制.方法 健康SD大鼠80只随机分为四组,正常对照组、0.9%氯化钠溶液组、单纯用药组和联合用药组.采用烙闭巩膜上静脉联合术后结膜下注射5-FU（5-氟尿嘧啶）的方法制作大鼠持续性高眼压模型,所有大鼠定期测量并记录眼压.4周、8周、12周、16周、20周后分别处死大鼠,摘取眼球,TUNEL法检测视网膜神经细胞（Retinal ganglion Cells,RGCs）凋亡;AgNOR染色检测RGCs的活性;免疫组织化学检测视网膜节细胞层半胱氨酸蛋白酶-9（caspase-9）的表达.结果 术后眼压维持在（36.55±2.27）mm Hg为4周至20周左右;视网膜神经节细胞层TUNEL阳性细胞数与正常对照组差异有统计学意义;正常对照组和联合用药组RGC8细胞核内银染颗粒数比较差异无统计学意义（P〉0.05）;各组视网膜神经节细胞层caspase-9蛋白的表达较正常对照组明显增强.结论PNS对持续性高眼压导致的视网膜神经节细胞损伤有较显著保护作用.联合降眼压药控制眼压,PNS对大鼠视网膜神经节细胞的保护作用更突出.PNS能抑制视网膜神经节细胞Caspase-9的表达从而保护大鼠视网膜神经节细胞.     

米诺环素对兔慢性高眼压视网膜功能的影响

目的研究米诺环素（minocycline）对兔慢性高眼压视网膜神经节细胞（retina／ganglia／cells,RGC）损伤的保护作用。方法成年健康色素兔30只随机分为A、B、C三组,每组各10只。A组为空白组;B组为模型组;C组为给药组。选B、C组右眼作高眼压模型,每眼抽取房水0．1ml,随后注射0．3％复方卡波姆溶液0．1ml。C组给予米诺环素（minocycline）口服给药,50mg／ks／24h,连续30d。用Schiotz眼压计测量并记录眼压,一周一次。30d时,A、B、C组右眼均行光学相干眼底断层扫描（OCT）检测视神经纤维层厚度。SPSS13．0统计学分析软件对结果进行统计学分析。结果眼压测量结果统计分析显示：B、C组眼压符合慢性高眼压造模标准,且差异无统计学意义（P〉0．05）,B、c组眼压较A组高,且差异有统计学意义（p〈0．05）。OCT所检测视神经纤维层厚度测量结果统计分析显示：视神经纤维层厚度由薄到厚B〈C〈A,差异均具有统计学意义（P〈0．05）。结论米诺环素对慢性高眼压下视网膜功能改变有保护作用。     

重组牛碱性成纤维细胞生长因子治疗视神经损伤的药理学研究

目的：研究重组牛碱性成纤维细胞生长因子（rbFGF)在视神经损伤修复中的作用。方法：视神经部分损伤后，球后分别注射生理盐水、维生素B12、bFGF，伤后4周测量闪光视神经诱发电位（F－VEP），进行轴突定量、视网膜神经节细胞（RGCs)定量以及RGCs凋亡的检测，观察视神经损伤修复情况。结果：伤后4周时生理盐水维生素B12组对照刺激无反应，bFGF组F－VEP接近正常，800U、1600U和2400UbFGF对RGCs挽救率分别为24．5％、27．3％、28．5％，800U、1600U和2400UbEGF组未发生演变的轴突数分别是损伤末治疗组的2．03、2．43、2．31倍。流式细胞仪检测结果显示，bFGF治疗7d后，RGCs凋亡率显著减少。结论：bFGF可挽救视网膜神经节细胞的存活，减少轴突溃变，有抗凋亡作用，对视神经损伤有显著地促功能修复作用。     

富氢生理盐水对大鼠视网膜缺血再灌注损伤神经保护作用的研究

目的：本文应用大鼠视网膜缺血再灌注损伤模型,探讨富氢生理盐水对其是否具有神经保护作用。方法成年雄性SD大鼠随机分为4组：正常组、视网膜缺血再灌注组（ RIR）、富氢生理盐水组（ HRS）、生理盐水组（ NS）。正常组大鼠不进行任何手术操作,其他3组大鼠均行前房穿刺,造成缺血60min后恢复灌注,RIR 组期间不给予任何干预措施,HRS 组和 NS 组于再灌注前10min 及再灌注开始时分别腹腔内注射3mLHRS或2mL NS。应用免疫组化法观察缺血再灌注损伤视网膜神经节细胞存活情况,另外用相应试剂盒检测再灌注24h及7d后大鼠血清中SOD活性及MDA水平。结果缺血再灌注7d后,RIR组大鼠神经节细胞数明显减少（P＜0．01）,而 HRS 组视网膜神经节细胞数明显较多（P＜0．05）;另外,与正常组相比,RIR组 SOD活性明显降低（P＜0．01）,MDA水平明显升高（24h P＜0．05,7d P＜0．01）,与 RIR 组相比,HRS 组SOD活性显著增加（24h P＜0．05,7d P＜0．01）,7d时MDA含量显著降低（P＜0．01）。结论腹腔内注射富氢生理盐水能够明显减少神经节细胞凋亡,并可显著提高血清中内源性抗氧化酶活性,降低氧化产物水平。     

MK-801对大鼠坐骨神经缺血再灌注损伤保护作用的实验研究

目的探讨MK-801阻断N-甲基-D-天冬氨酸(NMDA)受体与周围神经缺血再灌注损伤之间的关系及大鼠坐骨神经缺血再灌注损伤的机制。方法 24只健康清洁级SD雄性大鼠,随机分为对照组(假手术组)、缺血组、MK-801组各8只(再灌注前15min腹腔内注射MK-801,1mg/kg)。采用比色法检测血浆丙二醛(MDA)、一氧化氮(NO)和坐骨神经诱导型一氧化氮合酶(iNOS)水平;光镜、电镜观察坐骨神经组织病理改变情况;RT-PCR法测定坐骨神经肿瘤坏死因子α(TNF-α)mRNA表达。结果 MK-801能明显降低大鼠血浆MDA、NO和坐骨神经iNOS水平;下调坐骨神经TNF-α基因表达;减轻坐骨神经组织病理改变。结论兴奋性氨基酸参与了大鼠坐骨神经缺血再灌注损伤;其过程炎症细胞、炎症因子发挥着重要作用;MK-801对大鼠坐骨神经缺血再灌注损伤具有保护作用。     

Spatial learning deficit after NMDA receptor blockade and state-dependency

The non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801) (0.08 and 0.12 mg/kg, i.p.) was used to examine whether spatial memory is learned state-dependently. Rats pre-treated with drug or saline were trained for 9 days in an eight-arm radial maze, in which four arms were baited. On the tenth day MK-801-treated rats were injected with saline and one group of saline-treated rats were injected with MK-801 (0.12 mg/kg) while another received saline. Performance of spatial memory was analysed for state-dependency. Neither rats treated with 0.08 mg/kg nor 0.12 mg/kg of MK-801 for 9 days were impaired in recall of spatial memory under saline. However, MK-801 impaired acquisition of spatial memory, with deficits in working memory and less marked deficits in reference memory. Motor activity (speed) was enhanced at both doses. Thus, learning under NMDA receptor blockade does not necessarily produce a condition that impedes the expression of the learning task under a different condition.     

谷氨酸对大鼠纹状体神经元活动的影响

目的:研究谷氨酸(L-glutamic acid,GLU)及受体阻断剂MK-801对雄性大鼠纹状体(striatum,STR)神经元自发放电活动的影响。方法:应用微电泳方法记录纹状体神经元自发放电活动。结果:微电泳GLU使84.13%STR神经元自发放电频率加快。在43个STR神经元中直接微电泳MK-801可使62.79%STR神经元自发放电频率降低。在微电泳GLU产生兴奋效应的33个STR神经元中,微电泳GLU期间给予MK-801拮抗GLU的兴奋效应,可使90.91%已对GLU产生兴奋效应的STR神经元放电频率减慢。结论:GLU对STR神经元起兴奋作用,但其兴奋作用可被MK-801所拮抗,当直接微电泳MK-801时,可使STR神经元产生抑制效应。研究提示抗谷氨酸作用的药物有抗帕金森病(Parkinson disease,PD)的作用。     

Evidence for the participation of glutamate in reflexes involving afferent, substance P-containing nerve fibres in the rat.

1. Responses mediated, either peripherally or centrally, by substance P-containing primary afferent C-fibres were investigated in the rat following impairment of axonal transport by colchicine (120 micrograms kg-1, i.p., daily for 3 days), and after treatment with the tachykinin antagonist SR-140333 (10-100 micrograms kg-1, i.v.) or the N-methyl-D-aspartate (NMDA) antagonist MK-801 (100 micrograms kg-1). 2. Peripheral effects mediated by afferent C-fibres were measured by plasma protein extravasation (Evans blue method), following antidromic stimulation of the sciatic nerve, topical application of mustard oil and, as control, i.v. injection of substance P. SR-140333 (100 micrograms kg-1) reduced the effects by 86%, 75% and 74%, respectively. Colchicine reduced the effects of the first two stimuli by 31% and 33% and, as expected not the effect of substance P. The increase of paw skin temperature following capsaicin i.v. was inhibited by SR-140333, but not by colchicine. MK-801 had no effect on the plasma protein extravasation following antidromic sciatic nerve stimulation or on the rise of paw skin temperature induced by capsaicin i.v., thus excluding an effect of MK-801 on peripheral terminals of afferent neurones. 3. Depressor reflexes, which are known to be mediated by capsaicin-sensitive afferent neuones, such as those elicited (A) by a stimulating dose of 30 ng capsaicin i.a., (B) by distension of the ascending colon or (C) by afferent sciatic nerve stimulation were studied. Colchicine significantly reduced depressor reflexes A and B, but had no effect on reflex C. None of the reflexes was affected by SR-140333. MK-801 significantly inhibited all three reflexes. 4. Capsaicin, injected either i.v. (200 micrograms kg-1) or into the nucleus caudatus/putamen (i.c., 30 micrograms), induced an increase in paw skin temperature and a decrease in colon temperature. The rise in fore paw skin temperature (delta t = 2.3 +/- 0.4 degrees C) evoked by capsaicin i.v. was almost completely blocked by SR-140333 (100 micrograms kg-1, i.v.), but no inhibition was observed with MK-801, indicating that capsaicin had brought about a release of substance P from peripheral nerve terminals. Colchicine did not influence heat dissipation induced by i.v. capsaicin. 5. When capsaicin was injected i.c., the rise in paw skin temperature in colchicine- and SR-140333-pretreated groups did not differ from that of the control group. MK-801 totally prevented the heat loss reaction to i.c. capsaicin administration. Colchicine did not change the effects of i.v. or i.c. injected capsaicin: this excludes the involvement of a mechanism dependent on axonal transport of neurotransmitters. 6. The reduction of axonal transport by colchicine reduced plasma extravasation induced by mustard oil and antidromic sciatic nerve stimulation (peripheral functions) and depressor reflexes evoked by i.a. capsaicin and colon distension (central functions). It can be argued that afferent stimulation of the sciatic nerve includes the stimulation of A-fibres, which might be less sensitive to colchicine. SR-140333 was effective only on peripherally mediated responses. 7. The recent evidence for the concomitant release of glutamate and substance P from central terminals of afferent C-fibres, known to mediate reflexes abolished after capsaicin treatment allows the following conclusions: (a) the inhibition by MK-801 indicates an essential role for glutamate in the central transmission of these reflexes; (b) tachykinin antagonists such as SR-140333 do not affect these responses when administered systemically. Centrally released substance P could be involved in functions of the CNS other than those investigated here unless the access of neurokinin antagonists to their receptors in the CNS is insufficient.     

Differential actions of dizocilpine (MK-801) on the mesolimbic and mesocortical dopamine systems: role of neuronal activity

The significance of impulse activity in the dopamine neurons of the ventral tegmental area for the dopamine release evoked by systemic administration of the psychotomimetic drug dizocilpine (MK-801) was investigated. Dual probe microdialysis was utilized in freely moving rats implanted with one probe in the ventral tegmental area and a second ipsilateral probe in either the nucleus accumbens or the medial prefrontal cortex. Dialysates were analyzed with high-performance liquid chromatography with electrochemical detection for dopamine. The ventral tegmental area was perfused with the sodium channel blocker tetrodotoxin (1 microM) or vehicle (perfusion solution). A total of 2 h after the onset of tetrodotoxin perfusion of the ventral tegmental area, MK-801 (0.1 mg/kg) was injected subcutaneously. Tetrodotoxin perfusion of the ventral tegmental area significantly reduced dialysate levels of dopamine both in the nucleus accumbens and the medial prefrontal cortex to approximately 30% of baseline. When given alone, MK-801 caused a significant, i.e. 50%, increase in extracellular dopamine levels in the nucleus accumbens, and an even larger increase in the medial prefrontal cortex, i.e. 150%. Tetrodotoxin perfusion of the ventral tegmental area completely blocked the systemic MK-801 induced increase in extracellular concentrations of dopamine in the nucleus accumbens. However, the MK-801-evoked increase in dopamine levels in the medial prefrontal cortex was not significantly affected. Thus, the present results allow the conclusion that basal dopamine output in mesolimbic and mesocortical dopamine nerve terminal regions is predominantly dependent on nerve impulses generated in the ventral tegmental area. Moreover, also the MK-801 evoked dopamine release in the mesolimbic projection is almost entirely dependent on the impulse activity of the dopamine neurons, in agreement with our previous results. However, the MK-801 evoked dopamine release in the mesocortical projection is, in contrast, largely independent of the nerve impulse activity in the dopamine cells. The dysfunctions of mesolimbic and mesocortical dopamine neurons induced by systemic administration of non-competitive NMDA receptor antagonists may have direct bearing on the neurobiology of psychotic states, in particular as regards the generation of emotional and cognitive impairments.     

MK-801对吗啡依赖大鼠戒断症状及中枢cAMP含量的影响

目的观察MK-801对吗啡依赖大鼠戒断症状及脊髓和脑干cAMP含量的影响。方法选择♂性SD大鼠32只,随机分为盐水对照组、吗啡依赖组、吗啡戒断组和MK-801组,每组8只。各组在纳洛酮激发戒断后立即观察戒断症状30min,纳洛酮激发戒断后1h,处死大鼠,分离脊髓和脑干,用放射免疫法检测cAMP的含量。结果MK-801组戒断症状总分为26.06±1.98,低于吗啡戒断组61.15±3.28(P<0.01)。MK-801组脊髓cAMP含量为0.8±0.26μmol.g-1,低于吗啡戒断组(P<0.05),而与吗啡依赖组相近(P>0.05);MK-801组脑干cAMP含量为1.62±0.38μmol.g-1,低于吗啡戒断组(P<0.05),而与吗啡依赖组相近(P>0.05)。结论MK-801减轻吗啡戒断症状的机制可能与其降低大鼠中枢cAMP的水平有关。     

Cerebral oligemic hypoxia and MK-801 treatment: effect on alternation behavior in mice

It is known that glutamatergic system is one of neurotransmitter systems affected by a transiently reduced oxygen supply. The aim of the present study was to examine the effects of MK-801, a noncompetitive NMDA receptor antagonist, on spontaneous alternation in mice exposed to cerebral oligemic hypoxia. Spontaneous alternation behavior and locomotor activity were evaluated using the Y-maze task. Transient cerebral oligemia was induced by bilateral clamping of carotid arteries (BCCA) for 30 min under pentobarbital anesthesia. MK-801 was injected 48 h after BCCA or sham surgery, 30 min before the test session. Treatment with MK-801 (0.1 mg/kg ip) impaired spontaneous alternation both in sham-operated and BCCA mice. MK-801 (0.1 mg/kg ip) significantly enhanced the locomotion of mice. The effects of MK-801 were not exacerbated by BCCA. These results show that cerebral oligemic hypoxia induced by BCCA does not change alternation behavior of mice treated with MK-801.     

Effects of MK-801 and nicotine combinations on memory consolidation in CD1 mice

RATIONALE: Recent experiments have shown that pre-trial administrations of nicotine to rats tested in a 16-arm radial maze attenuated the MK-801-induced deficit in both working and reference memory performance. Memory consolidation can be influenced in laboratory animals, by post-training administration of drugs. OBJECTIVE: In the present study we have investigated the effects on memory consolidation of CD1 mice exerted by: a) the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]cyclo-hepten-5, 10-imine-maleate] b) nicotine, and c) combinations of MK-801 and nicotine. METHODS: Different groups of mice were injected intraperitoneally (IP) with the single drugs and with their combinations, immediately after training in a passive avoidance task. Additional groups of animals were also injected 2 h post-training with the highest effective dose of MK-801 (0.3 mg/kg), with the highest effective dose of nicotine (0.5 mg/kg) or with the combination of an otherwise ineffective dose of MK-801 (0.1 mg/kg) with the highest effective dose of nicotine, respectively. Their performances were compared with those of mice injected with saline, with the vehicle of nicotine and with the other treatment combinations, respectively RESULTS: The results showed that MK-801 exerted deleterious effects, while nicotine exerted facilitatory effects on mice performances. Further, an otherwise ineffective dose of MK-801 (0.1 mg/kg) antagonized the facilitatory effects of nicotine (0.25 and 0.5 mg/kg). In the 2 h post-training injected groups the treatments were ineffective, showing that the immediate post-training drug administrations affected memory consolidation processes. CONCLUSIONS: In conclusion, from the present research, it is evident that NMDA glutamate and nicotinic acetylcholine receptor systems interact in modulating memory consolidation in CD I mice.     

A preliminary study of the levels of testis oxidative stress parameters after MK-801-induced experimental psychosis model: protective effects of CAPE

We evaluated the effects of caffeic acid phenethyl ester (CAPE) on antioxidant enzyme levels and histopathologic changes in dizocilpine (MK-801) induced schizophrenic rat testis. A total of 30 adult male Wistar-Albino rats were divided into three groups. Group-I was used as control. Rats in the Group-II were intraperitoneally injected with MK-801, whereas those in Group-III were intraperitoneally injected with CAPE in addition to MK-801. The testes were collected for biochemical and histopathological examinations. Antioxidant enzyme activities, malondialdehyde, protein carbonyl and nitric oxide levels in testicular tissues were analyzed with spectrophotometric methods. Induction of schizophrenia resulted in a significant oxidative stress by increasing the levels of antioxidant enzymes. Tissue malondialdehyde and protein carbonyl levels were also increased. Treatment with CAPE led to significant decrease in oxidative injury. Administration of CAPE reduced the detrimental histopathologic changes caused by MK-801. The results showed that experimentally induced schizophrenia caused oxidative stress in testes of rats and treatment with CAPE reduced these harmful effects.