maFGF对慢性衰老大鼠脑组织中ATP酶活力的影响

目的观察改构型酸性成纤维细胞生长因子(maFGF)对D-半乳糖致衰老大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力的影响,探讨maFGF抗衰老的机制。方法选择成年Wistar大鼠40只,采用皮下注射D-半乳糖建立衰老模型,衰老模型成功后随机分为衰老对照组、NS对照组和maFGF治疗组。另10只不注射D-半乳糖作为正常对照组。maFGF治疗组按12μg/kg剂量肌内注射,1次/d,共14 d,NS对照组肌肉注射与maFGF治疗组相同容量的生理盐水,1次/d;衰老对照组不作任何干预。各组大鼠到相对应的时间点取出各组大鼠脑组织,测定脑组织匀浆中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力。结果与正常对照组相比,衰老对照组大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力均明显著降低(P<0.01);maFGF治疗组脑组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于衰老对照组、NS对照组(P<0.05)。结论 maFGF能升高衰老大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,对衰老大鼠脑损伤有一定保护作用。     

改构型酸性成纤维细胞生长因子对衰老模型大鼠自由基与脂质过氧化物的影响*

背景：有研究表明改构型酸性成纤维细胞生长因子是多功能生长因子,但其抗衰老作用至今尚未见报道。 目的：观察改构型酸性成纤维细胞生长因子对D-半乳糖致衰老大鼠脑组织、肝组织及血清中超氧化物歧化酶活力、丙二醛含量和抑制羟自由基能力的影响。 方法：选择成年Wistar大鼠皮下注射D-半乳糖建立衰老模型,建模成功后随机分为模型组、生理盐水对照组和改构型酸性成纤维细胞生长因子治疗组,另设正常对照组。改构型酸性成纤维细胞生长因子组按12 µg/kg剂量肌肉注射改构型酸性成纤维细胞生长因子,生理盐水对照组肌肉注射等量的生理盐水,模型组不作干预。 结果与结论：与模型组和生理盐水对照组相比,改构型酸性成纤维细胞生长因子治疗组脑组织、肝组织及血清中超氧化物歧化酶活力和抑制羟自由基能力均显著升高(P < 0.01或P < 0.05),丙二醛含量均显著降低(P < 0.01或P < 0.05)。结果证实,改构型酸性成纤维细胞生长因子可通过降低自由基,提高机体的抗氧化能力来发挥延缓衰老的作用。     

异丙酚对大鼠脑缺血再灌注损伤线粒体能量代谢的影响

目的 探讨静脉麻醉药异丙酚对脑缺血再灌注损伤模型大鼠的神经保护作用.方法 SD大鼠48只按随机数字表法分为假手术组、模型组、50 mg/kg异丙酚和100 mg/kg异丙酚组,每组12只.后3组大鼠均制备脑缺血(2 h)再灌注(24 h)模型,恢复灌注后分别经腹腔内注射等体积生理盐水和50、100 mg/kg异丙酚.再灌注24 h后对大鼠进行神经功能缺损评分,应用TTC染色观察脑梗死的范围,化学比色法检测脑组织线粒体琥珀酸脱氢酶(SDH)、Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶活性的改变.结果 与模型组比较,50、100mg/kg异丙酚组大鼠神经功能缺损评分较低,脑组织线粒体SDH、Na+-K+-ATP酶、Ca2+Mg2+-ATP酶活性增高,差异有统计学意义(P＜0.05);与50mg/kg异丙酚组[(45.9±25.1)U/mg pro,(5.24±0.85)分]比较,100mg/kg异丙酚组SDH活性[(96.1±20.8)U/mgpro]较高,神经功能缺损评分(4.40±0.79)较低,差异有统计学意义(P＜0.05).结论异丙酚对脑缺血再灌注损伤大鼠具有神经保护作用,促进线粒体SDH、Na+-K+-ATP酶、Ca2+Mg2+-ATP酶活性的恢复、保护线粒体功能是其机制之一.     

桃仁红花煎剂对大鼠缺血再灌注后脑组织的保护作用

目的研究桃仁红花煎剂对大鼠局灶性脑缺血再灌注后脑组织的影响。方法 45只雄性SD大鼠随机平均为给药组、模型组和对照组。采用线栓法阻塞大鼠右侧大脑中动脉,使其缺血2h后再灌注24h建立局灶性脑缺血再灌注模型。术前2h和术后3、12h分3次灌胃给予桃仁红花煎剂,总剂量是40g/kg。通过神经行为评分评定大鼠神经功能变化,按干湿重法测定脑含水量,用氯化三苯基四氮唑法测定脑梗死范围,分光光度法测定缺血区脑组织中Na+-K+-ATP酶和Ca2+-ATP酶的活性。结果在缺血再灌注3h和24h后,给药组神经行为评分明显高于模型组(P<0.05)。缺血再灌注24h,给药组脑含水量和脑梗死体积明显少于模型组(P<0.05);给药组缺血脑皮层中Na+-K+-ATP酶和Ca2+-ATP酶活性明显高于模型组(P<0.05)。结论桃仁红花煎剂对大鼠缺血再灌注后脑组织有保护作用,其机制可能与其增强Na+-K+-ATP酶和Ca2+-ATP酶的活性、减轻脑水肿有关。     

原花青素对大鼠脑缺血再灌注损伤代谢障碍的影响

目的 探讨原花青素(PC)对大鼠脑缺血再灌注损伤代谢障碍的影响.方法 采用Zea-Longa线栓法制备大鼠局灶性脑缺血再灌注模型.术前0.5 h和脑缺血2 h时给予大鼠PC溶液50、100、200 mg/kg,假手术组和模型组分别给予等量的生理盐水.观察不同剂量PC溶液对大鼠脑缺血再灌注后神经功能状态、脑组织含水量及乳酸含量、能量代谢酶(Na+-K+-ATP酶和Ca2+-ATP酶)活性的影响.结果 PC中、高剂量组神经功能行为学评分和脑组织含水量显著低于模型组(P＜0.05).PC低、中、高剂量组脑组织乳酸含量显著低于模型组(P＜0.05).PC中、高剂量组Na+-K+-ATPase活性较模型组升高(P＜0.05).PC高剂量组Ca2+-ATPase活性较模型组有所增高(P＜0.05).结论 PC可通过减轻脑水肿、改善脑组织的代谢障碍而发挥脑保护作用.     

maFGF对衰老大鼠脑组织SOD、MDA和羟自由基及神经细胞凋亡的影响

目的观察改构型酸性成纤维细胞生长因子(maFGF)对D-半乳糖致衰老大鼠脑组织SOD活力、MDA含量和羟自由基含量及神经细胞凋亡的影响,探讨maFGF对慢性衰老大鼠的抗衰老作用。方法选择成年Wistar大鼠48只,采用皮下注射D-半乳糖建立衰老模型,衰老模型成功后随机分为衰老模型组、生理盐水(NS)对照组和maFGF治疗组。另16只不注射D-半乳糖作为正常对照组。各组大鼠到相对应的时间点取出脑组织,测定脑组织中SOD活力、MDA含量和抑制羟自由基能力;TUNEL法测定大鼠大脑皮质神经细胞凋亡数目。结果衰老模型组大鼠脑组织SOD活力显著降低,MDA含量和羟自由基含量升高,皮质神经细胞凋亡数明显增多;经过用maFGF治疗慢性衰老大鼠后脑组织SOD活力显著升高,MDA含量和羟自由基含量均显著降低,皮质神经细胞凋亡数明显减少。结论 maFGF起到降低自由基,提高脑组织的抗氧化能力,减少皮质神经细胞凋亡数量,具有抗衰老     

碱性成纤维细胞生长因子对脑出血大鼠大脑组织、海马SOD和MDA的影响

目的 观察碱性成纤维细胞生长因子对大鼠脑出血后出血灶周围脑组织和出血侧海马超氧化物歧化酶(SOD)、丙二醛(MDA)的影响.方法 采用脑内注射胶原酶建立大鼠脑出血模型,脑出血模型建立成功的动物分为模型组、生理盐水对照组和碱性成纤维细胞生长因子治疗组,每组又分为1、3、7d 3个时间点.碱性成纤维细胞生长因子治疗组按8 μg/kg剂量肌内注射.然后检测各组血肿周围脑组织和出血侧海马中SOD活力和MDA含量.结果 (1)碱性成纤维细胞生长因子治疗组与生理盐水对照组比,3d、7d时血肿周围脑组织SOD活力均明显增高(P＜0.05),而3d和7d时血肿周围脑组织MDA含量均明显下降(P＜0.05).(2)碱性成纤维细胞生长因子治疗组与生理盐水对照组比,7d时出血侧海马SOD活力增高(P＜0.05),而7 d时出血侧海马MDA含量下降(P＜0.05) .结论 碱性成纤维细胞生长因子能提高大鼠脑出血后大脑脑组织和海马SOD活力,降低MDA含量.     

骨骼肌肌浆网Na+，K+-ATP酶和Ca2+-ATP酶活性在不同训练条件下的变化

背景：Na+,K+-ATP酶和Ca2+-ATP酶在物质运送、能量转换以及信息传递方面具有重要作用。肌浆网在肌肉兴奋-收缩耦联过程中起关键作用,与运动性骨骼肌疲劳的发生密切关。 目的：通过建立SD大鼠有氧和无氧训练模型,观察不同训练负荷条件对大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶活性的影响。 方法：参照Bedford TG标准,建立有氧和无氧运动大鼠跑台训练模型,有氧运动组采用递增负荷训练,无氧运动组采用高速间歇训练,正常对照组大鼠正常笼内生活,不运动。各组动物训练结束后用超速离心法提取大鼠骨骼肌肌浆网,紫外分光光度计检测大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性。 结果与结论：训练4周后,两个运动组大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性逐渐升高(P < 0.05);训练6周,仅有氧运动组升高(P < 0.05),无氧运动组则活性降低(P < 0.05)。结果提示有氧训练更有利于保护大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性,但需要一定的时间累积。     

有氧运动对大鼠骨骼肌线粒体Na+，K+-ATP酶和Ca2+-ATP酶及线粒体肿胀的影响

背景：研究表明有氧运动可提高线粒体功能,但在不同时期的作用特点还不明确。 目的：观察不同周期有氧运动对大鼠骨骼肌线粒体Na+,K+-ATP酶和Ca2+-ATP酶以及线粒体肿胀的影响。 方法：将SD大鼠随机分为正常对照组,有氧运动2,4和6周组。正常对照组不进行有氧运动,其余3组则参照BedfordTG标准,采用跑台运动方式,建立有氧运动模型进行相应的运动周期锻炼。测定各组大鼠骨骼肌线粒体Na+,K+-ATP酶和Ca2+-ATP酶的活性以及线粒体肿胀程度。 结果与结论：有氧运动2周组各指标与对照组比较无差异。有氧运动4和6周组线粒体Na+,K+-ATP酶、Ca2+-ATP酶活性均增高(P < 0.05),线粒体肿胀程度降低(P < 0.05)。实验结果表明,有氧运动可保护线粒体Na+,K+-ATP酶、Ca2+-ATP酶的活性,提高线粒体功能,但需要一定的时间积累。     

高温对重型颅脑损伤后乳酸、Na+-K+-ATP酶和脑水肿的影响

目的 探讨大鼠重型颅脑损伤后高温对伤灶区脑组织乳酸、Na+-K+-ATP酶和脑水肿的影响.方法 90只SD大鼠随机分为假手术组、颅脑损伤组、伤后高温组,每组又按处死时间点(伤后4 h、1 d、3 d、5 d和7 d)分为五个亚组,每亚组6只.取伤灶区脑组织测含水量、乳酸含量和Na+-K+-ATP酶活性并行电镜检查.结果 高温组脑组织含水量和乳酸含量在伤后各时间点均显著高于颅脑损伤组和假手术组(P＜0.05),而Na+-K+-ATP酶含量显著低于颅脑损伤组和假手术组(P＜0.05),电镜检查发现高温组神经细胞肿胀、血脑屏障破坏程度较颅脑损伤组明显加重.结论 颅脑损伤后高温增加脑组织乳酸生成,同时Na+-K+-ATP酶活性下降,脑水肿加重,故在颅脑损伤后应保持体温在正常范围内,避免体温升高.     

肠淋巴再灌注加重肠系膜上动脉闭塞性休克大鼠的脑损伤*

目的：观察肠淋巴再灌注（MLR）对肠系膜上动脉闭塞性（SMAO）休克大鼠脑组织形态学的影响；从氧自由基、一氧化氮、中性粒细胞、膜泵、能量代谢等方面揭示其机制。方法：24只Wistar雄性大鼠均分为4组：Sham组，仅麻醉与手术；MLR组，夹闭肠系膜淋巴管（ML）1h，再灌注2h；SMAO组，夹闭肠系膜上动脉（SMA）1h，再灌注2h；MLR+SMAO：夹闭ML和SMA1h，再灌注2h。于再灌注2h后，选择固定位置留取脑组织，制备病理切片，观察形态学；同时制备脑组织匀浆，用于检测LA、MDA、SOD、NO、NOS、MPO、ATPase及ATP。结果：Sham与MLR组大鼠脑组织结构基本正常；SMAO组大鼠可见神经元有坏死、变性，偶见肿胀；MLR+SMAO组神经元损伤情况较SMAO组重。MLR与Sham组脑组织匀浆各项指标均无统计学差异；SMAO与MLR+SMAO组脑匀浆MDA、NO、LA含量、NOS与MPO活性均显著高于MLR与Sham组，且MLR+SMAO组脑匀浆MDA、NO含量、NOS与MPO活性均显著高于SMAO组；SMAO组脑匀浆SOD、Na+- K+-ATPase活性显著低于Sham与MLR组、Mg2+-ATPase活性、ATP含量显著低于MLR组；MLR+SMAO组脑匀浆的SOD、Na+- K+-ATPase、Ca2+-ATPase、Mg2+-ATPase及Ca2+-Mg2+- ATPase活性均显著低于Sham与MLR组，且Ca2+-ATPase、Mg2+-ATPase及Ca2+-Mg2+-ATPase活性、ATP含量均显著低于SMAO组。结论：MLR加重SMAO休克大鼠的脑损伤，其机制可能与MLR加重或增加脑组织氧自由基损伤、NO合成与释放、中性粒细胞扣押、能量代谢障碍及降低脑组织细胞膜泵活性等因素有关。     

Hyperbaric oxygen treatment induces dynamic ATPase activity changes in the rat brain following transient global cerebral ischemia-reperfusion*

BACKGROUND： Energy depletion, induced by ischemia or hypoxia, is one of the first events in neuronal injury. OBJECTIVE： To investigate the dynamic changes of Na^＋-K^＋-ATPase and Ca^2＋-ATPase activity in the rat brain following transient global cerebral ischemia-reperfusion （IR）, as well as the effects of hyperbaric oxygen （HBO） treatment. DESIGN, TIME AND SETTING： A randomized and controlled animal study was performed in the Department of Biochemistry and Molecular Biology, Capital Medical University between February and December 2006. MATERIALS： Clean-grade, female, Sprague Dawley rats were provided by the Animal Research Department of Capital Medical University （License number： SYXK11-00-0047）. Na^＋-K^＋-ATPase and Ca^2＋-ATPase kits were provided by Nanjing Jiancheng Bioengineering Institute （Nanjing, China）. A hyperbaric oxygen chamber （DWC150-300） was supplied by Shanghai 701 Medical Oxygen Chamber Factory （Shanghai, China）. METHODS： Sixty-three rats were randomly divided into nine groups： sham operated group （sham-O） as control, groups of IR, and groups treated with hyperbaric oxygen （HBO） after IR. Animal from the IR and HBO groups were sacrificed after four different survival intervals of 6, 24, 48 and 96 hours, respectively. Each group consisted of seven rats. The rats of HBO groups were placed into the hyperbaric chamber. The HBO chamber was flushed with pure oxygen for 5 minutes, followed by a gradual rise in pressure over 5 minutes and stabilization at 0.2 MPa. Then, pure oxygen was supplied for 45 minutes in stabilized pressure, followed by gradually reduced pressure over 15 minutes. The rats of the 6-h HBO group were placed into the HBO chamber following reperfusion for 3 hours on the first day, which was repeated on three consecutive days, always at the same time. Rats in the sham-O group and IR group remained under normal atmospheric pressure. MAIN OUTCOME MEASURES： The Na^＋-K^＋-ATPase and Ca^2＋-ATPase activity in rat brain homogenate     

Mesenteric lymph reperfusion may exacerbate brain injury in a rat model of superior mesenteric artery occlusion shock

BACKGROUND:The intestinal lymphatic pathway and intestinal ischemia/reperfusion are mainly involved in mesenteric lymph duct ligation or drainage; moreover,intervention by reducing the lymph liquid reflux might relieve lung and other organ dysfunction induced by intestinal ischemia/reperfusion; however,research addressing mesenteric lymph reperfusion (MLR) and brain injury has not yet to be reported.OBJECTIVE:To observe the effect of MLR on brain tissue in a rat model of superior mesenteric artery occlusion (SMAO) shock,and to explore the molecular mechanism of MLR.DESIGN,TIME AND SETTING:A randomized,controlled,animal experiment at a neuro-pathophysiology level was performed at the Institute of Microcirculation,Hebei North University; Department of Pathophysiology,Basic Medical College; Department of Pathology,the First Hospital of Hebei North University between December 2007 and March 2009.MATERIALS:Adenosine triphosphate (ATP) standard was provided by the National Institute for the Control of Pharmaceutical and Biological Products; lactic acid (LA),superoxide dismutase (SOD),malonaldehyde (MDA),nitrogen monoxidum (NO),nitric oxide synthase (NOS),myeloperoxidase (MPO) and ATPase assay kits were provided by Nanjing Jiancheng Bioengineering Institute,China.METHODS:A total of 24 male Wistar rats were randomly divided into four groups.In the sham-surgery group (n = 6),both the mesenteric lymph duct and the superior mesenteric artery were not blocked; in the MLR group (n = 6),the mesenteric lymph duct was occluded for 1 hour followed by 2-hour reperfusion; in the SMAO group (n = 6),the superior mesenteric artery was occluded for 1 hour followed by 2-hour reperfusion; in the MLR + SMAO group (n = 6),both the mesenteric lymph duct and superior mesenteric artery were occluded for 1 hour followed by 2-hour reperfusion.MAIN OUTCOME MEASURES:Mean arterial blood pressure prior to and following ischemia/reperfusion; brain tissue morphology levels of LA,MDA,SOD,NO,NOS,MPO,ATPase and ATP following reperfusion.RESULTS:MLR did not cause changes in mean arterial blood pressure,brain tissue morphology,LA,MDA,NO,ATP,SOD,NOS,MPO and ATPase.However,SMAO caused a rapid decrease and gradual increase of mean arterial blood pressure.Neuronal necrosis,degeneration and swelling were observed in brain tissue.Contents of MDA,NO,LA and ATP as well as activities of NOS and MPO were significantly increased (P< 0.05),but activities of SOD and Na+-K+-ATPase were significantly decreased (P < 0.05).MLR aggravated neuronal damage in a rat model of SMAO shock.Following MLR,mean arterial blood pressure was significantly decreased (P < 0.05),contents of MDA and NO as well as activities of NOS and MPO were significantly increased (P <0.05),but activities of Ca2+-ATPase,Mg2+-ATPase and Ca2+-Mg2+-ATPase as well as ATP content were significantly decreased (P< 0.05).CONCLUSION:MLR aggravates brain injury in a rat model of SMAO shock,which correlates with oxygen-derived free radical injury,NO synthesis and release,sequestration of neutrophilic granulocytes,decreasing activity of cell membrane pumps and energy metabolism dysfunction.Pathogenesis of the intestinal lymphatic pathway should be thoroughly investigated to prevent ischemia/reperfusion injury.     

Cromakalin pretreatment affects mitochondrial structure and function in a rat model of ischemia/reperfusion injury

BACKGROUND: Mitochondrial structural changes and energy dysmetabolism frequently occur subsequent to cerebral ischemia. Adenosine triphosphate (ATP)-sensitive potassium channel openers exhibit protective effects on cerebral ischemia/reperfusion injury. OBJECTIVE: To validate the effects of cromakalin on mitochondrial structure and function in ischemic penumbra brain tissue in a rat model of middle cerebral artery occlusion (MCAO). DESIGN, TIME AND SETTING: The present single-factor analysis of variance, randomized, controlled, animal experiment was performed at the Institute of Brain Science, Affiliated Hospital of Qingdao University Medical College between October 2007 and March 2008. MATERIALS: Forty male, Wistar rats were randomly divided into four groups, with 10 rats per group: sham-operated, MCAO, MCAO ATP-sensitive potassium channel opener (cromakalin), and MCAO eromakalin ATP-sensitive potassium channel blocking agent (glibenclamide). METHODS: Focal cerebral ischemia/reperfusion injury was induced by MCAO in all groups except the sham-operated group. The MCAO cromakalin group was administered 10 mg/kg cromakalin (i.p.) prior to MCAO induction. The MCAO cromakalin glibenclamide group received an injection of 10 mg/kg cromakalin (i.v.), and subsequently an injection of 10 mg/kg cromakalin (i.p.) prior to MCAO induction. MAIN OUTCOME MEASURES: At 24 hours after cerebral ischemia/reperfusion injury, cellular apoptosis was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick-end labeling technique. Cytochrome C expression was measured by immunohistochemistry. In addition, mitochondrial swelling, membrane fluidity, membrane phospholipid and malonaldehyde (MDA) contents, as well as Na -K -ATPase, Ca2 -ATPase, and superoxide dismutase (SOD) activities were determined. RESULTS: Compared with the sham-operated group, the three ischemia groups exhibited significantly elevated mitochondrial MDA content, reduced membrane phospholipid and ATP contents, down-regulated membrane fluidity, and reduced Na -K -ATPase, Ca2 -ATPase, and SOD activities (P < 0.05-0.01 ). In the MCAO eromakalin group, the number of apoptotic cells decreased, and cytochrome C expression, as well as MDA content, were reduced. However, ATP content and Na -K -ATPase, Ca2 -ATPase, and SOD activities significantly increased compared with the MCAO group (P < 0.05-0.01 ). Glibenclamide noticeably antagonized cromakalin protection of mitochondria.CONCLUSION: Pretreatment with the ATP-sensitive potassium channel opener cromakalin increased mitochondrial Na -K -ATPase, Ca2 -ATPase, and SOD activities, decreased neuronal apoptosis, and inhibited cytochrome C expression following MCAO.     

The effects of the pre-treatment of intravenous nimodipine on Na(+)-K+/Mg+2 ATPase, Ca+2/Mg+2 ATPase, lipid peroxidation and early ultrastructural findings following middle cerebral artery occlusion in the rat

Excessive calcium influx has been implicated in the pathophysiology of ischemic cerebral damage. The effects of nimodipine, a calcium antagonist, on the Na(+)-K+/MG+2 ATPase activity, Ca+2/Mg+2 ATPase, lipid peroxidation, and early ultrastructural findings were examined at the acute stage of ischemia in the rat brain. Ischemia was produced by permanent unilateral occlusion of the middle cerebral artery. In Group I, the rats which had no ischemia and not received medication were used for determining Na(+)-K+/Mg+2 ATPase, Ca+2/Mg+2 ATPase, the extent of lipid peroxidation by measuring the malondialdehyde content and normal ultrastructural findings. In Group II, the rats which had only subtemporal craniectomy without occlusion and received saline solution were used for determining the effect of the surgical procedure on the biochemical indices and ultrastructural findings. In Group III, the rats received saline solution following the occlusion in the same amount of nimodipine and in the same duration as used in Group IV. In Group IV, nimodipine pre-treatment 15 min before occlusion (microgram kg-1 min-1 over a 10 min period) was applied i.v. Na(+)-K+/Mg+2 ATPase and Ca+2/Mg+2 ATPase activities decreased significantly and promptly as early as 10 min and remained at a lower level than the contralateral hemisphere in the same group and at the normal level in Group I. Nimodipine pre-treatment immediately attenuated the inactivation of Na(+)-K+/Mg+2 ATPase (p < 0.05) but there was no change on Ca+2/Mg+2 ATPase activity (p < 0.05). Malondialdehyde content increased significantly in Group III following ischemia as early as 30 min. Nimodipine pre-treatment decreased the malondialdehyde level in Group IV (p < 0.05). This study supports the possibility that nimodipine pre-treatment effects the membrane stabilizing properties via inhibiting the lipid peroxidation and subsequently restoring some membrane bound and lipid dependent enzymes' activity such as Na(+)-K+/Mg+2 ATPase and the ultrastructural findings.     

Chlordecone toxicity: effect of withdrawal of treatment on ATPase inhibition

Adult male Sprague-Dawley rats were treated P.O with 10 mg/kg/day chlordecone for 10 days. Five rats from control group receiving corn oil and five rats from chlordecone group were sacrificed for tissue preparations. The remaining rats in chlordecone group were withdrawn from treatment and left in cages for 45 days. At 15, 30 and 45 days after withdrawal, 5 rats from each group with equal number of controls were sacrificed. Brain, liver and kidney were removed and subcellular fractions were prepared. Na+-K+, oligomycin-sensitive and oligomycin-insensitive Mg2+ ATPases were determined. Rats treated with chlordecone for 10 days showed a significant reduction of Na+-K+ ATPase activity in brain and kidney. The decreased enzyme activity in kidney but not in brain returned to normal within 15 days of treatment withdrawal. In brain the enzyme activity stayed at reduced level throughout the experimental period. Oligomycin-sensitive Mg2+ ATPase activity in all the tissues was decreased significantly in chlordecone treated rats. The enzyme activity returned to normal levels in all tissues gradually by 30 days of treatment withdrawal. Oligomycin-insensitive Mg2+ ATPase activity was not decreased in any tissue by chlordecone treatment. These results suggest that chlordecone effects on ATPase system are reversible except for Na+-K+ ATPase in brain.     

缺血后处理对糖尿病大鼠局灶性脑缺血再灌注损伤线粒体的影响

目的观察缺血后处理(I-Post)对糖尿病大鼠局灶性脑缺血再灌注损伤线粒体超微结构和功能的影响,探讨I-Post诱导的脑保护的可能机制。方法采用链脲佐菌(STZ)腹腔注射建立糖尿病大鼠模型,在此基础上通过线栓法建立大鼠大脑中动脉阻塞/再灌注模型。SD糖尿病大鼠随机分为4组(n=10),空白对照组、假手术组、缺血再灌注组(I/R组)、缺血后处理组(I-Post组)。于缺血90min再灌注6h后电镜下观察线粒体超微结构、测定缺血侧脑组织线粒体中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、Na+/K+-ATPase和Ca2+-ATPase活性。结果缺血后处理能明显减轻I/R引起的线粒体超微结构的损伤,提高线粒体SOD、GSH-Px、Na+/K+-ATPase和Ca2+-ATPase的活性(P<0.05或0.0),降低MDA的含量(P<0.05)。结论线粒体可能在I-Post诱导的脑保护中起关键性作用,I-Post诱导的脑保护机制可能与SOD、Na+/K+-ATP酶、Ca2+-ATP酶和GSH-Px活性增加有关。