环孢素A对DSS结肠炎小鼠肠黏膜通透性影响及其机制的研究

目的探讨环孢素A(CsA)对葡聚糖硫酸钠(DSS)结肠炎小鼠肠黏膜通透性的影响及作用机制。方法 C57BL/6J小鼠(6～8周龄、体质量20 g±2 g、♂),实验分为正常对照组(饮用无菌蒸馏水+腹腔注射0.9%NS)、DSS模型组(DSS溶液+腹腔注射0.9%NS)、环孢素A组(DSS溶液+腹腔注射CsA)。小鼠自由饮用5%DSS溶液1周制备结肠炎模型,环孢素A(0.025 mg.g-1)腹腔注射给药,每天1次,共7 d。每日行DAI评分,实验结束后取结肠进行HE染色评分,结肠匀浆检测MPO活性、TNF-α、IFN-γ、IL-13和IL-17水平,另取小鼠小肠黏膜进行透射电镜检查和肌球蛋白轻链激酶(MLCK)活性测定,采用Evans blue和异硫氰酸荧光素-葡聚糖(FITC-D)方法检测小肠黏膜通透性。结果与正常对照组比较,模型对照组小鼠1周后出现明显体重减轻、便血和腹泻,DAI评分和HI评分增高,同时结肠黏膜MPO活性明显增高。电镜检查小鼠回肠黏膜上皮绒毛萎缩、排列不规则,细胞间连接复合体缩短、变宽,细胞间隙扩大,小肠黏膜通透性增高。小鼠结肠匀浆中TNF-α、IFN-γ、IL-13和IL-17水平均有不同程度增高,小肠黏膜中MLCK活性明显增高。与DSS模型组比较,环孢素A组小鼠DAI评分和HI评分明显降低,结肠黏膜MPO活性减低,回肠黏膜上皮细胞绒毛排列整齐,小肠黏膜通透性降低,小肠黏膜MLCK活性和结肠匀浆中TNF-α、IFN-γ、IL-13和IL-17水平均有不同程度降低。结论环孢素A具有明显的抗DSS小鼠结肠炎作用,机制可能与通过调控MLCK表达,改善肠黏膜通透性有关。     

不同NSAIDs肠病模型中肠黏膜通透性的比较研究

目的探讨不同NSAIDs肠病模型中肠黏膜通透性改变的研究。方法选用不同NSAIDs(阿司匹林、吲哚美辛、双氯芬酸钠)制备小鼠NSAIDs肠病模型。其中阿司匹林组(500 mg.kg-1)、吲哚美辛组(5 mg.kg-1)、双氯芬酸钠(10 mg.kg-1)灌胃给药3 d。在此基础上,进行不同剂量双氯芬酸钠不同时间灌胃给药。实验结束后取小鼠小肠进行Evans-blue通透性检测,并计算小肠溃疡数目。结果在不同NSAIDs肠病模型中,阿司匹林组小鼠小肠黏膜未见明显溃疡,小肠黏膜通透性轻度升高(621.1±114.2 vs 460.6±89.7μg.g-1),吲哚美辛组小鼠小肠黏膜损害明显,小肠溃疡明显增多(8.2±1.9 vs 0),小肠通透性显著升高(2132.0±315.7 vs 460.6±89.7μg.g-1),双氯芬酸钠组小肠黏膜损伤和小肠黏膜通透性升高均较吲哚美辛组减轻。随着双氯芬酸钠给药剂量增加和给药时间延长,小鼠小肠黏膜损害和肠黏膜通透性增高越明显。结论在不同NSAIDs肠病模型中,阿司匹林组小鼠小肠损害轻,吲哚美辛组小肠损伤严重,双氯芬酸钠2.5 mg.kg-1灌胃3 d可引起小肠黏膜通透性和肠黏膜损害,适用于NSAIDs肠病模型的研究。     

Balsalazine decreases intestinal mucosal permeability of dextran sulfate sodium-induced colitis in mice

Aim： To investigate the effect of balsalazine treatment on intestinal mucosal permeability in dextran sulfate sodium （DSS）-induced colitis and to determine the mechanism of the balsalazine-induced changes.
Methods： Experimental colitis was induced in C57BL/6J mice by the administration of 5% DSS. Balsalazine was administered intragastrically at doses of 42, 141, and 423 mg/kg. The disease activity index （DAI） score was evaluated and colon tissue was collected for the assessment of histological changes. The amount of malondialdehyde （MDA） in the colon was determined, along with the activity of myeloperoxidase （MPO）, superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px）. Mucosa from the small intestine was collected to determine the levels of tumor necrosis factor （TNF）-α and interferon （IFN）-γ. The mucosa was ultrastructurally examined with transmission electron microscopy and intestinal permeability was assayed using Evans blue.
Results： Balsalazine was found to reduce the DAI score and the histological index （HI） score, decrease the MDA content and the activity of MPO, and increase the activity of SOD and GSH-Px in colitis mice. At the same time, balsalazine ameliorated microvillus and tight junction structure, resulting in a decrease in the amount of Evans blue permeating into the intestinal wall and the levels of TNF-α and IFN-γ in colitis mice.
Conclusion： In colitis mice, the anti-colitis effect of balsalazine results in a decrease in intestinal mucosal permeability. The mechanism of this effect is partly associated with balsalazine＇s antioxidative and anti-inflammatory effects.     

丁酸钠对大鼠放射性肠损伤的保护作用

目的 构建放射性肠损伤大鼠模型,观察丁酸钠对肠损伤的保护作用。方法 SPF级成年SD大鼠90只,分为对照组、模型组和丁酸钠组,每组各30只。除对照组外,造模大鼠暴露腹部上至胸骨剑突下至耻骨联合,VarianClinic600直线加速器6MV高能X射线定位照射,其余部位用5 cm厚铅砖屏蔽,单次照射,总吸收剂量10 Gy。造模前3 d,丁酸钠组SD大鼠ig 40 mg/kg丁酸钠,1次/d,照射后继续给药3 d,对照组和模型组ig生理盐水。多普勒血流仪检测肠黏膜血流量;FITC荧光标记的葡聚糖检测肠黏膜血管通透性;ELISA法检测外周血浆二胺氧化酶（DAO）活性和肠组织一氧化氮（NO）水平;肠黏膜组织切片HE染色,显微镜下测量肠黏膜绒毛高度、黏膜厚度。结果 丁酸钠组造模成功率为83.3%,显著低于模型组的100%（P<0.05）。模型组和丁酸钠组肠黏膜血流量、黏膜绒毛高度和黏膜厚度显著低于对照组（P<0.05、0.01）,丁酸钠组肠黏膜血流量、黏膜绒毛高度和黏膜厚度显著高于模型组（P<0.05）。模型组和丁酸钠组肠黏膜葡聚糖、DAO和NO显著高于对照组（P<0.05）,丁酸钠组肠黏膜葡聚糖、DAO和NO显著低于模型组（P<0.05）。结论 丁酸钠可以增加放射性肠损伤大鼠肠黏膜血流量,降低NO表达,发挥肠黏膜保护作用。     

地塞米松对双氯芬酸钠肝损伤的保护作用

目的探讨地塞米松(dexamethasone,Dex)对双氯芬酸钠诱导的大鼠药物性肝损伤的保护作用及部分机制。方法大鼠随机分为正常对照组、模型对照组、Dex(10 mg.kg-1)给药组。Dex(10 mg.kg-1)腹腔注射,1 h后腹腔注射双氯芬酸钠100 mg.kg-1,24 h后检测ALT和AST活性、测定肝匀浆中MDA、GSH含量和GSH-Px、SOD活性,观察肝组织病理学变化,并测肝线粒体膜电位、线粒体肿胀度、NADH水平、SDH及ATPase活性。结果模型对照组血清ALT、AST升高,光镜下可见肝小叶内肝细胞片状坏死,肝匀浆MDA含量升高,GSH、GSH-Px和SOD含量降低,肝线粒体NADH含量、SDH及ATPase活性降低。Dex可明显降低ALT、AST活性(P<0.05),减轻肝脏炎症,降低肝匀浆中MDA含量(P<0.01),升高GSH含量、GSH-Px和SOD活性以及线粒体中NADH含量、SDH及ATPase活性(P<0.01)。结论 Dex对双氯芬酸钠诱导的大鼠药物性肝损伤有保护作用,作用机制可能与减轻线粒体损伤有关。     

乳酸菌对DSS诱导的溃疡性结肠炎小鼠肠道通透性影响

目的观察乳酸菌制剂对溃疡性结肠炎(UC)小鼠肠黏膜通透性影响。方法采用葡聚糖硫酸钠(DSS)诱导小鼠UC模型。小白鼠60只分为4个组,正常对照组、模型对照组、乳酸菌1组、乳酸菌2组。乳酸菌1组、2组用菌液灌胃,正常对照组模型对照用0.9%氯化钠溶液灌胃。9 d后各组小鼠每日记录疾病活动指数(DAI)评分,观察小鼠结肠黏膜组织学改变,应用酶联免疫法检测小鼠血D-乳酸含量。结果与模型组比较,乳酸菌1组、2组小鼠DAI与组织学损伤评分(CMDI)均下降(P<0.01),血D-乳酸的含量明显降低(P<0.01),乳酸菌1组、2组各指标差异无统计学意义。结论乳酸菌制剂灌胃可降低溃疡性结肠炎小鼠结肠黏膜通透性。     

褪黑素对四氯化碳小鼠肝损伤的保护作用

目的　探讨褪黑素对四氯化碳肝毒性的保护作用。方法　给予小鼠四氯化碳（５ ｍｌ·ｋｇ － １ ） ,继后每隔６ ｈ ｉｐ 褪黑素１０ ｍ ｇ·ｋｇ － １ 。用胶原酶消化法分离小鼠肝细胞后,依次加用褪黑素（１０ － ５ ～１０ － １ １ ｍｏｌ· Ｌ－ １ ） 和四氯化碳（２０ ｍ ｍ ｏｌ· Ｌ－ １ ） 。以测定丙氨酸氨基转换酶（ Ａ Ｌ Ｔ） ,丙二醛（ Ｍ Ｄ Ａ） 和谷胱甘肽过氧化物酶活力,作为四氯化碳肝损伤的指标。用 Ｍ Ｔ Ｔ 法检测肝细胞活力。结果　四氯化碳可使小鼠血液 Ａ Ｌ Ｔ 活性和肝 Ｍ Ｄ Ａ 含量明显上升。体内应用 Ｍ Ｔ １０ ｍ ｇ·ｋｇ － １ ,则明显降低肝匀浆 Ｍ Ｄ Ａ 含量（ Ｐ＜ ００１） , 对血浆 Ａ Ｌ Ｔ 活性无明显影响。体外应用 Ｍ Ｔ（１０ － ５ ～１０ － ７ ｍｏｌ· Ｌ－ １ ） 亦可使肝细胞 Ｍ Ｄ Ａ 含量下降（ Ｐ＜ ００５） ,同时还可使肝细胞 Ａ Ｌ Ｔ 释放率下降,细胞活力上升（ Ｐ＜ ００５） 。结论　 Ｍ Ｔ 拮抗 Ｃ Ｃｌ４ 肝毒性的作用可能与其抗氧化能力有关     

梓醇对鱼藤酮致小鼠中脑和纹状体线粒体酶活性改变的改善作用

目的研究梓醇对鱼藤酮致小鼠脑组织线粒体酶活性的影响。方法昆明小鼠分别ip给予梓醇10 mg.kg-1,连续7 d后,改ip给予鱼藤酮1.5 mg.kg-1,连续28 d;或ip给予鱼藤酮1.5 mg.kg-1,连续28 d后,改ip给予梓醇10 mg.kg-1,连续7 d。取小鼠中脑和纹状体提取线粒体测定线粒体复合物酶Ⅰ、Ⅱ、Ⅱ+Ⅲ、Ⅳ、线粒体一氧化氮合酶(mtNOS)活性、线粒体膜电位以及线粒体内活性氧(ROS)。结果与正常对照组相比,鱼藤酮组中脑和纹状体线粒体复合物Ⅰ和Ⅳ活性明显下降(P<0.01),预防或治疗性地给予梓醇后活性明显上升(P<0.05);线粒体复合物Ⅱ和Ⅱ+Ⅲ活性各组间无明显差异。与正常组相比,鱼藤酮组小鼠中脑和纹状体线粒体膜电位下降(P<0.01),mtNOS活性升高(P<0.05),ROS的生成增多(P<0.05),预防或治疗性地给予梓醇后中脑和纹状体线粒体膜电位升高(P<0.01),mtNOS活性降低(P<0.05),ROS的生成减少(P<0.05)。结论梓醇可能通过恢复脑内线粒体复合物酶活性和膜电位水平、减少线粒体内ROS生成的作用而抑制鱼藤酮诱导的脑损伤。     

槲皮素等对烫伤后小鼠肠粘膜损伤的保护作用

目的　研究槲皮素、芸香苷、黄色素母酮 3种黄酮类化合物对烫伤所致小鼠肠粘膜损伤的保护作用。方法　观察小肠肠粘膜损伤指数的变化 ,检测肠粘膜中蛋白质、DNA含量变化 ,DTNB法测定肠粘膜中GSH的含量 ,并应用DNA解旋的荧光检测法测定DNA损伤程度。结果　槲皮素等三种黄酮类化合物连续 3d灌胃可不同程度的改善烫伤所致肠粘膜损伤状况 ,使肠粘膜损伤指数降低 ,蛋白质、DNA、GSH含量增加 ,DNA损伤程度减轻。其中尤以槲皮素作用较为明显。结论　槲皮素、芸香苷、黄色素母酮 3种黄酮类化合物可明显改善烫伤所致小鼠肠粘膜损伤 ,其机制可能与其抗氧化作用有关。     

A review of the protective effect of melatonin in pesticide-induced toxicity

Introduction: Pesticides are among the most important chemicals used in agriculture sector. However, their extensive use has polluted the environment and increased human vulnerability to various chronic diseases. Pesticide exposure causes genetic and epigenetic modifications, endocrine disruption, mitochondrial dysfunction and oxidative stress.

Areas covered: This review is based on the literature studies currently reported on pesticide-induced toxicity and the protective role of melatonin. Scientific databases such as PubMed, Scopus and Web of Science were searched using keywords ‘pesticide’ and ‘melatonin’ up to January 2016. Full length articles related to animal and human exposure were retrieved. A total number of 181 records were obtained, and after excluding the duplicates, 97 papers were further screened on the basis of relevance to the topic.

Expert opinion: Melatonin as a broad-spectrum antioxidant is able to penetrate cellular compartments specifically the mitochondria. It is a potent free radical scavenger with low toxicity and desirable solubility in organic and aqueous phases. We are of the opinion that melatonin is a promising agent in minimizing organ injuries induced by pesticides.     

褪黑素增强内皮细胞抗LPS损伤能力的研究

目的探讨褪黑素对体外培养的内皮细胞抗内毒素损伤的影响。方法体外培养内皮细胞,加入5mg/L脂多糖(LPS)和(或)褪黑素(0.1mmol/L)干预培养24h后,检测细胞乳酸脱氢酶释放率、丙二醛含量;应用RT-PCR检测各组细胞肿瘤坏死因子(TNF-α)转录水平的改变;噻唑蓝(MTT)法检测细胞存活率。结果 LPS刺激24h后,TNF-αmRNA表达量显著升高,细胞存活率下降、而丙二醛含量和乳酸脱氢酶释放率均增高(P<0.05);加用褪黑素后,TNF-αmRNA表达量下降,细胞存活率提高、丙二醛含量和乳酸脱氢酶释放率下降。结论褪黑素可增强体外培养内皮细胞的抗LPS损伤能力     

肝硬化患者肠黏膜通透性改变与肝功能分级的关系研究

目的探讨肝硬化患者肠黏膜通透性改变与肝功能分级的关系。方法以2020年11月至2022年4月经郑州市第六人民医院医学检验科收治肝硬化患者96例为观察组, 按Child-Pugh肝功能分级分为A组(35例)、B组(43例)、C组(18例)3个亚组;同期选择无肝硬化的健康体检者40例为对照组。A组男25例、女10例, 年龄(55.01±8.71)岁;B组男30例、女13例, 年龄(55.19±8.76)岁;C组男14例、女4例, 年龄(55.34±8.81)岁;对照组男27例、女13例, 年龄(54.52±8.56)岁。收集粪便标本, 通过细菌培养测定肠道主要菌群变化, 测定肠黏膜通透性指标[D-乳酸(D-LAC)、内毒素(ETX)及二胺氧化酶(DAO)]。Pearson相关性分析分析肠黏膜通透性指标之间的相关性, Spearman相关性分析分析肠黏膜通透性指标与Child-Pugh肝功能分级的相关性, 并使用受试者工作特征曲线(ROC)分析肠黏膜通透性指标的预测价值。计量资料采用F检验、独立样本t检验, 计数资料采用χ2检验。结果 A、B、C组肠杆菌[(8.61±0.42)lgCFU/g...     

褪黑素对损毁弓状核大鼠所致肥胖的干预研究

目的 观察褪黑素对损毁弓状核大鼠所致肥胖的干预作用.方法 皮下注射谷氨酸钠,建立大鼠弓状核损毁所致中枢性肥胖,比较各组大鼠体质量指数(BMI) ;测定体温变化、摄食量和脂肪重;检测甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)等和血压;观察弓状核病理学变化.结果 褪黑素处理肥胖大鼠后,体温逐渐升高,其中高、低剂量给药组大鼠的BMI均明显回降(P<0.05,P<0.01),血压降低(P<0.01,P<0.05).褪黑素高、低剂量组大鼠体内白色脂肪重量,较模型组明显降低(P<0.01,P<0.05),棕色脂肪量明显增多(P<0.05,P<0.01).甘油三酯、高密度脂蛋白和低密度脂蛋白含量,褪黑素治疗组明显降低(P<0.01).结论 褪黑素对损毁大鼠弓状核所致肥胖具有干预作用,可能是由于其使能量消耗增多对肥胖有一定的抵抗作用.     

褪黑素对在体大鼠心肌缺血再灌注损伤的作用

目的　探讨外源性褪黑素(MLT)对在体大鼠心肌急性缺血再灌注损伤的保护作用。方法　36只大鼠随机分为对照组、缺血再灌注(I/R)组及缺血再灌注+褪黑素(I/R+MLT)组,I/R组及I/R+MLT组在体大鼠心脏左冠状动脉前降支完全阻断10min,再灌15min,术中监测记录心电及血流动力学的变化,随后测定局部受损心肌中MDA(丙二醛)的含量和SOD(超氧化物歧化酶)的活性并用电镜检查心肌结构。结果心脏血流动力学指标I/R+MLT组好于I/R组(P<0 .01);I/R组MDA的含量明显高于对照组及I/R+MLT组(P<0.01 ),SOD活性明显低于对照组及I/R+MLT组(P<0 .01),I/R+MLT组MDA含量及SOD活性与对照组无明显差异(P>0 .05);电镜下I/R组心肌细胞结构损伤明显,而I/RMLT组心肌细胞结构基本正常。结论　褪黑素对在体大鼠心肌急性缺血再灌注损伤具有保护作用,其作用与抗氧化损伤有关。     

褪黑素对吗啡依赖小鼠的作用及其与脑啡肽关系的研究

目的观察褪黑素（ＭＴ）对吗啡（Ｍｏｒ）致依赖性的作用及机制分析。方法连续ｉｐＭｏｒ与纳络酮催促建立小鼠依赖模型，甩尾法，淋巴细胞增殖反应和脑啡肽（Ｍｅｔ－Ｅｎｋ）放免测定。结果Ｍｏｒ依赖组小鼠痛阈下降，跳跃次数增加，肛温降低，伴有胸腺细胞增殖能力的低下，Ｍｏｒ依赖小鼠的脑和血浆Ｍｅｔ－Ｅｎｋ亦明显降低。本文首次发现ｉｇＭＴ（３０、９０ｍｇ·ｋｇ－１×７ｄ）能明显提高依赖性小鼠的痛阈，减少跳跃次数，恢复其肛温，阻止Ｍｏｒ对淋巴细胞功能的抑制，并能维持脑、血浆Ｍｅｔ－Ｅｎｋ接近正常对照水平。结论ＭＴ具有对抗Ｍｏｒ致小鼠依赖性作用，其机制与维持内源性Ｍｅｔ－Ｅｎｋ水平有关。     

褪黑素对年龄相关性黄斑变性模型小鼠视网膜氧化损伤的保护机制研究

目的探讨褪黑素(MEL)对年龄相关性黄斑变性(AMD)模型小鼠视网膜氧化损伤的保护作用及对沉默信息调节因子1/叉头状转录因子1(SIRT1/FOXO1)通路的影响。方法 90只小鼠按随机数字表法分为正常组,模型组,MEL低、中、高剂量组,每组18只。除正常组外,其余各组尾静脉注射25μL/g NaIO3制备AMD小鼠模型,MEL低、中、高剂量组分别以10、20、40 mg/kg MEL灌胃,正常组、模型组灌胃等体积生理盐水,1次/d,连续1周。眼底荧光造影仪进行荧光素眼底血管造影(FFA),光学相干断层扫描(OCT)检测视网膜厚度;HE染色检测视网膜形态;试剂盒检测眼眶静脉血血清中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性;Westernblot法检测小鼠视网膜中SIRT1、FOXO1、Ac-FOXO1蛋白水平。结果模型组视盘消失,血管出现收缩现象,视网膜变白,血管出现破裂,视网膜各层细胞排列紊乱,外核层排列松散,细胞嵌入内节段/外节段,内核层细胞变大且松散排列;随MEL剂量的升高,上述症状均逐渐改善。与正常组相比,模型组视网膜厚度,眼眶静脉...     

Protective effects of betulinic acid on intestinal mucosal injury induced by cyclophosphamide in mice

BackgroundBetulinic acid (BA) is a plant-derived pentacyclic triterpenoid with a variety of biological activities. The purpose of this study was to assess the potential protective role of BA against intestinal mucosal injury induced by cyclophosphamide (CYP) treatment.MethodsMice were pretreated with BA daily (0.05, 0.5, and 5.0 mg/kg) for 14 days, then injected intraperitoneally with CYP (50 mg/kg) for 2 days.ResultsBA pretreatment reduced the contents of malondialdehyde (MDA) and glutathione (GSH), decreased the activity of superoxide dismutase (SOD) in small intestine, increased villus hight/crypt depth ratio and restored the morphology of intestinal villi in CYP-induced mice. Moreover, BA pretreatment could significantly down-regulate the levels of pro-inflammatory cytokines interleukin-5 (IL-5), IL-17, IL-12 (P70) and tumor necrosis factor α (TNF-α), reduced production of chemokines macrophage inflammatory protein-1α (MIP-1α), macrophage inflammatory protein-1β (MIP-1β) and regulated upon activation, normal T-cell expressed and secreted (RANTES), and enhanced the levels of anti-inflammatory such as IL-2 and IL-10 in serum, and decreased the mRNA expressions of IL-1β and TNF-α in intestine of CYP-induced mice. Furthermore, RT-PCR demonstrated that BA improved intestinal physical and immunological barrier in CYP-stimulated mice by enhancing the mRNA expressions of zonula occluden 1 (ZO-1) and Claudin-1.ConclusionsBA might be considered as an effective agent in the amelioration of the intestinal mucosal resulting from CYP treatment.     

刺五加注射液对肠缺血再灌注损伤保护作用的实验研究

目的：通过建立大鼠肠系膜上动脉缺血再灌注（IR）模型,观察刺五加注射液对大鼠肠缺血再灌注损伤的保护作用。方法：健康Wistar大鼠40只随机分为A假手术组,B缺血再灌注组,C缺血再灌注＋生理盐水组,D缺血再灌注＋刺五加注射液组。后两组分别静脉注射生理盐水和刺五加注射液。实验结束后分别观察小肠粘膜损伤程度并行病理评分,检测各组超氧化物歧化酶（SOD）活性、丙二醛（MDA）、NO^2-／NO^3-和D-乳酸浓度。结果：D组与B组和C组比较,小肠组织匀浆SOD活性上升（P〈0．05）,MDA浓度降低（P〈0．01）,血浆中NO^2-／NO^3-浓度上升（P〈0．05）,D-乳酸明显降低（P〈0．01）,小肠粘膜损伤程度明显减轻（P〈0．01）。小肠粘膜损伤病理评分与D-乳酸水平呈正相关,与NO^2-／NO^3-水平和SOD活性呈负相关。结论：刺五加注射液对大鼠肠IR损伤有一定的保护作用,作用机制与其清除氧自由基,防止脂质过氧化和保护小肠粘膜上皮细胞有关。     

Deltamethrin induces mitochondrial membrane permeability and altered expression of cytochrome C in rat brain

Deltamethrin is a type II synthetic pyrethroid insecticide and is used extensively. Numerous studies have demonstrated that deltamethrin can cause severe central nervous system symptoms. The mechanism of neuro-toxicity caused by deltamethrin is still poorly understood. This study investigated the effect of deltamethrin on the mitochondria-mediated apoptosis pathway in rat brain. The cortex and hippocampus mitochondrial membrane potential, permeability transition, expression of cytochrome c and activity of cytochrome c oxidase was assayed at 5, 24, 48 and 72 h following deltamethrin treatment. The study observed that the membrane potential, change of absorbance at 540 nm (A(540)), intensities of cytochrome c in mitochondria and activity of cytochrome c oxidase in the cortex and hippocampus of treated groups were significantly lower than those of the control group. The results of the study demonstrated that deltamethrin induced a decreased mitochondrial membrane potential and increased permeability, and reduced the expression of cytochrome c, thus depressing the activity of cytochrome c oxidase significantly. It indicates that deltamethrin may have an effect on mitochondria-mediated apoptosis of nerve cells in the rat brain.