葛根素对糖尿病大鼠胰腺线粒体氧化应激及ATP酶的影响

目的 探讨葛根素对糖尿病大鼠胰腺线粒体氧化应激及ATP酶的影响.方法 将30只Wistar大鼠分为正常对照组、糖尿病组(DM组)和糖尿病治疗组(Pue组,采用葛根素注射液治疗),前两组注射等体积的O.9%氯化钠溶液.8周后,测3组大鼠血清葡萄糖、胰岛素、胰腺线粒体丙二醛(MDA)水平及起氧化物歧化酶(SOD)、Na+-K+-ATP酶(Na+-K+-ATPase)和Ca2+-ATP酶(Ca2+-ATPase)的活性.结果 (1)DM组大鼠血糖和MDA含量明显高于对照组(P<0.001),而血清胰岛素水平、SOD、Na2-K+-ATPase和ca2+-ATPase活性显著降低(P<0.05).(2)Pue组大鼠血糖及MDA含量较DM组显著降低(P<0.05),血清胰岛素水平、SOD、Na+-K+-ATPase和Ca2+-ATPase活性显著升高(P<0.05),差别有统计学意义.结论 葛根素可减轻糖尿病大鼠胰腺线粒体氧化应激水平.     

葛根素对糖尿病大鼠胰腺线粒体氧化应激及ATP酶的影响

目的探讨葛根素对糖尿病大鼠胰腺线粒体氧化应激及ATP酶的影响。方法将30只Wistar大鼠分为正常对照组、糖尿病组(DM组)和糖尿病治疗组(Pue组,采用葛根素注射液治疗),前两组注射等体积的0.9%氯化钠溶液。8周后,测3组大鼠血清葡萄糖、胰岛素、胰腺线粒体丙二醛(MDA)水平及超氧化物歧化酶(SOD)、Na+-K+-ATP酶(Na+-K+-ATPase)和Ca2+-ATP酶(Ca2+-ATPase)的活性。结果 (1)DM组大鼠血糖和MDA含量明显高于对照组(P<0.001),而血清胰岛素水平、SOD、Na+-K+-ATPase和Ca2+-ATPase活性显著降低(P<0.05)。(2)Pue组大鼠血糖及MDA含量较DM组显著降低(P<0.05),血清胰岛素水平、SOD、Na+-K+-ATPase和Ca2+-ATPase活性显著升高(P<0.05),差别有统计学意义。结论葛根素可减轻糖尿病大鼠胰腺线粒体氧化应激水平。     

芦荟苷预处理对缺血再灌注大鼠心肌细胞凋亡的影响

目的研究芦荟苷(Barb)对急性心肌缺血再灌注损伤大鼠心肌细胞凋亡的影响。方法结扎大鼠左冠状动脉前降支复制心肌缺血再灌注损伤模型,实验分为假手术组,缺血再灌注组(IR),Barb高、低剂量预处理组。采用原位缺口末端标记法(TUNEL)检测心肌细胞凋亡指数(AI),酶联免疫吸附试验(ELISA)法测定心肌细胞肿瘤坏死因子(TNF)-α水平,化学法测定线粒体Ca2+-ATPase活性。结果与IR组比较,Barb组AI和TNF-α水平显著降低(P<0.01或P<0.05),Ca2+-ATPase活性明显增高(P<0.05)。结论Barb能明显抑制IR引起的心肌细胞凋亡,其作用可能与降低TNF-α水平和提高Ca2+-ATPase活性有关。     

牛磺酸对2型糖尿病大鼠胰腺线粒体氧化应激的影响

目的探讨牛磺酸对糖尿病大鼠胰腺线粒体氧化应激的影响。方法将30只Wistar大鼠随机分为正常对照组、糖尿病组(DM组)和牛磺酸治疗组(Tau组,采用20g.L-1牛磺酸生理盐水溶液治疗,200mg·kg-1),前两组注射等体积的生理盐水溶液。8wk后,测3组大鼠血浆葡萄糖、胰岛素、丙二醛(MDA),胰腺线粒体MDA、Ca2+、超氧化物歧化酶(SOD)及Na+,K+-ATP酶(Na+,K+-ATPase)和Ca2+,Mg2+-ATP酶(Ca2+,Mg2+-ATPase)的活性。结果①DM组大鼠血糖、MDA和胰腺线粒体MDA、Ca2+含量明显高于对照组(P<0.01),而血浆胰岛素水平、SOD、Na+,K+-AT-Pase和Ca2+,Mg2+-ATPase活性明显降低(P<0.05)。②Tau组大鼠血糖、MDA及胰腺线粒体Ca2+、MDA含量较DM组明显降低(P<0.05),血浆胰岛素水平、SOD、Na+,K+-ATPase和Ca2+,Mg2+-ATPase活性明显升高(P<0.05)。结论牛磺酸可减轻2型糖尿病大鼠胰腺线粒体氧化应激水平。     

祁州漏芦不同溶剂提取物对急性肝损伤模型小鼠的保护作用

目的:研究祁州漏芦(以下简称"漏芦")不同溶剂提取物对急性肝损伤模型小鼠的保护作用。方法:60只KM种小鼠随机分为正常对照(等容生理盐水)组、模型(等容生理盐水)组、联苯双酯(100 mg/kg)组、漏芦乙醇粗提物(200 mg/kg)组、漏芦正丁醇提取物(200 mg/kg)组和漏芦水提取物(200 mg/kg)组。灌胃给药,每天1次,连续7 d。末次给药1 h后,一次性腹腔注射300 mg/kg对乙酰氨基酚(APAP)以复制小鼠急性肝损伤模型。比色法检测小鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)、白蛋白(ALB),肝匀浆丙二醛(MDA)、还原型谷胱甘肽(GSH)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)、谷胱甘肽-S-转移酶(GST),肝线粒体Na+-K+-ATP酶(Na+-K+-ATPase)、Ca2+-Mg2+-ATP酶(Ca2+-Mg2+-ATPase)水平。结果:与正常对照组比较,模型组小鼠血清ALT、AST和ALP活性增强,ALB含量降低;肝组织MDA含量增加,CAT、GPx、SOD、GST活性减弱,GSH含量减少;肝线粒体Na+-K+-ATPase和Ca2+-Mg2+-ATPase活性减弱,差异具有统计学意义(P<0.05)。与模型组比较,漏芦乙醇粗提物组小鼠血清ALT、AST活性减弱,ALB含量增加,肝匀浆MDA含量减少,GSH含量增加,CAT、GPx、SOD、GST活性增强,肝线粒体Na+-K+-ATPase和Ca2+-Mg2+-ATPase活性增强,差异具有统计学意义(P<0.05);漏芦正丁醇提取物组小鼠血清ALT、AST、ALP活性减弱,ALB含量增加,肝匀浆MDA含量减少,GSH含量增加,CAT、GPx、SOD、GST活性增强,肝线粒体Na+-K+-ATPase和Ca2+-Mg2+-ATPase活性增强,差异具有统计学意义(P<0.05);漏芦水提取物组小鼠血清ALT、AST活性减弱,ALB含量增加,肝匀浆MDA含量减少,GSH含量增加,GPx、GST活性增强,肝线粒体Na+-K+-ATPase和Ca2+-Mg2+-ATPase活性增强,差异具有统计学意义(P<0.05)。结论:漏芦不同溶剂提取物对APAP致小鼠急性肝损伤具有保护作用,其机制可能与其抗氧化作用有关。     

川芎嗪对大鼠加速型抗GBM抗体肾炎肾皮质的线粒体膜流动性和ATP酶活性的影响

目的 观察川芎嗪对大鼠加速型抗肾小球基底膜(GBM)抗体肾炎肾皮质线粒体膜流动性和ATP酶活性的影响。方法采用1,6-二苯基-1,3,5-己三烯(DPH)荧光偏振法研究抗GBM肾炎肾皮质的线粒体膜流动性,利用定磷法测定线粒体膜ATP酶的活性。结果川芎嗪能调节抗GBM抗体肾炎肾皮质的线粒体膜流动性,同时可以使Na^ -K^ -ATPase、Mg^ -ATPase、Ca^2 -ATPase活力升高。结论川芎嗪可能通过改善肾线粒体膜流动性,而保护线粒体膜结构及功能。     

早期糖尿病肾病大鼠肾脏线粒体Ca2+及细胞色素C变化

目的 观察早期糖尿病肾病大鼠肾脏线粒体Ca2+及细胞色素C(Cyt C)的变化.方法 将20只Wistar 大鼠随机分为对照组、模型组,每组10只.模型组建立链脲佐菌素诱导早期糖尿病肾病大鼠模型,对照组大鼠未经链脲佐菌素诱导.第10周末测定两组血糖、肾质量指数、24 h尿蛋白定量;检测两组大鼠肾脏线粒体Ca2+、CytC含量.结果 与对照组相比,模型组大鼠的血糖、肾质量指数、24 h尿蛋白定量均显著升高(均P＜0.01),线粒体Ca2+及胞浆Cyt C含量升高,线粒体Cyt C含量显著降低(P＜0.05).结论 早期糖尿病肾病大鼠肾脏线粒体内钙超载,线粒体Cyt C释放增加.     

穿心莲内酯抗大鼠心肌肥厚作用及其与ATPase活性的关系

目的:观察穿心莲内酯对异丙肾上腺素所致大鼠心肌肥厚的保护作用及其对心肌组织Na+-K+-ATPase、Ca2+-Mg2+-ATPase活性及羟脯氨酸含量的影响。方法:采用ISO1 mg.kg-1.d-1,背部皮下注射,连续10 d,建立大鼠心肌肥厚模型。造模第2天开始给予不同浓度的穿心莲内酯、二甲基亚砜或NS,连续14 d,末次给药后禁食12 h,称体质量,麻醉,取心脏,称全心及左心室质量,计算左心室质量指数,测定心肌组织Na+-K+-ATPase、Ca2+-Mg2+-ATPase活性及羟脯氨酸含量。结果:模型组左心室质量指数升高(P<0.01),心肌组织Na+-K+-ATPase(P<0.01)、Ca2+-Mg2+-ATPase(P<0.01)活性降低,羟脯氨酸含量升高(P<0.01);与模型组相比,低剂量组左心室质量指数降低(P<0.01),高剂量及低剂量穿心莲内酯治疗组心肌组织Na+-K+-ATPase、Ca2+-Mg2+-ATPase活性升高,羟脯氨酸含量均降低,且呈现剂量依赖性效应。结论:穿心莲内酯可通过提高Na+-K+-ATPase、Ca2+-Mg2+-ATPase的活性,降低羟脯氨酸含量,从而抑...     

三七总皂苷通过线粒体途径抑制顺铂诱导的大鼠肾细胞凋亡

目的探讨三七总皂苷(PNS)通过线粒体途径对顺铂肾损伤大鼠肾组织细胞凋亡的影响。方法将36只♂SD大鼠随机分为空白对照组、顺铂模型组、顺铂+PNS组;在给药8 d后,检测大鼠血清肌酐(Cr)、尿素氮(BUN)和尿β-N-乙酰胺基葡萄糖苷酶(NAG)水平。采用HE染色观察病理变化,利用透射电子显微镜观察大鼠肾脏线粒体形态,采用原位末端缺口标记法(TUNEL染色)检测肾细胞凋亡情况,通过免疫组化SP法检测凋亡相关蛋白Bax、caspase-9的表达,并采用Western blot检测Bcl-2蛋白的表达情况。结果与空白对照组比较,顺铂模型组大鼠血清Cr、BUN和尿NAG水平明显升高(P<0.01),肾小管上皮细胞线粒体损伤严重,肾组织的细胞凋亡率明显增加(P<0.01),肾组织Bax、caspase-9及Bcl-2表达均明显增强(P<0.01);与顺铂模型组比较,顺铂+PNS组血清Cr、BUN和尿NAG水平明显降低(P<0.01),肾小管上皮细胞线粒体损害明显改善,肾组织细胞凋亡率和Bax、caspase-9表达水平均明显降低(P<0.01),Bcl-2的表达则明显增强(P<0.01)。结论 PNS可能通过增加抑凋亡蛋白Bcl-2表达,减少促凋亡蛋白Bax和凋亡相关蛋白caspase-9的表达来调节细胞凋亡,从而发挥保护顺铂肾损害的作用。     

川芎嗪对大鼠心肌线粒体损伤的保护作用

目的 :观察川芎嗪对大鼠缺血再灌注心肌线粒体损伤的影响及其机制。方法 :结扎大鼠冠状动脉30min后灌注20min ,复制缺血再灌注模型。测定心肌线粒体中琥珀酸脱氢酶 (SDH)、细胞色素氧化酶 (CCO)、Ca2 + ·Mg2 + -ATP酶、Ca2 + -ATP酶、超氧化物歧化酶 (SOD)、谷光甘肽过氧化物酶 (GSH -PX)活力及细胞色素和丙二醛 (MDA)含量。结果 :川芎嗪保护组的SDH、CCO、Ca2 + -ATP酶、Ca2 + ·Mg2 + -ATP酶、SOD和GSH -PX活力显著高于缺血再灌注组 (P<0 05) ,其细胞色素aa3、细胞色素C和膜磷脂含量也显著高于缺血再灌注组 ,而MDA含量则显著性降低。结论 :川芎嗪对缺血再灌注时心肌线粒体膜酶活性变化及膜成分降解有较强的拮抗作用 ,其机理可能是通过提高对氧自由基的清除和抑制脂质过氧化。     

Chloral hydrate inhibition in vitro of ATPase in membrane of rat erythrocytes and in microsomes of dog kidney external medulla

The study of the general anesthetic chloral hydrate and its effects on rat erythrocyte membranes and dog kidney microsomes showed that ATPases were reversibly inhibited in every case. The inhibition was cooperative in the cases of (Mg2+ + Na+ + K+)-ATPase, Mg2+-ATPase and (Na+ + K+)-ATPase of rat erythrocyte membrane, while Ca2+-ATPase and (Mg2+ + Ca2+)-ATPase were non-cooperative. The chloral hydrate concentrations necessary to diminish the activity of the enzyme to half of the Vmax (I50) were 6 mM for Ca2+-ATPase from erythrocyte membranes and 82 mM for Mg2+-ATPase from intact external kidney medulla microsomes. When Ca2+-ATPase was studied in the absence of Mg2+ in these microsomes, the affinity for Ca2+ was very low, but the enzyme was sensitive to chloral hydrate.     

青龙衣多糖对H22型肿瘤细胞的ATPase活性影响的研究

目的 研究青龙衣多糖对H22型肿瘤细胞的ATPase活性的影响。方法 按照测定无机磷含量的方法对H22肿瘤细胞的Ca^2＋-ATPase、Na^＋K^＋-ATPase和Mg^2＋-ATPase活性进行了测定。结果 发现青龙衣多糖可以降低ATPase的活性，除青龙衣多糖中、高剂量组显著抑制Ca^2＋-ATPase活性。高、中、低剂量组都显著降低Na^＋-K^＋-ATPase和Mg^2＋-ATPase活性（P〈0．05）。结论 ATPase活性降低导致了膜电位下降。细胞容积降低．可能引起细胞凋亡发生．Ca^2＋．调节凋亡发生．Mg^2＋调控ATPase的活性,可能是青龙衣多糖抗肿瘤的机制之一。     

果糖二磷酸钠镁对失血性休克大鼠肾脏的保护作用

目的探讨果糖二磷酸钠镁(FDPM)对失血性休克大鼠肾脏的保护作用及其机制。方法按照Wiggers改良法建立失血性休克模型,模型成功后分别自股静脉注射FDPM(90.0、45.0、22.5mg.kg-1),1.6-二磷酸果糖(37.5mg.kg-1),硫酸镁(3.4mg.kg-1)及等容量生理盐水,于休克前、休克末、给药后10、、30、60min及回输血后0、30、60min检测平均动脉压的变化,并测定血清中的尿素氮(BUN)、肌酐(Cr)含量和肾脏组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)、Na+-K+-ATPase、Mg2+-ATPase、Ca2+-ATPase活性的变化。结果FDPM能够升高失血性休克大鼠的平均动脉压(MAP),减少血清中的BUN和Cr含量,同时降低肾脏组织MDA含量和提高SOD、Na+,K+-ATPase、Mg2+-ATPase、Ca2+-ATPase活性。结论FDPM能够有效的减轻失血性休克大鼠肾脏组织缺血缺氧性损伤,改善能量代谢,增加ATP酶活性,减轻自由基损伤,从而起到保护肾脏的作用。     

The protective effect of lipid emulsion in preventing bupivacaine-induced mitochondrial injury and apoptosis of H9C2 cardiomyocytes

Lipid emulsion (LE) has been shown to be effective in the resuscitation of bupivacaine-induced cardiac arrest, but the precise mechanism of this action has not been fully elucidated. Pursuant to this lack of information on the mechanism in which LE protects the myocardium during bupivacaine-induced toxicity, we explored mitochondrial function and cell apoptosis. H9C2 cardiomyocytes were used in study. Cells were randomly divided in different groups and were cultivated 6?h, 12?h, and 24?h. The mitochondria were extracted and mitochondrial ATP content was measured, as was mitochondrial membrane potential, the concentration of calcium ion (Ca2+), and the activity of Ca2+-ATP enzyme (Ca2+-ATPase). Cells from groups Bup1000, LE group, and Bup1000LE were collected to determine cell viability, cell apoptosis, and electron microscopy scanning of mitochondrial ultrastructure (after 24?h). We found that LE can reverse the inhibition of the mitochondrial function induced by bupivacaine, regulate the concentration of calcium ion in mitochondria, resulting in the protection of myocardial cells from toxicity induced by bupivacaine.     

Effect of plictran on beef heart mitochondrial ATPases

The in vitro effects of plictran on oligomycin-sensitive Mg2+-ATPase and Ca2+-ATPase activities in beef heart mitochondria were studied. Beef heart mitochondrial fractions were prepared by the conventional centrifugation method. ATPase activities were measured by determining the inorganic phosphate released by the hydrolysis of ATP. Plictran inhibited both oligomycin-sensitive (o.s.) Mg2+-ATPase and Ca2+ ATPase activities at nanomolar concentrations. However, plictran did not affect the oligomycin-insensitive (o.i.) Mg2+-ATPase activity at any concentration studied. Substrate activation kinetics revealed that plictran inhibited o.s. Mg2+-ATPase uncompetitively and Ca2+-ATPase non-competitively. These results clearly indicate that plictran affects ATP synthesis and calcium ion transport in beef heart mitochondria.     

Effect of 1 alpha-hydroxycholecalciferol on cellular calcium metabolism of kidney cortex (author's transl)]

Rats were provided a normal laboratory diet or a low Ca.vitamin D-deficient diet. After the administration of 1 alpha-hydroxycholecalciferol, mitochondria, microsomes and slices were prepared from kidney cortex of both control and treated rats. When 1 alpha-hydroxycholecalciferol was given to normal and low Ca.vitamin D-deficient rats, Ca accumulation in mitochondria was stimulated during 30 minutes and the high calcium content was maintained at the subsequent incubation. There was a significant decrease of mitochondrial Ca2+-ATPase and Mg2+-ATPase activities with low Ca.vitamin D depletion, but both enzyme activities were restored by 1 alpha-hydroxycholecalciferol treatment of the depleted rats. Ca2+-ATPase and Mg2+-ATPase activities of microsomes were not altered with the administration of 1 alha-hydroxycholecalciferol. In contrast to results of mitochondrial Ca transport, changes in Ca influx and efflux of slices were not significant in response to the treatment of low Ca.vitamin D-deficient rats with 1 alpha-hydroxycholecalciferol. The results of the present study suggest that 1 alpha-hydroxycholecalciferol plays a role in the process of Ca accumulation and ATP hydrolysis of mitochondria in kidney cortex.     

The effect of racemomycin-D, a nephrotoxic antibiotic, on cellular metabolism of rat kidney cortex in vitro

In vitro effects of racemomycin-D on cellular metabolism were examined in rat kidney. Racemomycin-D decreased the concentration gradient of Na+ and K+ across the cell membranes, but failed to influence water content and ATP concentration of kidney cortical slices. The antibiotic inhibited microsomal (Na+ + K+)-ATPase. Preincubation of the microsomes with racemomycin-D enhanced the inhibition about 1.8-fold. Succinoxidase activity of mitochondria remained unaltered in the presence of racemomycin-D, but the antibiotic potently decreased ATP-dependent Ca2+ and Mg2+ uptakes by mitochondria. These results suggest that racemomycin-D probably disorders intracellular homeostasis of Na+, K+ and Ca2+.     

Effects of nitrate and nitrite, chemical intermediates of inhaled nitrogen dioxide, on membrane components of red blood cells of rats

Rat blood was incubated at 37 degrees C for 60 min with either NaNO3 or NaNO2 to examine the relationship between the decrease in the hexose content and Ca2+,Mg2+-ATPase activity of red cell membranes, and NO3- and NO2-. The hexose content decreased depending on the NaNO2 concentration up to 100 microM reaching 76% (p less than 0.05) of the control value. NaNO3 had little effect on the hexose content. On the other hand, the Ca2+,Mg2+-ATPase activity decreased depending on the NaNO3 concentration up to 200 microM, where the activity reached 75% (p less than 0.01) of the control value. The effect of NaNO2 on this activity was smaller than that of NaNO3. The sialic acid content and the Na+,K+-ATPase activity did not show significant alterations by incubation with NaNO2 and NaNO3 at below 100 microM. To examine the in vivo effects of NO2- and NO3-, 50 mM NaNO3 was intravenously injected into rats five times at hourly intervals (dose: 1.0 ml/kg body weight), and blood was collected 1 hr after the last injection. The activities of Ca2+,Mg2+- and Na+,K+-ATPases of red cell membranes were decreased to 68% (p less than 0.05) and 80% of the control value, respectively. Reduction by injection of 50 mM NaNO2 was smaller than that by 50 mM NaNO3. The results show that the hexose content and the Ca2+,Mg2+-ATPase activity of red cell membranes were decreased by NO-x that increased in the blood during short-term exposure of rats to NO2.     

氯丙嗪和维拉帕米对大鼠镉肾毒性的影响(英文)

目的研究氯丙嗪(CPZ)和维拉帕米(Ver)对由镉引起的大鼠肾毒性是否有预防作用。方法32只大鼠随机分成4组,分别为对照组、单纯染镉组、CPZ和Ver预处理组。单纯染镉组大鼠sc7μmol·kg-1氯化镉;CPZ和Ver预处理组分别ipCPZ5mg·kg-1和Ver4mg·kg-1,1h后sc7μmol·kg-1氯化镉;对照组在相应时间内给予生理盐水,注射容量均为2mL·kg-1。最后一次注射24h后,收集24h尿样,测定尿乳酸脱氢酶(LDH)活性、尿蛋白、尿镉、肾镉和肾皮质中的Na+K+ATP酶,Ca2+ATP酶和蛋白激酶C(PKC)的活性。结果单纯染镉组与对照组比较,尿镉和肾镉含量明显升高。CPZ和Ver预处理组尿镉明显低于单纯染镉组,但肾镉无明显变化。与对照组比较,单纯染镉组尿LDH活性、尿蛋白和肾皮质中的Na+K+ATP酶,Ca2+ATP酶和PKC活性明显升高。CPZ和Ver预处理组大鼠尿LDH活性、尿蛋白和肾皮质中的Na+K+ATP酶,Ca2+ATP酶和PKC活性明显低于单纯染镉组。结论镉能激活Na+K+ATP酶,Ca2+ATP酶和PKC的活性,而且,CPZ和Ver均可不同程度地减轻肾毒性。     

咖啡酸苯乙酯通过Nrf-2途径抑制地塞米松诱导的成骨细胞凋亡

目的 探讨Nrf-2途径在咖啡酸苯乙酯(CAPE)抑制地塞米松(DEX)诱导成骨细胞凋亡中的作用.方法 用细胞贴壁法培养小鼠颅顶前骨细胞(MC3T3-E1),采用10μmol/L DEX建立细胞损伤模型,以不同浓度CAPE(0.05、0.25、1μmol/L)预处理细胞2h后加入地塞米松共孵育24h;细胞增殖-毒性检测试剂盒(CCK-8)检测细胞增殖活性;依据CCK-8检测结果确定药物浓度后将实验分为对照组、咖啡酸苯乙酯组(CAPE组)、地塞米松组(DEX组),咖啡酸苯乙酯+地塞米松组(CAPE+DEX组);DCFH-DA荧光探针检测细胞内活性氧(reactive oxygen species,ROS)水平;Caspase-3活性检测试剂盒检测Caspase-3酶活性,Western blot法检测Nrf-2 途径相关蛋白Nrf-2和血红素氧合酶1(heme oxygenase,HO-1)蛋白表达水平;流式细胞仪检测细胞凋亡率.结果 10μmol/L DEX作用下细胞形态发生明显变化,损伤作用明显.与对照组相比,DEX组内细胞存活率显著下降(P＜0.01),而细胞内 ROS水平、细胞凋亡率及Caspase-3酶活性显著增加(P＜0.01);同时,Nrf-2途径相关蛋白 Nrf-2及HO-1表达量减少,差异有统计学意义(P＜0.01).与DEX组相比,CAPE+DEX组细胞存活率显著上升(P＜0.01),Nrf-2途径相关蛋白 Nrf-2及HO-1表达明显增加(P＜0.01);此外,CAPE+DEX组细胞内 ROS 水平、细胞凋亡率及Caspase-3酶活显著降低,差异有统计学意义(P＜0.01).结论 咖啡酸苯乙酯可以通过Nrf-2途径降低细胞内ROS水平进而减轻地塞米松诱导的氧化应激所致细胞损伤及凋亡.