松果菊苷对过氧化氢损伤的PC12细胞的保护作用及机制研究

目的研究松果菊苷(echinacoside,ECH)对过氧化氢(H2O2)诱导的PC12细胞损伤的保护作用及机制。方法用终浓度为0.4 mmol.L-1的H2O2损伤PC12细胞,测定细胞存活率和Na+,K+-ATP酶的活性;用激光共聚焦法(LSCM)检测线粒体膜电位(MMP);用RT-PCR法检测Bcl-2和p53 mRNA表达量的变化。结果10 mg.L-1松果菊苷可以提高H2O2损伤的PC12细胞存活率和Na+,K+-ATP酶的活力、升高线粒体膜电位、降低p53 mRNA水平但增高Bcl-2 mRNA水平(P<0.05或P<0.01)。结论松果菊苷可保护H2O2诱导的PC12细胞损伤,升高MMP、下调p53mRNA和上调Bcl-2 mRNA可能是其作用机制。     

MCI-186对PC12细胞缺血性损伤的保护作用

目的:研究MCI-186对PC12细胞缺血损伤的保护作用.方法:以氰化钠(NaCN)合并培养基质缺糖以及连二亚硫酸钠(Na2S2O4)合并培养基质缺糖造成PC12细胞缺血性损伤模型,观察活体细胞的形态,并采用MTT比色法测定PC12细胞存活率.结果:10-5mol·L-1MCI-186可改善缺血引起的PC12细胞形态学变化,提高细胞存活率,对2种模型造成的缺血性损伤的抑制率分别为29 5%及14.3%.结论:MCI-186对NaCN及Na2S2O4造成的PC12细胞缺血性损伤有一定的保护作用.     

大豆异黄酮活性组分对H2O2诱导的PC12细胞损伤的影响

目的:探讨大豆异黄酮活性组分对H2 O2 诱导的PC12细胞损伤的保护作用。方法:以H2 O2 损伤PC12细胞为氧化应激损伤的模型,采用光学显微镜观察细胞形态,MTT法判断细胞的存活率,LDH法检测细胞的损伤程度。结果:不同浓度大豆异黄酮能明显改善H2 O2 导致的细胞甲瓒减少,大豆异黄酮处理组细胞存活率明显高于H2 O2 处理组(P <0 .0 1) ;而LDH漏出率则明显低于H2 O2 处理组(P <0 .0 5 )。结论:大豆异黄酮活性组分对H2 O2 诱导的PC12细胞损伤具有保护作用。     

补骨脂素逆转多药耐药细胞系K562/ADR耐药性研究

目的　研究补骨脂素对白血病细胞阿霉素耐药株(K5 6 2 /ADR)多药耐药 (multidrugresistance,MDR)性的逆转作用及其机制。方法　采用MTT法检测药物细胞毒性作用 ,高效液相色谱法检测细胞内阿霉素 (ADR)的浓度 ,流式细胞术测定细胞P 糖蛋白 (P gp)的表达。 结果　补骨脂素 (1～ 2 0 μmol·L-1)能不同程度地降低ADR对K5 6 2 /ADR细胞的IC50 。 2 0 μmol·L-1能显著提高ADR在K5 6 2 /ADR细胞内的浓度 ,降低K5 6 2 /ADR细胞P gp的表达。 结论　补骨脂素能逆转K5 6 2 /ADR细胞的MDR ,其机制与抑制P gp的功能及其表达 ,增加细胞内ADR的积累有关     

α-硫辛酸注射液对过氧化氢致PC12细胞损伤的保护作用

目的 研究α-硫辛酸注射液(抗氧化剂)对H2O2致PC12细胞损伤的保护作用.方法 600 μmol·L-1H2O2与细胞共同孵育4 h,建立PC12细胞氧化应激损伤模型,用MTT法,测定细胞生长抑制率;培养介质中的LDH测定,用紫外分光光度法,用流式细胞术测定细胞凋亡率和线粒体膜电位.结果 与模型组相比,3个剂量(10,1 μmol·L-1)α-硫辛酸注射液能提高H2O2损伤的PC12细胞的存活率,减少LDH的漏出,降低细胞凋亡率,抑制线粒体膜电位的下降(P＜0.05,P＜0.01).结论 α-硫辛酸注射液对H2O2致PC12细胞损伤模型具有较好的保护作用.     

二氢石蒜碱对过氧化氢损伤的PC12细胞的保护作用

目的:探讨二氢石蒜碱(DL)对H2O2诱导的PC12细胞氧化损伤的影响及其可能机制。方法:用H2O2(200μmol.L-1)处理PC12细胞建立氧化应激模型,并加入二氢石蒜碱预处理作为保护。噻唑蓝(MTT)法和乳酸脱氢酶(LDH)检测细胞存活率和细胞损伤程度,利用荧光探针DCFH-DA和JC-1分别检测细胞内活性氧(ROS)和线粒体膜电位。结果:H2O2作用于PC12细胞后,细胞存活率下降,LDH活性和ROS含量增高,线粒体膜电位降低,与正常对照组比较具有显著性差异(P<0.01);10-7～10-5mol.L-1DL预处理后,细胞存活率提高,LDH和ROS变低,线粒体膜电位回升,且在一定范围呈剂量依赖性。结论:DL对H2O2诱导PC12细胞氧化损伤具有保护作用,其作用机制可能与减少ROS产生和稳定线粒体膜电位有关。     

丹皮酚对过氧化氢诱导的PC12细胞凋亡的抑制作用(英文)

目的探讨丹皮酚对过氧化氢(H2O2)诱导的PC12细胞凋亡的抑制作用及其机制。方法建立H2O2致PC12细胞损伤模型,采用MTT法测定细胞存活率,流式细胞术测定细胞凋亡率及细胞内活性氧含量,化学比色法测定乳酸脱氢酶(LDH)释放量及细胞内丙二醛(MDA)含量。结果PC12细胞经H2O2100μmol.L-1处理10 h可致细胞存活率下降,并能诱导细胞凋亡,LDH释放量及细胞内活性氧和MDA含量明显增加;丹皮酚(12,25和50μmol.L-1)预处理1 h可提高细胞存活率,减少细胞凋亡、LDH释放量及细胞内活性氧和MDA含量。结论丹皮酚对H2O2诱导的PC12细胞凋亡具有抑制作用,该作用可能与其抗氧化作用有关。     

新的四氢异喹啉类化合物CPUE1逆转K562/A02细胞的多药耐药性

目的 :研究新的四氢异喹啉类化合物CPUE1逆转K5 6 2 A0 2细胞多药耐药性的作用及机制。方法 :在CPUE1的作用下 ,用MTT法检测长春新碱(vincristine ,VCR)对K5 6 2 A0 2多药耐药细胞的细胞毒作用的变化 ,使用DNA分析和Annexin Ⅴ PI双染法研究CPUE1对VCR诱导K5 6 2 A0 2细胞凋亡的影响 ,流式细胞仪检测CPUE1对P 糖蛋白 (P glycop rotein ,P gp)外排罗丹明 12 3(rhodamine12 3,Rh12 3)的作用。结果 :CPUE1能明显提高VCR对K5 6 2 A0 2多药耐药细胞的细胞毒作用以及凋亡诱导作用 ,10 μmol·L-1的CPUE1能使K5 6 2 A0 2对VCR的IC50值由 6 0 .5 4μmol·L-1降至 4 .17μmol·L-1。CPUE1还能抑制Rh12 3外排从而增加细胞内Rh12 3的蓄积浓度。结论 :CPUE1通过抑制P gp的活性逆转K5 6 2 A0 2细胞的多药耐药性。     

胡黄连苷-Ⅱ在体外对PC12神经细胞损伤的保护作用

目的 :考察胡黄连苷 Ⅱ对PC12神经细胞损伤的保护作用。方法 :采用细胞培养的方法 ,建立PC12神经细胞双氧水 (H2 O2 )损伤模型。通过观察细胞形态 ,测定细胞存活率 (MTT法 ) ,乳酸脱氢酶(LDH)漏出率 ,细胞内氧化活性物质 (ROS)水平 ,检测胡黄连苷 Ⅱ对PC12细胞损伤的保护作用。结果 :同造模组比较 ,胡黄连苷 Ⅱ 0 .5、5 .0mmol·L-1能减轻H2 O2 引起的对PC12神经细胞的损伤 ,明显提高细胞的存活率 ,减少LDH的释放量 ,降低细胞内ROS水平。结论 :胡黄连苷 Ⅱ对PC12神经细胞损伤具有明显的保护作用。     

甘西鼠尾草注射液与丹参注射液对PC12细胞H2O2损伤保护作用比较研究

目的：比较甘西鼠尾草注射液与丹参注射液对PC12细胞H2O2损伤的保护作用。方法：采用细胞株培养的方法,建立PC12细胞H2O2损伤模型,通过MTT法和流式细胞分析仪检测细胞存活率和凋亡率;采用免疫细胞化学染色法检测PC12细胞bcl-2和bax表达。结果：PC12细胞经H2O2损伤后,细胞存活率降低、凋亡率增加,甘西鼠尾草注射液与丹参注射液处理组均可有效缓解上述改变（P〈0.05）;两药均使bcl-2表达增加（P〈0.05）,bax表达减少（P〈0.05）。结论：甘西鼠尾草注射液与丹参注射液对PC12细胞H2O2损伤具有明显保护作用。其机理可能与增强凋亡抑制因子bcl-2表达、抑制凋亡促进因子bax表达,进而抑制细胞凋亡有关。     

CJX2, an amlodipine derivative,reverses p‐glycoprotein‐mediated multidrug‐resistance in doxorubicin‐resistant human myelogenous leukemia (K562/DOX) cells

P‐glycoprotein‐mediated drug efflux can yield a multidrug‐resistance (MDR) phenotype that is associated with a poor response to cancer chemotherapy. Development of safe and effective MDR‐reversing agents is an important approach in the clinic. The aim of this study was to observe the effects of CJX2, an amlodipine derivative, on the inhibition of P‐gp function and P‐gp‐mediated MDR in K562/DOX cells and parental K562 cells. Based on the flow cytometric technology, the uptake, accumulation, and efflux of rhodamine123 (Rh123) were detected in these cells by measuring Rh123‐associated mean fluorescence intensity (MFI). The effects of CJX2 on the doxorubicin cytotoxicity were evaluated by assaying for MTT (3‐(4,5‐dimethylthiazol)‐2,5‐diphenyltetrazolium bromide) reduction and the reversal fold (RF) values. The DNA content, percentage of apoptosis, and cell cycle analysis were monitored with flow cytometry. Intracellular accumulation of doxorubicin was also assessed by the determination of doxorubicin‐associated MFI. Verapamil was employed as a comparative agent. Incubation of K562/DOX cells with CJX2 caused a marked increase in accumulation, uptake, and a notable decrease in efflux of Rh123. No such results were found in parental K562 cells. The inhibitory effect of the agent on P‐gp function was reversible, but it persisted at least for 90 min after removal of 2.5 µM CJX2 from incubation medium. The doxorubicin‐induced cytotoxicity, apoptosis, and cell cycle perturbations were significantly potentiated by CJX2. The intracellular accumulation of doxorubicin was enhanced in the presence of various concentrations of CJX2. The CJX2 exhibited potent effects in vitro in the reversal of P‐gp‐mediated MDR, suggesting that the compound may become a candidate for an effective MDR‐reversing agent in cancer chemotherapy. Drug Dev. Res. 66:278–285, 2006. © 2006 Wiley‐Liss, Inc.     

盐酸千金藤碱逆转K562/ADR细胞多药耐药性及其机制

研究盐酸千金藤碱(cepharanthine hydrochloride,CH)逆转K562/ADR细胞多药耐药性及其机制。采用MTT法检测多柔比星(adriamycin,ADR)单用及分别与CH、维拉帕米(verapamil,VER)合用的细胞毒作用;采用流式细胞仪,测定CH对细胞内ADR蓄积、罗丹明123(Rho123)蓄积和泵出及P糖蛋白(P-gp)表达的影响。结果表明,CH(4μmol.L1)使K562/ADR细胞对ADR的敏感性增加7.43倍,逆转活性是VER的3.19倍,但对K562敏感株基本无影响。同时CH浓度依赖性地增加K562/ADR细胞内ADR和Rho123的蓄积,减少Rho123的泵出,抑制P糖蛋白的表达,但对K562细胞均无明显影响。CH在体外逆转肿瘤细胞多药耐药性的作用可能与其抑制P糖蛋白的功能和表达有关。     

Sambutoxin sensitizes K562/ADR to adrimycin by inhibiting expression of P-glycoprotein

OBJECTIVE To investigate the reverse effects of sambutoxin, a representative derivative of 4-hydroxy-2-pyridone with antibacterial, antifungal and antitumor effects, on multidrug resistance(MDR) of K562/ADR cells to adriamycin(ADR) and to elucidate its potential molecular mechanism. METHODS We first investigated the dose-dependent cytotoxic effects of sambutoxin as single treatment on K562 and K562/ADR cells by MTT and CCK-8 assay in order to select the suitable dosage of sambutoxin in the combination treatment. The cytotoxicity of ADR combined with sambutoxin on K562 and K562/ADR cells were also determined by MTT and CCK-8 assays. Then, effects of sambutoxin on the intracellular accumulation of ADR in K562/ADR cells were determined using flow cytometry. The effect of sambutoxin on the efflux function and expression of P-gp in K562/ADR cells was evaluated by Rhodamine123(Rh123) accumulation assay and Western blotting assay respectively. 3 D interactions of human P-gp with sambutoxin, verapamil and adriamycin predicted by docking studies conducted using Sybyl2.1 sofware. Next, the effect of combination treatment of sambutoxin and ADR on the apoptosis of K562/ADR cells was determined by Hoechst 33342 nuclear staining. The expression of the apoptosis related proteins were detected by Western blotting assay. Effect of sambutoxin and ADR on reactive oxygen species(ROS) level in K562/ADR cells was evaluated detected by the DCFH-DA method using fluorescence microscopy and flow cytometry. Effect of sambutoxin and ADR on EGFR/MAPK and PI3 K/AKT/m TOR signaling pathways in K562/ADR cells was evaluated by Western blotting assay. RESULTS Sambutoxin treatment potently enhanced the susceptibility of K562/ADR cells to ADR in a dose manner and the reversal effect was much more prominent in K562/ADR cells. Sambutoxin increased the intracellular accumulation of ADR and Rh123 in K562/ADR cells. Sambutoxin inhibited protein expression of P-gp through Akt/NF-κB pathway in K562/ADR cells. Molecular docking display sambutoxin with P-gp(PDB code:6 QEX) formed two hydrogen bonds with GLN-725 and ASN-721, total Score was 8.29. Co-administration ADR with sambutoxin remarkably increased ADR-induced apoptosis through mitochondrial pathway, including down-regulation of anti-apoptotic protein Bcl-2, up-regulation of proapoptotic protein Bax, up-regulation of cleaved caspase3, and cleaved PARP, augmented ROS in K562/ADR cells. Moreover, ADR combined with sambutoxin could down-regulate the EGFR/MAPK and PI3 K/AKT/m TOR survival pathway in K562/ADR cells. CONCLUSION Sambutoxin reverses MDR of K562/ADR cells to ADR by downregulating P-gp expression and increasing ROS level, as well as, inducing apoptosis. These fundamental findings provide evidence for further clinical research in application of sambutoxin as an assistant agent for chemotherapy of cancer.     

CJZ3, a lomerizine derivative,reverses P‐glycoprotein‐mediated multidrug‐resistance in doxorubicin‐resistant human myelogenous leukemia (K562/DOX) cells

P‐glycoprotein‐mediated drug efflux can yield a multidrug‐resistance (MDR) phenotype that is associated with a poor response to cancer chemotherapy. The development of safe and effective MDR‐reversing agents is an important approach in the clinic. The aim of this study was to examine the effects of CJZ3, a lomerizine derivative, on the inhibition of P‐gp function and P‐gp‐mediated MDR in K562/DOX cells and parental K562 cells. Incubation of K562/DOX cells with CJZ3 caused a marked increase in accumulation and uptake and a notable decrease in efflux of Rh123, No such results were found in parental K562 cells. The inhibitory effect of the agent on P‐gp function was reversible, but it persisted for at least 90 min after removal of 2.5 &µM CJZ3 from the incubation medium. The doxorubicin‐induced cytotoxicity, apoptosis, and cell‐cycle perturbations were significantly potentiated by CJZ3. The intracellular accumulation of doxorubicin was enhanced in the presence of various concentrations of CJZ3. The CJZ3 exhibited potent effects in vitro in the reversal of P‐gp‐mediated MDR, suggesting that the compound may be an effective MDR reversing agent in cancer chemotherapy. Drug Dev. Res. 67:862–869, 2006. © 2007 Wiley‐Liss, Inc.     

Substituted tetrahydroisoquinoline compound B3 inhibited P-glycoprotein-mediated multidrug resistance in-vitro and in-vivo

P-glycoprotein (P-gp) mediated multidrug resistance (MDR) is one of the main obstacles in tumour chemotherapy. A promising approach to reverse MDR is the combined use of nontoxic and potent P-gp inhibitor with conventional anticancer drugs. We have examined the potential of a newly synthesized tetrahydroisoquinoline derivative B3 as a MDR-reversing agent. The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was used to examine the effect of B3 on the cytotoxicity in K562/A02 and MCF-7/ADM cells caused by doxorubicin (adriamycin). Accumulation and efflux of P-gp substrate rhodamine123 in K562/A02 and primary cultured rat brain microvessel endothelial cells (RBMECs) were measured to evaluate the inhibitory effect of B3 on P-gp. The K562/A02 xenograft model in nude mice was established to examine MDR-reversing efficacy of B3 in-vivo. The results indicated that co-administration of B3 resulted in an increase on chemosensitivity of K562/A02 and MCF-7/ADM cells to doxorubicin in a dose-dependent manner. Rhodamine123 accumulation in K562/A02 cells and RBMECs were significantly enhanced after the incubation with various concentrations of B3. Furthermore, B3 inhibited the efflux of rhodamine123 from RBMECs. Co-administration of B3 with doxorubicin significantly decreased weight and volume of tumour in nude mice. In conclusion, B3 is a novel and potent MDR reversal agent with the potential to be an adjunctive agent for tumour chemotherapy.     

洛美利嗪对大鼠脑微血管内皮细胞上P-糖蛋白活力的影响与P-gp及mdr1基因mRNA表达无关

目的：研究洛美利嗪对原代培养的大鼠脑微血管内皮细胞（RBMECs）上P-糖蛋白（P-gP）功能和表达的影响。方法：使用流式细胞术分析洛美利嗪对P-gp底物-罗丹明123（rhodaminel23，Rh123）在RBMECs中外排的影响，使用流式细胞术分析了洛美利嗪对RBMECs上P-gp表达的影响，应用RT-PCR技术分析了洛美利嗪对RBMECs mdr1基因mRNA水平表达的影响，还使用Transwell模型研究了洛美利嗪对Rh123通透RBMECs单层细胞转运的影响。结果：洛美利嗪通过抑制了RBMECs胞内Rh123的外排；洛美利嗪对P—gP功能的影响与RBMECs上P-gp及mdr1基因mRNA表达无关；在Transwell模型中，洛美利嗪还能显著增加Rh123跨RBMECs单层细胞膜的、经上室至下室的转运，并抑制相反方向的Rh123的转运。结论：洛美利嗪能显著地抑制RBMECs上P-gp的活性，并对P-gp底物的跨细胞转运产生影响。     

咯萘啶逆转肿瘤多药耐药及其作用机制

目的:利用mdr1~ 的人白血病和乳腺癌多药耐药(MDR)细胞系K562/A02和MCF-7/ADR研究咯萘啶(pyronaridine,PND)对MDR的逆转作用及其机制.方法:采用MTT法、荧光分光光度法、荧光显微镜法、流式细胞仪法和RT-PCR法分别测定PND单独或与阿霉素(DOX)合用,对肿瘤细胞的生长抑制、诱导凋亡、细胞内药物浓度、mdr1基因表达的影响.结果:PND对敏感及耐药细胞均具有生长抑制作用,半数抑制剂量(IC_(50))根据不同细胞在5.10-18.66μmol/L之间;低毒剂量PND显著增强DOX对耐药细胞的细胞毒和诱导凋亡作用,且增加DOX在耐药细胞内的蓄积及减少罗丹明(Rh123)的外排.RT-PCR结果显示,PND对mdr1基因无下调作用.结论:PND可作为第三代P-糖蛋白(P-gp)抑制剂,通过下调P-gp药物外排泵功能而产生强大的逆转MDR效应.     

姜黄素衍生物C15对白血病K562/A02细胞多药耐药的逆转作用

目的: 探讨姜黄素衍生物C15对人白血病K562/A02细胞多药耐药(multidrug resistance,MOR)的逆转作用及其作用机制。方法: 四甲基偶氮唑蓝(MTT)法检测细胞增殖;流式细胞术检测P-糖蛋白(P-gp)外排泵功能和细胞周期;免疫印迹法检测蛋白表达;P-gp-Glo^TM Assay System试剂盒检测P-gp ATP水解酶(ATPase)活性。结果: C15对K562/A02细胞半数抑制浓度(IC₅₀)大于50 μmol·L^-1。对K562/A02细胞无明显细胞毒的浓度为2.5,5.0,10.0 μmol·L^-1的C15逆转对K562/A02细胞对阿霉素(ADR)耐药的倍数分别为2.60,5.39,11.39,对长春新碱(vincristine, VCR)耐药的倍数分别为4.50,18.07,124.35,但是对非P-gp底物的化疗药物顺铂(cisplatin, CIS)和敏感细胞K562基本无逆转效果。2.5,5.0,10.0 μmol·L^-1 C15可以增加耐药细胞K562/A02胞内罗丹明123(Rh-123)的蓄积量分别为1.93,2.30,2.47倍。C15增加阿霉素(adriamycin, ADR)在K562/A02细胞中的蓄积水平,降低P-gp介导的Rh-123外排速率。2.5,10.0 μmol·L^-1 C15与300 nmol·L^-1VCR联合作用后,可使K562/A02细胞的G2/M期比例从9.36%增加到67.57%和69.38%。C15对P-gp蛋白和ATPase的活性没有抑制作用。结论: C15可能是P-gp的非衣物型抑制剂,且具有逆转K562/A02细胞MDR的作用,该作用与其抑制细胞P-gp的外排泵功能有关。     

尼莫地平含药脑脊液对体外PC12细胞损伤的保护作用

目的观察尼莫地平含药脑脊液对多种PC12细胞损伤模型的保护作用,对脑脊液药理实验条件的规范化及其应用进行探讨。方法采用噻唑蓝（MTT）法,观察不同取样时间、不同添加量、不同灭活方法处理的尼莫地平大鼠含药脑脊液对氯化钾损伤的PC12细胞存活力的影响,确定尼莫地平大鼠含药脑脊液的制备条件。并进一步考察该条件制备的尼莫地平大鼠含药脑脊液对过氧化氢、连二亚硫酸钠及谷氨酸钠等因素引起的PC12细胞损伤的保护作用。结果尼莫地平含药脑脊液对氯化钾致PC12细胞损伤的保护率随添加量的增加而提高;相同添加量多次给药（2次·d^-1×3.5d）含药脑脊液的保护率均高于单次给药的含药脑脊液;热灭活、乙醇灭活及丙酮灭活含药脑脊液对PC12细胞均有显著保护作用,其保护率与未灭活含药脑脊液无显著性差异;根据确定条件制备的尼莫地平大鼠含药脑脊液对过氧化氢、连二亚硫酸钠及谷氨酸钠等因素损伤的PC12细胞均具有显著的保护作用。结论尼莫地平含药脑脊液的制备以连续多次给药方案,无需灭活处理,体外添加终体积的10%为宜;对氯化钾等多种原因引起的PC12细胞损伤均具有明显保护作用。     

姜黄素对H_2O_2损伤PC12细胞的保护作用

目的　探讨姜黄素 (curcumin ,Cur)对氧化应激损伤PC12细胞的保护作用。方法　以H2 O2 损伤PC12细胞为氧化应激损伤的模型 ,采用甲氮甲唑蓝 (3 [4 ,5 dimethylthia zol 2 yl] 2 ,5diphenyltetrazoliumbromide ,MTT)法检测细胞增殖状况 ,碘化丙啶 (Propidiumiodide,PI)染色流式细胞术(flowcytometry ,FCM )检测细胞凋亡 ,罗丹明 12 3(Rho damine12 3,Rh12 3)染色FCM检测细胞线粒体膜电位 (mito chondrialpotentialmembrane ,△Ψm) ,双氢罗丹明 12 3(Dihy drohodamine12 3,DHR)染色FCM检测细胞内活性氧 (reac tiveoxygenspecies,ROS)的含量。 结果　 2 0和 4 0 μmol·L-1Cur均可使 2 5～ 4 0 0 μmol·L-1H2 O2 作用 2 4h后对PC12细胞生长的抑制率下降 ,可明显抑制 10 0和 2 0 0 μmo·L-1H2 O2 作用 2 4h后对PC12细胞凋亡的诱导作用和对PC12细胞△Ψm的降低作用 ,可明显降低 10 0和 2 0 0 μmol·L-1H2 O2 作用 12h后细胞内ROS的含量。结论　Cur对氧化应激损伤PC12细胞具有保护作用 ,其机制可能与降低细胞内ROS的含量 ,进而抑制△Ψm的降低有关。