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1.
Heme oxygenase-1 (HO-1) has been strongly highlighted because of its induction in many cell types by toxic stimuli, including oxidative stress. The intense HO-1 immunostaining in the substantia nigra of Parkinson disease (PD) patients suggests its involvement in the pathogenesis of this neurodegenerative disease. In this work we investigated HO-1 expression in rat substantia nigra postnatal cell cultures under conditions mimicking dopamine toxicity and its modulation by glial cell line-derived neurotrophic factor (GDNF), a potent neuroprotective factor for dopaminergic neurons. In neuron–glia cultures, we found that H2O2, a product of dopamine metabolism, or l-3,4-dihydroxyphenylalanine (l-DOPA), the dopamine precursor used in the therapy of PD, induced a fast up-regulation of HO-1 mRNA and protein levels, followed by a secondary down-regulation. H2O2 and l-DOPA also increased HO-1 expression in astrocyte cultures, but with a delayed time course in H2O2-treated cultures. HO-1 expression was decreased in neuron–glia cultures under conditions under which GDNF up-regulation was observed. Because exogenously applied GDNF prevented HO-1 up-regulation in cultures treated with H2O2 or l-DOPA, and antibody neutralization of GDNF prevented the secondary HO-1 down-regulation observed in neuron–glia cultures, we propose that GDNF negatively modulates HO-1 expression induced by oxidative stress. To our knowledge, this is the first report showing the modulation of HO-1 expression by GDNF.  相似文献   

2.
目的:探讨不同氧浓度下小鼠骨骼肌卫星细胞系(C2C12细胞)对H2O2刺激反应的变化及其机制。方法:小鼠骨骼肌卫星细胞系(C2C12细胞),经培养复苏后,将细胞分为7组,每组设8个复孔,各组分别加入浓度为0.1 mmol/L、0.25 mmol/L、0.5 mmol/L、0.75 mmol/L、1 mmol/L、2 mmol/L的H2O2,分别作用1 h、2 h后测细胞活力,选择细胞H2O2刺激的最佳作用时间和浓度;C2C12细胞分为不同氧浓度组:21% O2、12% O2、8% O2、5% O2每组设8个复孔,12 h后,H2O2作用1 h,收集细胞;检测细胞Nrf2蛋白荧光和蛋白表达量,测定Nrf2和抗氧化酶SOD1、SOD2、CAT、NQO-1、HO-1、GPX-1 的mRNA表达量及细胞ROS水平。结果:选择H2O2作用时间相对较短的1 h和浓度0.5 mmol/L作为本实验的H2O2刺激条件。与21%O2组相比,12%O2组细胞Nrf2蛋白荧光增强,Nrf2 的mRNA和蛋白表达以及抗氧化酶SOD1、SOD2、CAT、NQO-1、HO-1、GPX-1的 mRNA表达均显著增加(P<0.05或P<0.01),细胞 ROS水平明显降低(P<0.01);8%O2组仅GPX-1 mRNA显著增加(P<0.05),其他指标变化不大;5%O2组细胞 Nrf2 mRNA和蛋白表达以及抗氧化酶SOD1、SOD2、NQO-1、GPX-1的 mRNA表达均明显降低(P<0.05或P<0.01),细胞 ROS水平则明显升高(P<0.01)。结论:不同氧浓度下C2C12细胞中Nrf2介导的抗氧化系统对H2O2刺激反应不同,12 h的12% O2浓度可促进C2C12细胞Nrf2的抗氧化作用,而5% O2浓度的严重低氧则作用相反。  相似文献   

3.
Cho ES  Lee KW  Lee HJ 《Mutation research》2008,640(1-2):123-130
Oxidative stress induced by reactive oxygen species has been strongly associated with the pathogenesis of neurodegenerative disorders, including Alzheimer's disease. In this study, we investigated the possible protective effects of a cocoa procyanidin fraction (CPF) and procyanidin B2 (epicatechin-(4β-8)-epicatechin) – a major polyphenol in cocoa – against apoptosis of PC12 rat pheochromocytoma (PC12) cells induced by hydrogen peroxide (H2O2). CPF (1 and 5 μg/ml) and procyanidin B2 (1 and 5 μM) reduced PC12 cell death caused by H2O2, as determined by MTT and trypan blue exclusion assays. CPF and procyanidin B2 attenuated the H2O2-induced fragmentation of nucleus and DNA in PC12 cells. Western blot data demonstrated that H2O2 induced cleavage of poly(ADP-ribose)polymerase (PARP), downregulated Bcl-XL and Bcl-2 in PC12 cells. Pretreatment with CPF or procyanidin B2 before H2O2 treatment diminished PARP cleavage and increased Bcl-XL and Bcl-2 expression compared with those only treated with H2O2. Activation of caspase-3 by H2O2 was inhibited by pretreatment with CPF or procyanidin B2. Furthermore, H2O2-induced rapid and significant phosphorylation of c-Jun N-terminal protein kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), and both of these effects were attenuated by CPF or procyanidin B2 treatment. These results suggest that the protective effects of CPF and procyanidin B2 against H2O2-induced apoptosis involve inhibiting the downregulation of Bcl-XL and Bcl-2 expression through blocking the activation of JNK and p38 MAPK.  相似文献   

4.
Alteration of mitochondrial mass of human 143B osteosarcoma cells upon exposure to hydrogen peroxide (H2O2) was investigated. We found that mitochondrial mass and the intracellular level of H2O2 were increased by exogenous H2O2, which was accompanied with up-regulation of functional PKCδ. To investigate the role of PKCδ in H2O2-induced increase of mitochondrial mass, we treated 143B cells with PKCδ activator, bistratene A, and PKCδ inhibitor, rottlerin, respectively. The results show that bistratene A caused an increase of mitochondrial mass and that the H2O2-induced increase of mitochondrial mass was completely suppressed by rottlerin. Furthermore, we found that activation of PKCδ by bistratene A increased the intracellular levels of H2O2 and MnSOD protein expression. By contrast, suppression of PKCδ by rottlerin decreased the intracellular levels of H2O2 and MnSOD protein expression. Moreover, we noted that MnSOD expression was highly correlated with the expression of p53, which was controlled by PKCδ. Finally, we demonstrated that PKCδ was overexpressed in skin fibroblasts of patients with MERRF syndrome. Taken together, we conclude that PKCδ is involved in the regulation of mitochondrial mass and intracellular H2O2 in human cells and may play a key role in the overproliferation of mitochondria in the affected tissues of patients with mitochondrial diseases such as MERRF syndrome.  相似文献   

5.
A solid tumour undergoes ischemia/reperfusion due to deficient vascularization and subsequent formation of new blood vessels. This study investigated the effect of transient oxygen and glucose deprivation (OGD) on proliferation of C6 glioma cells. The cells were subjected to 18 h of OGD followed by reoxygenation in the presence of glucose and different extra-cellular H2O2 concentrations since H2O2 affects cell proliferation. After reoxygenation, the cellular H2O2 concentration was increased returning to control levels within 24 h. Within this period, increase in cell number and MTT-reduction were impaired. Regeneration was completed on the third day of reoxygenation. MTT-reduction increased faster than cell number, indicating an OGD-dependent up-regulation of protein expression. It is concluded that ischemia/reperfusion stress promotes proliferation of tumour cells. An essential factor is a distinct H2O2 concentration. Massive elevation as well as significant reduction of H2O2 concentration impairs the proliferation process.  相似文献   

6.
To examine the involvement of p38 mitogen-activated protein kinase (p38 MAPK) and extra-cellular signal-regulated kinase (ERK) in the oxidative stress-induced increase of permeability in endothelial cells, the effects of a p38 MAPK inhibitor (SB203580) and ERK inhibitor (PD90859) on the H2O2-induced increase of permeability in bovine pulmonary artery endothelial cells (BPAEC) were investigated using a two-compartment system partitioned by a semi-permeable filter. H2O2 at 1 mM caused an increase of the permeation rate of fluorescein isothiocyanate (FITC)-labeled dextran 40 through BPAEC monolayers. SB203580 inhibited the H2O2-induced increase of permeability but PD98059 did not, though activation (phosphorylation) of both p38 MAPK and ERK was observed in H2O2-treated cells in Western blot analysis. An H2O2-induced increase of the intracellular Ca2+ concentration ([Ca2+]i) was also observed and an intracellular Ca2+ chelator (BAPTA-AM) significantly inhibited the H2O2-induced increase of permeability. However, it showed no inhibitory effects on the H2O2-induced phosphorylation of p38 MAPK and ERK. The H2O2-induced increase of [Ca2+]i was not influenced by SB203580 and PD98059. These results indicate that the activation of p38 MAPK and the increase of [Ca2+]i are essential for the H2O2-induced increase of endothelial permeability and that ERK is not.  相似文献   

7.
The aim was to study the effects of a scuba diving session on the lymphocyte antioxidant system, NO synthesis, the capability to produce reactive oxygen species and the antioxidant response in neutrophils. For that purpose seven male divers performed an immersion at a depth of 40 m for 25 min. The same parameters were measured after an hyperbaric oxygen (HBO) treatment at resting conditions in a hyperbaric chamber. Lymphocyte H2O2 production rose after diving and after HBO treatment. Glutathione peroxidase (GPx) and catalase activities increased after diving in lymphocytes, while after HBO exposure only increased GPx activity. Lymphocyte HO-1 mRNA expression increased after diving and after HBO exposure, while iNOS levels and nitrite levels significantly increased after diving. The hyperoxia associated to scuba diving leads to a condition of oxidative stress with increased lymphocyte H2O2 production, HO-1 expression, NO synthesis and antioxidant enzyme adaptations in order to avoid oxidative damage.  相似文献   

8.
Oligodendrocytes have the highest rate of metabolic activity in the brain and are highly vulnerable to oxidative stress. In this work we determined the protective effect of Trolox, a water-soluble analogue of vitamin E, and insulin, a peptide shown to be neuroprotective, in oligodendrocyte lesion induced by hydrogen peroxide (H2O2). Exposure of primary cultures of rat oligodendrocytes to H2O2 dose-dependently decreased their reducing capacity, as determined by the MTT assay. H2O2 (100 μM) had no effect on Bax levels, active-caspase-3, DNA fragmentation or lactate dehydrogenase (LDH) leakage. Nevertheless, under these conditions, H2O2 decreased the levels of myelin basic protein (MBP), used as a marker for oligodendrocyte myelin membrane. Treatment with insulin alone increased MBP levels, but no changes were observed in the presence of insulin plus H2O2. In contrast, incubation with Trolox completely prevented H2O2-induced decrease in MBP expression, suggesting that vitamin E analogues may prevent against oligodendrocyte oxidative damage.  相似文献   

9.
10.
Two new multi-cobalt-containing polyoxotungstates K4Na6Co2(H2O)12{Co(H2O)4[Co2(H2O)10Co4(H2O)2(B--SiW9O34)2]2} · 40H2O (1) and K10Na2[Co4(H2O)2(GeW9O34)2] · 20H2O (2) have been obtained by the routine synthetic reactions in aqueous solution. The polyoxoanion framework of 1 consists of two sandwich-type polyoxoanions [Co4(H2O)2(B--SiW9O34)2]12− connected together by a [CoO2(H2O)4] cluster to constitute the sandwich dimer, and then, four isolated Co(H2O)5 cations coordinate to the dimer through four μ2-O atoms. The polyoxoanion 2 is isomorphic to the sandwich-type polyoxoanion [Co4(H2O)2(B--SiW9O34)2]12− in 1. The magnetic property of compound 1 has been studied by measuring its magnetic susceptibility in the temperature range 2.0–300.0 K, indicating the existence of intramolecular ferromagnetic Co–Co interactions, and, the electrochemical properties of 1 and 2 are detected in the pH 4 buffer solution.  相似文献   

11.
The role of H2O2 as a mediator of UVB-induced apoptosis in keratinocytes   总被引:5,自引:0,他引:5  
Apoptosis is an active form of cell death that is initiated by a variety of stimuli, including reactive oxygen species (ROS) and ultraviolet (UV) radiation. Previously, it has been reported that UVB-irradiation of keratinocytes leads to intracellular generation of hydrogen peroxide (H2O2) and that antioxidants can inhibit ROS-induced apoptosis. Although both UVB-irradiation and H2O2-incubation led to increased intracellular H2O2 levels, the antioxidants catalase and glutathione monoester (GME), inhibited apoptosis only when induced by H2O2, not by UVB. Furthermore, extracellular signal-regulated kinase (ERK), a prominent member of the mitogen-activated protein kinase (MAPK) family, was found to be activated by treatment with both UVB and H2O2. Inhibition of ERK phosphorylation by pre-treatment with PD98059 resulted in enhanced apoptosis after H2O2-exposure. However, no significant difference of apoptosis was observed between cells with and without inhibitor pre-treatment upon UVB-irradiation. DNA damage in the form of cyclobutane pyrimidine dimers was observed after exposure to UVB, but no photoproducts were found in H2O2-treated cells. These results suggest a ROS-independent pathway of UVB-induced apoptosis. Although UVB-irradiation causes moderate increase in H2O2, the generation of H2O2 does not contribute to the induction of apoptosis. Moreover, activation of ERK only blocks H2O2-dependent apoptosis but has no impact on UVB-induced apoptosis.  相似文献   

12.
Glial cell line-derived neurotrophic factor (GDNF) improves motor dysfunction associated with aging in rats and non-human primates, in animal models of Parkinson's disease, and may improve motoric function in patients with advanced Parkinson's disease. These improvements are associated with increased dopamine function in the nigrostriatal system, but the molecular events associated with this increase are unknown. In these studies, 100 micro g of GDNF was injected into the striatum of normal aged (24-month-old) male Fischer 344 rats. The protein levels and phosphorylation of TH, ERK1/2, and related proteins were determined by blot-immunolabeling of striatum and substantia nigra harvested 30 days after injection. In GDNF-treated rats, TH phosphorylation at Ser31 increased approximately 40% in striatum and approximately 250% in the substantia nigra. In the substantia nigra, there was a significant increase in ERK1 phosphorylation. In striatum, there was a significant increase in ERK2 phosphorylation. Microdialysis studies in striatum showed that both amphetamine- and potassium-evoked dopamine release in GDNF recipients were significantly increased. These data show that GDNF-induced increases in dopamine function are associated with a sustained increase in TH phosphorylation at Ser31, which is greatest in the substantia nigra and maintained for at least one month following a single striatal administration of GDNF. These findings, taken from the nigrostriatal system of normal aged rats, may help explain the long lasting effects of GDNF on dopamine function and prior studies supporting that a major effect of GDNF involves its effects on dopamine storage and somatodendritic release of dopamine in the substantia nigra.  相似文献   

13.
Hydrogen peroxide (H2O2) is known to both induce and inhibit apoptosis, however the mechanisms are unclear. We found that H2O2 inhibited the activity of recombinant caspase-3 and caspase-8, half-inhibition occurring at about 17 μM H2O2. This inhibition was both prevented and reversed by dithiothreitol while glutathione had little protective effect. 100–200 μM H2O2 added to macrophages after induction of caspase activation by nitric oxide or serum withdrawal substantially inhibited caspase activity. Activation of H2O2-producing NADPH oxidase in macrophages also caused catalase-sensitive inactivation of cellular caspases. The data suggest that the activity of caspases in cells can be directly but reversibly inhibited by H2O2.  相似文献   

14.
Heme catalases are considered to degrade two molecules of H2O2 to two molecules of H2O and one molecule of O2 employing the catalatic cycle. We here studied the catalytic behaviour of bovine liver catalase at low fluxes of H2O2 (relative to catalase concentration), adjusted by H2O2-generating systems. At a ratio of a H2O2 flux (given in μM/min- 1) to catalase concentration (given in μM) of 10 min- 1 and above, H2O2 degradation occurred via the catalatic cycle. At lower ratios, however, H2O2 degradation proceeded with increasingly diminished production of O2. At a ratio of 1 min- 1, O2 formation could no longer be observed, although the enzyme still degraded H2O2. These results strongly suggest that at low physiological H2O2 fluxes H2O2 is preferentially metabolised reductively to H2O, without release of O2. The pathways involved in the reductive metabolism of H2O2 are presumably those previously reported as inactivation and reactivation pathways. They start from compound I and are operative at low and high H2O2 fluxes but kinetically outcompete the reaction of compound I with H2O2 at low H2O2 production rates. In the absence of NADPH, the reducing equivalents for the reductive metabolism of H2O2 are most likely provided by the protein moiety of the enzyme. In the presence of NADPH, they are at least in part provided by the coenzyme.  相似文献   

15.
Little is currently known concerning the mechanisms responsible for the excessive deposition of redox-active iron in the substantia nigra of subjects with Parkinson's disease (PD). In the present study, we demonstrate that dopamine promotes the selective sequestration of non-transferrin-derived iron by the mitochondrial compartment of cultured rat astroglia and that the mechanism underlying this novel dopamine effect is oxidative in nature. We also provide evidence that up-regulation of the stress protein heme oxygenase-1 (HO-1) is both necessary and sufficient for mitochondrial iron trapping in dopamine-challenged astroglia. Finally, we show that opening of the mitochondrial transition pore (MTP) mediates the influx of non-transferrin-derived iron into mitochondria of dopamine-stimulated and HO-1-transfected astroglia. Our findings provide an explanation for the pathological iron sequestration, mitochondrial insufficiency, and amplification of oxidative injury reported in the brains of PD subjects. Pharmacological blockade of transition metal trapping by "stressed" astroglial mitochondria (e.g., using HO-1 inhibitors or modulators of the MTP) may afford effective neuroprotection in patients with PD and other neurological afflictions.  相似文献   

16.
We examined the mechanism through which leptin increases Na+, K+-ATPase activity in the rat kidney. Leptin was infused under anaesthesia into the abdominal aorta proximally to the renal arteries and then Na+, K+-ATPase activity was measured in the renal cortex and medulla. Leptin (1 μg/kg min) increased Na+, K+-ATPase activity after 3 h of infusion, which was accompanied by the increase in urinary H2O2 excretion and phosphorylation level of extracellular signal regulated kinase (ERK). The effect of leptin on ERK and Na+, K+-ATPase was abolished by catalase, specific inhibitors of epidermal growth factor (EGF) receptor, AG1478 and PD158780, as well as by ERK inhibitor, PD98059, and was mimicked by both exogenous H2O2 and EGF. The effect of leptin was also prevented by the inhibitor of Src tyrosine kinase, PP2. Leptin and H2O2 increased Src phosphorylation at Tyr418. We conclude that leptin-induced stimulation of renal Na+, K+-ATPase involves H2O2 generation, Src kinase, transactivation of the EGF receptor, and stimulation of ERK.  相似文献   

17.
Glial cell line-derived neurotrophic factor (GDNF) is a potent neuroprotective molecule for dopaminergic neurons of the nigrostriatal pathway that degenerate in Parkinson's disease. We have previously shown that H2O2- or l-3,4-dihydroxyphenylalanine (l-DOPA)-challenged dopaminergic neurons trigger the release of soluble factors that signal ventral midbrain astrocytes to increase GDNF expression. In the present work, we evaluated whether the factors released by ventral midbrain-challenged cells were able to alter GDNF expression in striatal cells, the targets of dopaminergic neurons projecting from the substantia nigra, and investigated the signalling pathways involved. Our data showed that soluble mediators released upon H2O2- or l-DOPA-induced dopaminergic injury up-regulated GDNF in striatal cells, with different temporal patterns depending on the oxidative agent used. Conditioned media from H2O2- or l-DOPA-challenged midbrain astrocyte cultures failed to up-regulate GDNF in striatal cultures. Likewise, there was no direct effect of H2O2 or l-DOPA on striatal GDNF levels suggesting that GDNF up-regulation was mediated by soluble factors released in the presence of failing dopaminergic neurons. Both phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways were involved in striatal GDNF up-regulation triggered by H2O2-induced dopaminergic injury, while diffusible factors released in the presence of l-DOPA-challenged dopaminergic neurons induced GDNF expression in striatal cells through the activation of the MAPK pathway. These soluble mediators may constitute, in the future, important targets for the control of endogenous GDNF expression enabling the development of new and, hopefully, more efficient neuroprotective/neurorestorative strategies for the treatment of Parkinson's disease.  相似文献   

18.
Continuous chemostat cultures of a recombinant strain of Aspergillus niger (B1-D), engineered to produce the marker protein hen egg white lysozyme, were investigated with regard to their susceptibility to oxidative stress. The culture response to oxidative stress, produced either by addition of exogenous hydrogen peroxide (H2O2) or by high dissolved oxygen tension (DOT), was characterised in terms of the activities of two key defensive enzymes: catalase (CAT) and superoxide dismutase (SOD). Since the morphology is so critical in submerged fungal bioprocesses, the key morphological indices were analysed using a semi-automated image analysis system. Both oxidant stressors, H2O2 and elevated DOT, increased both enzyme activities, however, the extent was different: exogenous H2O2 led mainly to increased CAT activity, whereas gassing with O2 enriched air, which resulted in a DOT of 165% of air saturation, increased both enzyme activities more than 2-fold compared with the control steady state culture. Addition of exogenous H2O2 resulted in shorter hyphae compared with control steady state cultures. These findings indicate that it is unsound to use exogenous H2O2 to simulate oxidative stress induced by elevated dissolved oxygen levels since the response to each might be quite different, both in terms of enzymatic (defensive) responses and in terms of culture morphology.  相似文献   

19.
目的探讨微小RNA-142-3p(miR-142-3p)对过氧化氢诱导的心肌细胞损伤的影响及其作用机制。 方法构建氧化应激损伤模型,以H9C2心肌细胞为研究对象,实验将心肌细胞转染后分为正常对照组、H2O2组、H2O2+miR-142-3p组、H2O2+miR阴性对照组、H2O2+?si-?ELAVL1组、H2O2+siRNA对照组、H2O2+miR-142-3p+pcDNA-ELAVL1组、H2O2+miR-?142-3p+pcDNA组。分别采用qRT-PCR与Western Blot检测细胞中miR-142-3p与ELAVL1表达;检测各组活性氧(ROS)生成水平;MTT检测细胞存活率,流式细胞术检测细胞凋亡。双荧光素酶报告实验验证miR-142-3p与ELAVL1的靶向作用。Western Blot检测细胞中Cleaved Caspase-3、STAT3、Caspase-3、p-STAT3蛋白表达。两组间比较采用两样本t检验;多组间比较采用单因素方差分析,两两比较采用LSD-t检验。 结果H2O2组心肌细胞中miR-142-?3p(0.26±0.06)、p-STAT3表达水平(0.36±0.04)、细胞存活率(61.73±6.48)﹪与正常对照组相比下降(P均< 0.01),而ROS水平(1?566.38±121.57)、细胞凋亡率(27.46±1.73)﹪、Cleaved Caspase-3(0.68±0.08)及ELAVL1表达水平(4.23±0.31)均升高(P均< 0.01);双荧光素酶报告实验证实ELAVL1是miR-142-3p的靶基因;miR-142-3p过表达或沉默ELAVL1表达可明显促进心肌细胞存活、上调p-STAT3表达,而抑制细胞凋亡及Cleaved Caspase-3表达;ELAVL1过表达可逆转miR-142-3p对过氧化氢处理H9C2细胞的保护作用。 结论miR-142-?3p可通过抑制ELAVL1表达进而减轻过氧化氢诱导的心肌细胞损伤,其可能通过影响STAT3信号通路而保护心肌细胞。  相似文献   

20.
Excessive generation of reactive oxygen species (ROS) in the central nervous system (CNS) is a leading cause of neuronal injury. Despite yet unknown mechanisms, oxidant compounds such as H2O2 have been shown to stimulate the release of arachidonic acid (AA) in a number of cell systems. In this study, H2O2 and menadione, a compound known to release H2O2 intracellularly, were used to examine the phospholipases A2 (PLA2) responsible for AA release from primary murine astrocytes. Both H2O2 and menadione dose-dependently stimulated AA release, and the release mediated by H2O2 was completely inhibited by catalase. H2O2 also stimulated phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). However, complete inhibition of cPLA2 phosphorylation by U0126, an inhibitor for mitogen-activated protein kinase kinase (MEK) and GF109203x, a nonselective PKC inhibitor preferring the conventional and novel isoforms, only reduced H2O2-stimulated AA release by 50%. MAFP, a selective, active, site-directed, irreversible inhibitor of both cPLA2 and the Ca2+-independent iPLA2, nearly completely inhibited H2O2-mediated AA release; but, HELSS, a potent irreversible inhibitor of iPLA2, only inhibited H2O2-mediated AA release by 40%. Along with the observation that H2O2-mediated AA release was only partially inhibited upon chelating intracellular Ca2+ by BAPTA, these results indicate the involvement of both cPLA2 and iPLA2 in H2O2-mediated AA release in murine astrocytes.  相似文献   

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