共查询到20条相似文献，搜索用时 15 毫秒
1.
AIM: To explore the mechanism of ET-1, NO and PGI2 release from coronary artery endothelial cells(CAEC) induced by acute hypoxia. METHODS: Bovine coronary artery endothelial cells were cultured and [45 Ca2+] was used to investigate the difference of calcium uptake between normoxia group and hypoxia group(3% O2). The contents of ET-1, NO and PGI2 in media of normoxia group, hypoxia group and hypoxia + verapamil group were measured 24 h after hypoxia. RESULTS: [ 45 Ca2+] uptake by CAEC in hypoxia group was 1.9 times more than normoxia group(P< 0.01). Hypoxia + verapamil group released more PGI2, ET-1 and less NO than hypoxia group(P< 0.05). CONCLUSION: Changes of ET-1, NO and PGI2 releases during hypoxia may be caused by the inflow of Ca2+ into coronary artery endothelial cells. 相似文献
2.
AIM:To investigate the effect of lipopolysaccharide (LPS) priming on macrophage(MΦ).METHODS:Macrophage cell line RAW264.7 were pretreated with or without LPS for 1 h, then challenged with PMA, or LPS, muramyl dipeptide(MDP), Zymosan, formyl-methionyl-leucyl-phenylalanine(FMLP) for 1 h. O2- production in supernatants and intracellular free calcium([Ca2+]i) were measured, and changes in [Ca2+]i and LPS induced O2- production were compared.RESULTS:LPS pretreatment significantly increased O2- production in RAW264.7 cells challenged with the stimuli, and in a certain extent, both O2- production and increase of resting intracellular [Ca2+]i were dose- and time-dependent on LPS pretreatment.Furthermore, the peak [Ca2+]i was significantly higher in LPS pretreated groups than that of LPS unpretreated groups when challenged with PMA. Pretreatment with Ca2+ inophore A23187 mimicked the LPS priming effects on O2- production, but pretreatment with Ca2+ chelator BAPTA and EGTA blocked this priming effect.CONCLUSION:LPS-induced MΦ priming effect on O2- production is dependent on elevation of resting intracellular [Ca2+]i. 相似文献
3.
AIM: To study the effects of cyproheptadine (Cyp) and anisodamine (Ani) on the changes of intracellular free Ca2+ concentration ([Ca2+]i) induced by tumor necrosis factor (TNFα) in single endothelial cells, and to explore the mechanisms of TNFα mediated shock and antishock actions of Cyp and Ani. METHODS: Human umbilical vein endothelial cell strains (ECV304) were seed in 35 mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca2+]i in single endothelial cell was determined by laser scanning confocal microscopy (LSCM). RESULTS: [Ca2+]i in single endothelial cell after stimulation of TNFα rapidly increased in a dose-dependent manner and approached the peak value within 60 seconds, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca2+]i elevation was more obvious in nuclear than in cytoplasma, and decreased slowly. Cyp (3×10-5, 6×10-5 mol/L) and Ani (2×10-5, 4×10-5 mol·L-1) markedly inhibited TNFα (1.2×10-9 mol·L-1)-induced [Ca2+]i elevation. CONCLUSIONS: TNFα markedly induces elevation of [Ca2+]i in single endothelial cell, it may be an important mechanism of TNFα-induced shock and tissue injury. Cyp and Ani obviously suppress TNFα-induced [Ca2+]i elevation, which probably is one of the mechanisms of their antishock effects. 相似文献
4.
AIM:To study the effects of oxidized high-density lipoprotein (oxHDL) on the expression of monocyte chemoattractant protein-1(MCP-1) and intercellular adhesion molecule-1(ICAM-1) and intracellular free calcium concentration ([Ca2+]i) level in cultured human umbilical venous endothelial cells(HUVECs). METHODS:The MCP-1 protein content in the medium of conditioned HUVEC was measured by ELISA, and the ICAM-1 on HUVECs was detected by indirect immunofluorescence, and [Ca2+]i was determined by Fluo-3/AM, the injury of cells was observed by scanning electron microscopy (SEM).RESULTS:oxHDL could induce the expression of MCP-1 and ICAM-1 in HUVECs. In oxHDL group (HUVECs were incubated with 100 mg protein/L oxHDL for 24 h), the levels of MCP-1, ICAM-1 and [Ca2+]i increased by 160%, 60% and 70% respectively compared with the control group (P＜0.01). When HUVECs were incubated with 300 mg protein/L oxHDL for 24 h, cells were injured obviously. CONCLUSION:By inducing the expression of ICAM-1 and MCP-1 in endothelial cells, oxHDL may promote monocyte-endothelium adhesion and monocyte migration to intima, it may promote atherosclerosis as oxidized low-density lipoprotein (oxLDL). 相似文献
5.
AIM: To investigate the role of reactive oxygen species (ROS) and calcium overload in the apoptosis of MC3T3-E1 cells induced by high glucose. METHODS: Cultured mouse skull bone-derived osteoblast cell line MC3T3-E1 was treated with high concentration of D-glucose to induce apoptosis. The proliferation of MC3T3-E1 cells was detected by MTT assay after treated with different concentrations of D-glucose for 24 h and 48 h. The apoptotic rate and the intracellular levels of calcium and ROS were also measured after the cells were treated with high glucose (35 mmol/L) for 24 h. RESULTS: After high glucose treatment, the cell proliferation was inhibited. The early apoptosis and total cell death increased to (24.16?3.53)% and (63.74?4.32)%,respectively. High glucose treatment significantly increased intracellular levels of ROS and Ca2+. The increased apoptotic rate was reduced by addition of antioxidant N-acetylcysteine and calcium chelator BAPTA-AM. Inhibition of store-operated Ca2+ channels by La3+ also decreased the intracellular level of Ca2+ and cell apoptosis induced by high glucose. CONCLUSION: High glucose increases intracellular ROS level and the release of Ca2+ through the store-operated Ca2+ channels, thus resulting in intracellular Ca2+ overload and leading to apoptosis of osteoblasts. 相似文献
6.
AIM:To explore the effects of levcromakalim(Lev) on pulmonary arterial endothelial cells (PAEC) and smooth muscle cells (PASMC) exposed to hypoxia and the mechanisms involved.METHODS:The effects of Lev on [Ca2+]i, and expression of PKCα, eNOS, iNOS and PDGF-B mRNA and protein levels were observed. The nitrite (NO2-) and entothelin-1(ET-1) concentrations in supernatant in cultured PAEC and PASMC were measured. The proliferation and apoptosis of PASMC was also detected.RESULTS:When PASMC were exposed to hypoxia, Lev reduced concentration of ET-1 in cultured cell supernatant, lowed the expression of PKCα, iNOS and PDGF-B both at mRNA and protein levels, decreased [Ca2+]i concentration, increased proliferation and promoted the apoptosis in PASMC. However, in the presence of Lev, the [Ca2+]i concentration was not changed in the hypoxic PAEC. The NO2- concentration in cultured cell supernant and expression of eNOS at mRNA and protein levels in hypoxic PASMC and PAEC were also unchanged. The downregulated ET-1 activity in PASMC and PAEC and proliferation in PASMC involved in the inhibition of PKCα signaling pathway.CONCLUSIONS:Lev reduce some disadvatage effect of hypoxia on PASMC and PAEC. The mechanism of Lev action may partly involve in the downregulation of PKCα signaling functions. 相似文献
7.
AIM: To investigate the effects of salidroside on intracellular free calcium concentration [Ca2+]i, apoptosis, mitochondrial membrane potential (MMP) and activity during injury induced by hypoxia/hypoglycemia in cultured SH-SY5Y cells. METHODS: Mitochondrial activity was measured by methylthiazolyl tetrazolium test. MMP,[Ca2+]i and apoptosis were measured by flow cytometry. RESULTS: SH-SY5Y cells were cultured in a hypoxia/hypoglycemia condition for 2, 4, 6 and 12 h,[Ca2+]i and apoptosis rate significantly increased compared with control group (P<0.01). After hypoxia /hypoglycemia cultures, MMP and mitochondrial activity declined 29.17% (P<0.01) and 38.80% (P<0.01) at 2 h, 56.72% (P<0.01) and 63.58% (P<0.01) at 12 h, were lower than that in control group (P<0.01). Salidroside significantly decreased [Ca2+]i and apoptosis rate, and increased MMP and mitochondrial activity in hypoxia /hypoglycemia-treated SH-SY5Y cells. CONCLUSIONS: Salidroside might inhibit the decline in MMP and mitochondrial activity induced by hypoxia /hypoglycemia, and has an inhibitory effects on neuronal apoptosis. The mechanism might be related to inhibiting intracellular calcium overload. 相似文献
8.
AIM: To determine whether nuclear Ca2+ is independently regulated from the cytosolic Ca2+ and nuclear Ca2+ oscillation induced by many modulating factors in cultured rat neonatal myocytes and its mechanism. METHODS: Rat neonatal cardiac myocytes were cultured, and fluo-4/AM was loaded as calcium probe. The changes of cytosolic and nuclear Ca2+ were observed by confocal laser microscopy. RESULTS: Calcium fluorescent intensity oscillated slightly in myocardiocytes and the average intensity was much higher in the nucleus than that in the cytosole. Ca2+ oscillation in nucleus and cytosole induced by norepinephrine, isoproperenol, ATP were completely blocked by Ca2+-ATPase antagonist thapsigargin (10-6 mol/L),L-type Ca2+ channel blocker verapermil (500 μmol/L) and KCl (20 mmol/L). Ca2+-ATPase antagonist thapsigargin completely blocked the propagation of Ca2+ waves and simutaneouly induced a temporary Ca2+ increase followed by a magnificient drop and loss of response to norepinephrine. CONCLUSIONS: The results suggested that generation and maintenance of calcium oscillation both in cytosole and nucleus depended on extracellular Ca2+ influx, membrane potential, Ca2+ release and uptake of cytosolic and nuclear calcium stores. The difference between cytosolic calcium and nuclear calcium indicated that calcium regulating system relatively independent of cytosole may exist in nucleus. 相似文献
9.
Pulmonary hypertension induced by high pulmonary blood flow involves a variety of complex mechanisms, including endothelial damage, pulmonary artery smooth muscle relaxation-contraction disorder and vascular remodeling. Besides, the factor of ion channels in pulmonary artery smooth muscle cells is also highly correlated to vasoconstriction. In recent years, many studies have shown that activation of Ca2+-activated Cl- channels is responsible for the membrane depolarization of pulmonary artery smooth muscle cells, and plays an important role in the regulation of vascular tone and vasoconstriction. This article reviews the biophysical and pharmacological characteristics of Ca2+-activated Cl- channels as well as the influence of Ca2+-activated Cl- channels in high pulmonary blood flow-induced pulmonary hypertension. 相似文献
10.
AIM: To study the effect of endothelial cell activation on the homing of hematopoietic stem cells (HUHSC) during transplantation. METHODS: Human umbilical vein endothelial cells (HUVEC) were cultured to single layer and activated by vascular endothelial growth factor (EVGF), granulocyte colony stimulating factor (G-CSF) and lipopolysaccharide (LPS), respectively. The HUHSC, enriched by eliminating red blood cells, granulocytes, monocytes and lymphocytes from cord blood, were cocultured with activated HUVEC to make adhesion. The adhesive ability of activated HUVEC to C-Kit+ HUHSC was assayed by ELISA. Anti-VCAM-1 monoclonal antibody was used to detect the effect of activation on HUVEC and HUHSC interactions. RESULTS: Resting HUVEC had a little adhesive ability to HUHSC. A great enhancement of adhesive ability was showed when HUVEC was activated by VEGF, G-CSF and LPS. In the presence of anti-VCAM-1, the adhesive ability of activated HUVEC was decreased remarkablely. CONCLUSION: HUHSC homing may be related to the activation of endothelial cells and adhesion molecules. 相似文献
11.
AIM: To explore regulation of lipopolysaccharide (LPS)-induced elevation of Ca2+ intracellular level in alveolar macrophages(AMs) from patients with chronic bronchitis by Angelica Sinensis and nifedipine.METHODS:AMs was obtained from 7 patients with chronic bronchitis and 6 normal controls by bronchoalveolar lavage and intracellular Calevel was detected after adding Angelica Sinensis, nifedipine or LPS to the supernatant of AMs loaded by Fura-2. RESULTS: In contrast with normal control group (99.65±32.21 nmol/L), intracellular Ca2+ level in AMs from chronic bronchitis group (189.47±23.69 nmol/L) was increased significantly in the absence of extracellular Ca2+ but not 1 mmol/L. Intracellular Ca2+ level in AMs from chronic bronchitis group were significantly increased by adding 10 μg/mL LPS to the supernatant of AMs. LPS-induced elevation of intracellular Ca2+ level in AMs from chronic bronchitis group was completely inhibited by Angelica Sinensis or nifedipine.CONCLUSION: Both Anelica Sinensis and nifedipine may inhibit activation of AMs from patients with chronic bronchitis by reducing LPS-induced elevation of intracellular Ca2+ level in AMs, suggested that these two medicines may inhibit non-specific inflammation of airways in chronic bronchitis. 相似文献
12.
MA Jie WANG Jiao-jiao WANG Lu LI Xin-juan WANG Guo-hong ZHAO Hong-gang LI Dong-liang 《园艺学报》2016,32(8):1408-1412
AIM: To investigate the effects of sodium hydrosulfide (NaHS), a donor of hydrogen sulfide (H2S), on the membrane permeability, intracellular Ca2+ concentration ([Ca2+]i) and the release of IL-1β induced by adenosine triphosphate (ATP) in rat microglia, and to explore the effect of H2S on ATP-P2X purinergic signaling pathway and the molecular mechanism of its neuroprotective effect. METHODS: Rat microglia in logarithmic growth phase were used in the study. The[Ca2+]i was detected by Fura-2/AM staining. Fluorescent dye YO-PRO-1 was used to observe the membrane permeability. Interleukin-1β (IL-1β) was measured by rat IL-1β ELISA kits. RESULTS: The YO-PRO-1 fluorescence intensity was obviously elevated by ATP induction in a dose-dependent manner in the rat microglia, but this effect was counteracted by NaHS pretreatment (P<0.05).[Ca2+]i rapidly increased and then decreased slowly, forming a stable platform for a long time when rat microglia were treated with ATP. Ca2+ spike activity induced by ATP had no change, but the platform disappeared (P<0.05) after NaHS pretreatment. The ATP and LPS together facilitated the release of IL-1β, but the phenomenon was inhibited by NaHS (P<0.05). CONCLUSION: Hydrogen sulfide may decrease the membrane permeability, calcium inflow and IL-1β release in rat microglia activated by high dose of ATP. The cytoprotection of hydrogen sulfide may be mediated by purinergic signaling pathway. 相似文献
13.
XING Yan-yan WANG Jun-bing XIE Sai GONG Zheng LU Da-xiang DONG Jun TANG Hong-mei PAN Rui DENG Qin-ying XIONG Guo-yin 《园艺学报》2012,28(10):1746-1750
AIM: To study the possible mechanism of curcumin on actinomycin D (ActD)/tumor necrosis factor α (TNF-α)-induced injury in PC12 cells and rat hippocampal neurons. METHODS: PC12 cells were divided into control group, TNF-α group, ActD group, curcumin group, ActD/TNF-α group and curcumin+ActD/TNF-α group. The cells were cultured for 24 h. Inverted fluorescence microscopy was used to observe the morphological changes of the cells in each group. Annexin V/PI double staining was applied to analyze the apoptosis of PC12 cells. The level of intracellular Ca2+ was detected by Fluo-3 AM staining. Rat hippocampal slices were prepared and divided into the same groups as the PC12 cells. Extracellular microelectrode recording technique was used to observe and calculate the changes of long-term potentiation (LTP) in different groups. RESULTS: Apoptosis of PC12 cells was induced by ActD/TNF-α. Curcumin protected the PC12 cells from ActD/TNF-α-induced apoptosis (P<0.05). ActD/TNF-α increased the intracellular Ca2+ concentration. Curcumin significantly reduced ActD/TNF-α-induced apoptosis by decreasing the intracellular Ca2+ concentration (P<0.05), inversed the effect of ActD/TNF-α on LTP in hippocampal slices, and improved the synaptic plasticity (P<0.05). CONCLUSION: Curcumin protects ActD/TNF-α-induced neuronal damage by depressing the intracellular Ca2+ concentration and maintaining the homostasis of intracellular calcium. 相似文献
14.
AIM: To investigate the changes of cytosolic free calcium concentration([Ca2+]i) and expression of Bcl-2 in HL-60 cells treated by 6F isolated from Pteris semipinnata L.(PSL), and to discuss the relations between calcium ion and cytotoxicity and DNA fragment induction effects of 6F. METHODS: HL-60 cells were used as in vitro model. [Ca2+]i was measured on fluorescent spectrophotometry using Fura-2/AM as Ca2+ indicator. Bcl-2 expressing level was measured by flow cytometry. Tetrazolium salt(MTT) and diphenylamine staining methods were applied for cytotoxicity assay and DNA fragmentation detection, respectively. RESULTS: [Ca2+]i increased obviously in a dose and time dependent manner after treated HL-60 cells with 6F. 6F decreased the expressing level of Bcl-2. Adding 2 mmol/L Ca2+ to the medium, or 1 mmol/L EDTA to chelate Ca2+, or 4 μmol/L calcium ionophore A 23187 to increase the concentration of cytosolic Ca2+, the DNA fragment induction by 6F was not affected, whereas the cytotoxicity of 6F was enhanced. 250 μmol/L Zn2+ attenuated the DNA fragment induction, and the cytotoxicity of 6F against HL-60 cells was enhanced significantly. CONCLUSION: It was speculated that the decreased expressing of Bcl-2 by compound 6F was related to increased [Ca2+]i in HL-60 cells, and DNA fragment induction was possibly catalyzed by Ca2+ - independent DNase. 相似文献
15.
AIM:We examined the effect of interleukin-2 (IL-2) on calcium handling of rat cardiomyocytes. METHODS:The effects of steady state and transient changes in stimulus frequency on the intracellular calcium transient were investigated in the isolated ventricular myocytes with spectrofluorometry technique. RESULTS: Under the steady state (0.2 Hz), IL-2 at 2×105U/L decreased the peak [Ca2+] i and amplitude of the [Ca2+]i transient, increased the diastolic calcium level, and prolonged the decay of the calcium transient. At 1.25 mmol/L of extracellular [Ca2+], when increasing the stimulus frequency from 0.2 to 1.0 Hz, diastolic calcium level and peak [Ca2+] i as well as the amplitude of the transient were increased. The positive frequency relationship was blunted in the IL-2-treated myocytes and this was not normalized by increasing extracellular [Ca2+] to 2.5 mmol/L. The caffeine induced Ca2+ release was increased with increase in stimulus frequency. IL-2 inhibited the frequency relationship of caffeine induced Ca2+ release. The restitution was not different between control and IL-2 groups at the 1.25 mmol/L of extracellular [Ca2+], which was slowed in IL-2-treated myocytes when the extracellular [Ca2+] was increased to 2.5 mmol/L. CONCLUSIONS:It is concluded that the blunted frequency response of IL-2-treated myocytes was resulted from the decrease in SR Ca2+ release, which was related to depression of SR function. Despite the evidence of depressed SR Ca2+ uptake, the restitution of calcium transient at 1.25 mmol/L of extracellular remains unchanged, which maybe due to the increase in the Na+/Ca2+ exchanger activity. 相似文献
16.
LIU Xiao-ni CAO Dong-qing ZHANG Na-na TAO Ran DING Ying-jiong JIN Hui-ming LU Ning 《园艺学报》2016,32(12):2133-2138
AIM: To investigate the role of reactive oxygen species (ROS) in the regulation of intracellular Ca2+ induced by angiotensin II (Ang II) in the primarily cultured medullary neurons. METHODS: Primarily cultured medullary neurons were prepared from 14-day-old embryos of Sprague-Dawley rats in the study. The identification of medullary neurons was assessed by double-labeling immunofluorescence. To explore the role of ROS, mainly the superoxide (O2·), the O2·generation was measured using the fluorogenic probe dihydroethidium (DHE). To determine intracellular free calcium concentration ([Ca2+]i), the neurons were loaded with the Ca2+-specific dye Fura-2/AM. The cell viability after adding Ang II was also examined using CCK-8 assay. RESULTS: Most of the cultured cells were medullary neurons, more than 80% of which were glutamate positive neurons. Ang II (5 μmol/L) increased the level of ROS within 10 min in the medullary neurons. Ang II at 5 μmol/L induced a significant[Ca2+]i increase in the medullary neurons, and the effect of Ang II occurred rapidly and reached a peak within 20 min after administration. The level of[Ca2+]i started to decline after washout. The Ca2+ elevation induced by Ang II was significantly decreased by apocynin or TEMPOL. No significant difference in the cell viability between control group and 5 μmol/L Ang II treatment group was observed. CONCLUSION: ROS is involved in the regulation of[Ca2+]i induced by Ang II in the primarily cultured medullary neurons, suggesting a potential intracellular signaling mechanism involved in the Ang II-mediated oxidant regulation of central neural control of blood pressure. 相似文献
17.
AIM: To investigate intracellular free calcium ( [Ca2+]i ) alterations in hypothalamus of febrile rabbits induced by endotoxin (ET), and compare with the effect of ET and IL-1β on i in hypothalamic neurocytes from normothermia rabbits. METHOD: The concentration of [Ca2+]i was determined by using spectrofluorometer and fluorescent Ca2+ probe fura-2 /Am. RESULTS: 1. A minute dose of ET (2 ng/mL) induced a significant rise in [Ca2+]i in hypothalamic neurocytes from normothermia rabbits. The rise in [Ca2+]i in hypothalamic neurocytes from febrile rabbits induced by intravenous injection of ET was also observed. 2. In hypothalamic neurocytes from normotheria rabbits, IL-1β failed to affect [Ca2+]i at concentrations of 100, 500, 1 000ng/mL, respectively. CONCLUSION:The action site of low concentration of calcium that plays a regulatory role during fever seems unlikely to be in cytosolic compartment of hypothalamic neurons. The change of [Ca2+]i in hypothalamic neurocytes by ET can not be considered the direct effect of IL-1β. 相似文献
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19.
AIM: To study the effects of tetrandrine(Tet) and fructose-1, 6-diphosphate(FDP) on the elevated intrasynaptosomal [Ca2+]i induced by excitatory amino acids(EAA). METHODS: A rapid method for preparing synaptosomes was used, and intrasynaptosomal free calcium([Ca2+]i) was measured by using the fluorescent indicator quin-2. RESULTS: L-glutamate(Glu, 100 μmol/L), aspartate(Asp, 100 μmol·L-1), N-methy1-D-aspartate(100 μmol/L) and Glu(50 μmol/L) plus Asp(50 μmol/L) all elevated intrasynaptosomal [Ca2+]i in a dose-dependent manner. Pretreatment with Tet(10, 30, 60 μmol/L), FDP(15, 30, 75, 150 μmol/L), MK-801(10, 20 μmol/L) and Tet(15, 30 μmol/L) plus FDP(15, 30 μmol/L) all attenuated the increase in intrasynaptosomal [Ca2+]i induced by EAAs mentioned as above in a dose-dependent manner, and the effect of Tet plus FDP was most significant. CONCLUSION: Both Tet and FDP inhibited a rise in intrasynaptosomal [Ca2+]i induced by EAAs, which may be one of mechanisms that Tet and FDP pretect cerebral tissues against ischemia injury. 相似文献
20.
LI Xiu-juan SHEN Hui WEI Lin-yu WANG Guo-hong ZHANG Li-bing LI Chao-kun LI Xin-juan WANG Lu ZHAO Hong-gang SONG Jing-gui LI Dong-liang 《园艺学报》2017,33(9):1587-1592
AIM: To investigate the neuroprotective effect of progesterone against adenosine triphosphate (ATP)-injured human neuroblastoma SH-SY5Y cells.METHODS: The SH-SY5Y cells in the logarithmic phase were divided into different groups according to the progesterone and ATP concentrations. The cell viability was measured by CCK-8 assay. The membrane permeability was detected using fluorescent dye YO-PRO-1. Cytosolic Ca2+ concentration was measured with fluorescent dye Fluo-3/AM. The expression of purinergic P2X7 receptor was assessed by Western blot.RESULTS: The viability of the SH-SY5Y cells was significantly decreased (P<0.05) and YO-PRO-1 uptake was obviously increased (P<0.05) in a concentration-dependent manner compared with control group when SH-SY5Y cells were treated with ATP at 1, 3, 5 and 7 mmol/L for 2 h. The viability reduction of the SH-SY5Y cells induced by ATP was obviously counteracted by treatment with progesterone at 3, 10 and 30 nmol/L for 30 min (P<0.05) as compared with ATP group. YO-PRO-1 fluorescence enhancement induced by ATP in SH-SY5Y cells was significantly reduced (P<0.05) by progesterone (30 nmol/L) or P2X7 receptor antagonist KN-62 (500 nmol/L) pretreatment for 30 min, and no obvious difference between treatments with progesterone and KN-62 was observed. Cytosolic Ca2+ fluorescence intensity in normal group was a little, but that in ATP group was increased (P<0.05). Progesterone or KN-62 pretreatment significantly decreased the cytosolic fluorescence intensity of Ca2+ induced by ATP (P<0.05). However, no obvious difference between treatments with progesterone and KN-62 was found. The expression of P2X7 receptor in ATP group was significantly higher than that in control group (P<0.05), and progesterone inhibited ATP-induced P2X7 receptor expression (P<0.05).CONCLUSION: Progesterone inhibits P2X7 receptor expression, membrane pore formation, intracellular Ca2+ increase and cell death induced by ATP, so progesterone may protect SH-SY5Y cells against ATP-induced injuries. 相似文献