Polyamines （PA）, polyamine oxidases, copper amine oxidases, and nitric oxide （NO） play important roles in physiology and stress responses in plants. NO biosynthesis as a result of catabolism of PA by polyamine oxi...Polyamines （PA）, polyamine oxidases, copper amine oxidases, and nitric oxide （NO） play important roles in physiology and stress responses in plants. NO biosynthesis as a result of catabolism of PA by polyamine oxidases and copper amine oxidases may explain in part PA-mediated responses. Involvement of a copper amine oxidase gene, COPPER AMINE OXIDASEI （CuAO1）, of Arabidopsis was tested for its role in stress responses using the knockouts cuao1-1 and cuaol-2. PA-induced and ABA-induced NO production investigated bY fluorometry and fluorescence microscopy showed that the cuaol-1 and cuaol-2 are impaired in NO production, suggesting a function of CuAO1 in PA and ABA-mediated NO production. Furthermore, we found a PA-dependent increase in protein S-nitrosylation. The addition of PA and ABA also resulted in H2O2 increases, cuao1-1 and cuao1-2 showed less sensitivity to exogenous ABA supplementation during germination, seedling establishment, and root growth inhibition as compared to wild-type. In response to ABA treatment, expression levels of the stress-responsive genes RD29A and ADH1 were significantly lower in the knockouts. These observations characterize cuao1-1 and cuao1-2 as ABA-insensitive mutants. Taken together, our findings extend the ABA signal transduction network to include CuAO1 as one potential contributor to enhanced NO production by ABA.展开更多
Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this wo...Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this work, Our experiment showed that NO exists in guard cell of Vicia faba L., and NO is involved in signal transduction of JA- induced stomata closuring: (ⅰ) JA enhances NO synthesis in guard cell; (ⅱ) both JA and NO induced stomatal closure, and had dose response to their effects; (ⅲ) there are synergetic correlation between JA and lower NO concentration in regu- lation of stomatal movement; (ⅳ) JA-induced stomatal closure was largely prevented by 2-phenyl-4,4,5,5-tetrame- thylimidazoline-1-oxyl-3-oxide (PTIO), a specific NO scav- enger. An inhibitor of NO synthase (NOS) in mammalian cells, NG-nitro-L-Arg-methyl eater (L-NAME) also inhibits plant NOS, repressing JA-induced NO generation and JA-induced stomatal closure. We presumed that NO mainly comes from NOS after JA treatment.展开更多
The effects and the relationship between sali-cylic acid (SA) and nitric oxide (NO) on Vicia faba L. stomatal movement were studied. The results here showed that exogenous SA and NO induced stomatal closure, 100 mmol/...The effects and the relationship between sali-cylic acid (SA) and nitric oxide (NO) on Vicia faba L. stomatal movement were studied. The results here showed that exogenous SA and NO induced stomatal closure, 100 mmol/L SA induced a rapid and striking NO increase in the cytosol of guard cells. This phenomenon was largely pre- vented by 200 mmol/L 2-phenyl-4,4,5,5-tetramethylimida- zoline-1-oxyl-3-oxide (PTIO), a specific NO scavenger, and 25 mmol/L NG-nitro-L-Arg-methyl eater (L-NAME), an in- hibitor of NO synthase (NOS) in mammalian cells that also inhibits plant NOS. In addition, SA-induced stomatal closure was largely prevented by PTIO and L-NAME. These results provide evidence that guard cells generate NO in response to SA via NOS-like activity, and that such NO production is required for full stomatal closure in response to SA. H-(1,2,4)-oxadiazole-[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of guanylate cyclase, and nicotinamide, an antago- nist of cADPR production, inhibited the effects of SA- and NO-induced stomatal closure. It suggests that both cGMP and cADPR might mediate the signal transduction of SA and NO-induced stomatal closure.展开更多
Emerging evidence suggests that plasma membrane calcium ATPases (PMCAs) play a key role as regulators of calcium-triggered signal transduction pathways via interaction with partner proteins. PMCAs regulate these pathw...Emerging evidence suggests that plasma membrane calcium ATPases (PMCAs) play a key role as regulators of calcium-triggered signal transduction pathways via interaction with partner proteins. PMCAs regulate these pathways by targeting specific proteins to cellular sub-domains where the levels of intracellular freecalcium are kept low by the calcium ejection properties of PMCAs. According to this model, PMCAs have been shown to interact functionally with the calcium-sensitive proteins neuronal nitric oxide synthase, calmodulindependent serine protein kinase, calcineurin and endothelial nitric oxidase synthase. Transgenic animals with altered expression of PMCAs are being used to evaluate the physiological significance of these interactions. To date, PMCA interactions with calcium-dependent partner proteins have been demonstrated to play a crucial role in the pathophysiology of the cardiovascular system via regulation of the nitric oxide and calcineurin/nuclear factor of activated T cells pathways. This new evidence suggests that PMCAs play a more sophisticated role than the mere ejection of calcium from the cells, by acting as modulators of signaling transduction pathways.展开更多
Nitric oxide （NO） has been known as an important signal in plant antioxidative defense but its production and roles in water stress are less known. The present study investigated whether NO dependence on a NO syntha...Nitric oxide （NO） has been known as an important signal in plant antioxidative defense but its production and roles in water stress are less known. The present study investigated whether NO dependence on a NO synthase-like （NOS） activity is involved in the signaling of drought-induced protective responses in maize seedlings. NOS activity, rate of NO release and drought responses were analyzed when NO donor sodium nitroprusside （SNP）, NO scavenger c-PTIO （2-（4-carboxyphenyl）- 4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide） and NOS inhibitor L-NAME （NG-nitro-L-arginine methyl ester） were applied to both detached maize leaves and whole plants. Both NOS activity and the rate of NO release increased substantially under dehydration stress. The high NOS activity induced by c-PTIO as NO scavenger and NO accumulation inhibited by NOS inhibitor L-NAME in dehydration-treated maize seedlings indicated that most NO production under water deficit stress may be generated from NOS-like activity. After dehydration stress for 3 h, detached maize leaves pretreated with NO donor SNP maintained more water content than that of control leaves pretreated with water. This result was consistent with the decrease in the transpiration rate of SNP-treated leaves subjected to drought treatment for 3 h. Membrane permeability, a cell injury index, was lower in SNP-treated maize leaves under dehydration stress for 4 h when compared with the control leaves. Also, superoxide dismutase （SOD） activity of SNP combined drought treatment maize leaves was higher than that of drought treatment alone, indicating that exogenous NO treatment alleviated the water loss and oxidative damage of maize leaves under water deficit stress. When c-PTIO as a specific NO scavenger was applied, the effects of applied SNP were overridden. Treatment with L-NAME on leaves also led to higher membrane permeability, higher transpiration rate and lower SOD activities than those of control leaves, indicating that NOS-like activity was involved in the antioxidative defense under water stress. These results suggested that NO dependence on NOS-like activity serves as a signaling component in the induction of protective responses and is associated with drought tolerance in maize seedlings.展开更多
Objective:: To study signal transduction pathway of nitric oxide inducing death of PC12 cells. Methods: Cell survival rate was measured with MTT assay, and caspase-3 activity with caspase-3 assay kits after PC12 cells...Objective:: To study signal transduction pathway of nitric oxide inducing death of PC12 cells. Methods: Cell survival rate was measured with MTT assay, and caspase-3 activity with caspase-3 assay kits after PC12 cells were incubated with sodium nitroprusside (SNP), caspase-3 inhibitor Ⅱ plus SNP or p38 inhibitor-SB203580 plus SNP. Results: SNP induced death of PC12 cells in dose- and time-dependent manner and enhanced caspase-3 activity gradually. Both caspase-3 inhibitor Ⅱ and SB203580 reduced cell death, but SB203580 reduced caspase-3 activity significantly. Conclusions: NO may induce death of PC12 cells through activation of p38 and caspase-3.展开更多
Nitric oxide （NO） plays important roles in diverse physiological processes in plants. NO can provoke both beneficial and harmful effects, which depend on the concentration and location of NO in plant cells. This rev...Nitric oxide （NO） plays important roles in diverse physiological processes in plants. NO can provoke both beneficial and harmful effects, which depend on the concentration and location of NO in plant cells. This review is focused on NO synthesis and the functions of NO in plant responses to abiotic environmental stresses. Abiotic stresses mostly induce NO production in plants. NO alleviates the harmfulness of reactive oxygen species, and reacts with other target molecules, and regulates the expression of stress responsive genes under various stress conditions.展开更多
Nitric oxide and reactive oxygen species are two important signal molecules that play key roles in plant defense responses. Nitric oxide generation and oxidative burst and accumulation of reactive oxygen species are t...Nitric oxide and reactive oxygen species are two important signal molecules that play key roles in plant defense responses. Nitric oxide generation and oxidative burst and accumulation of reactive oxygen species are the early reactions of Taxus chinensis suspension cells to fungal elicitor prepared from the cell walls of Penicillium citrinum. In order to investigate the relationship and/or interactions of ni- tric oxide and reactive oxygen species in the elici- tor-induced Taxol biosynthesis of T. chinensis sus- pension cells, we treated the cells with nitric oxide specific scavenger 2-4-carboxyphenyl-4,4,5,5-tetra- methylimidazoline-1-oxyl-3-oxide (cPITO), nitric ox- ide synthase inhibitor S,S′-1,3-phenylene-bis(1,2-eth- anediyl)-bis-isothiourea (PBITU), membrane NAD(P) H oxidase inhibitor diphenylene iodonium (DPI), su- peroxide dismutases (SOD) and catalase. The results show that pretreatment of T. chinensis cells with cPITO and DPI inhibited not only the elicitor-induced nitric oxide biosynthesis and oxidative burst, but also the elicitor-induced Taxol production, suggesting that both nitric oxide and reactive oxygen species are involved in elicitor-induced Taxol biosynthesis. Fur- thermore, pretreatment of the cells with cPITO and PBITU suppressed the elicitor-induced oxidative burst, indicating that the oxidative burst might be dependent on NO. Application of nitric oxide via its donor sodium nitroprusside (SNP) triggered Taxol biosynthesis of T. chinensis cells. The nitric ox-ide-induced Taxol production was suppressed by DPI, showing that the oxidative burst is involved in NO-triggered Taxol biosynthesis. However, nitric ox- ide and the fungal elicitor induced Taxol biosynthesis even though the accumulation of reactive oxygen species wass completely abolished in T. chinensis cells. Our data show that nitric oxide may mediate the elicitor-induced Taxol biosynthesis of T. chinensis suspension cells through both reactive oxygen spe- cies-dependent and -independent signal pathways. Moreover, the results of our work show that the elici- tor- and nitric oxide-induced Taxol biosynthesis is inhibited by catalase, indicating that H2O2 from the oxidative burst might be the signal molecule involved in induced Taxol production of T. chinensis cells.展开更多
The depression of cardiac contractility induced by space microgravity is an important issue of aerospace medicine research, while its precise mechanism is still unknown. In the present study, we explored effects of si...The depression of cardiac contractility induced by space microgravity is an important issue of aerospace medicine research, while its precise mechanism is still unknown. In the present study, we explored effects of simulated microgravity on nitric oxide (NO) level, inducible nitric oxide synthase (iNOS) expression and related regulative mechanism using electron spin resonance (ESR) spectroscopy, immunocytochemistry and in situ hybridization. We found a remarkable in-crease of NO level and up-regulation of iNOS and iNOS mRNA expression in rat cardiac myocytes under simulated microgravity. Staurosporine (a nonselective protein kinase inhibitor), calphostin C (a selective protein kinase C inhibitor), partially inhibited the effect of simulated microgravity. Thus regulative effect of simulated microgravity on iNOS expression is mediated at least partially via activation of protein kinase C. These results indicate that NO system in cardiac myocytes is sensi-tive to simulated microgravity and may play an important role in the depression of cardiac contrac-tility induced by simulated microgravity.展开更多
To explore the roles of astrocytes in the epileptogenesis, astrocytes and neurons were isolated, purified and cultured in vitro from cerebral cortex of rats. The astrocytes were activated by ciliary neurotrophic facto...To explore the roles of astrocytes in the epileptogenesis, astrocytes and neurons were isolated, purified and cultured in vitro from cerebral cortex of rats. The astrocytes were activated by ciliary neurotrophic factor (CNTF) and astrocytic conditioned medium (ACM) was collected to treat neurons for 4, 8 and 12 h. By using Western blot, the expression of calmodulin dependent protein kinase Ⅱ (CaMKⅡ), inducible nitric oxide synthase (iNOS) and adenylate cyclase (AC) was de- tected in neurons. The results showed that the expression of CaMKⅡ, iNOS and AC was increased significantly in the neurons treated with ACM from 4 h to 12 h (P<0.05), and that of iNOS and AC peaked at 8 h and 12 h respectively. It was suggested that there might be some epileptogenic factors in the ACM and such signal pathways as NOS-NO-cGMP, Ca2+?CaM-CaMKⅡ and AC-cAMP-PKA might take part in the signal transduction of epileptogenesis.展开更多
文摘Polyamines （PA）, polyamine oxidases, copper amine oxidases, and nitric oxide （NO） play important roles in physiology and stress responses in plants. NO biosynthesis as a result of catabolism of PA by polyamine oxidases and copper amine oxidases may explain in part PA-mediated responses. Involvement of a copper amine oxidase gene, COPPER AMINE OXIDASEI （CuAO1）, of Arabidopsis was tested for its role in stress responses using the knockouts cuao1-1 and cuaol-2. PA-induced and ABA-induced NO production investigated bY fluorometry and fluorescence microscopy showed that the cuaol-1 and cuaol-2 are impaired in NO production, suggesting a function of CuAO1 in PA and ABA-mediated NO production. Furthermore, we found a PA-dependent increase in protein S-nitrosylation. The addition of PA and ABA also resulted in H2O2 increases, cuao1-1 and cuao1-2 showed less sensitivity to exogenous ABA supplementation during germination, seedling establishment, and root growth inhibition as compared to wild-type. In response to ABA treatment, expression levels of the stress-responsive genes RD29A and ADH1 were significantly lower in the knockouts. These observations characterize cuao1-1 and cuao1-2 as ABA-insensitive mutants. Taken together, our findings extend the ABA signal transduction network to include CuAO1 as one potential contributor to enhanced NO production by ABA.
基金This work was supported by the National Natural Science Foundation of China(Grant No.30370141)Doctor's Fund of College&University Education(Grant No.2002001918)Fund of Education Department of Shandong Province(Grant No.J04C13).
文摘Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this work, Our experiment showed that NO exists in guard cell of Vicia faba L., and NO is involved in signal transduction of JA- induced stomata closuring: (ⅰ) JA enhances NO synthesis in guard cell; (ⅱ) both JA and NO induced stomatal closure, and had dose response to their effects; (ⅲ) there are synergetic correlation between JA and lower NO concentration in regu- lation of stomatal movement; (ⅳ) JA-induced stomatal closure was largely prevented by 2-phenyl-4,4,5,5-tetrame- thylimidazoline-1-oxyl-3-oxide (PTIO), a specific NO scav- enger. An inhibitor of NO synthase (NOS) in mammalian cells, NG-nitro-L-Arg-methyl eater (L-NAME) also inhibits plant NOS, repressing JA-induced NO generation and JA-induced stomatal closure. We presumed that NO mainly comes from NOS after JA treatment.
基金the National KeyBasic Research Special Funds of China (Grant No. G1999011700)
文摘The effects and the relationship between sali-cylic acid (SA) and nitric oxide (NO) on Vicia faba L. stomatal movement were studied. The results here showed that exogenous SA and NO induced stomatal closure, 100 mmol/L SA induced a rapid and striking NO increase in the cytosol of guard cells. This phenomenon was largely pre- vented by 200 mmol/L 2-phenyl-4,4,5,5-tetramethylimida- zoline-1-oxyl-3-oxide (PTIO), a specific NO scavenger, and 25 mmol/L NG-nitro-L-Arg-methyl eater (L-NAME), an in- hibitor of NO synthase (NOS) in mammalian cells that also inhibits plant NOS. In addition, SA-induced stomatal closure was largely prevented by PTIO and L-NAME. These results provide evidence that guard cells generate NO in response to SA via NOS-like activity, and that such NO production is required for full stomatal closure in response to SA. H-(1,2,4)-oxadiazole-[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of guanylate cyclase, and nicotinamide, an antago- nist of cADPR production, inhibited the effects of SA- and NO-induced stomatal closure. It suggests that both cGMP and cADPR might mediate the signal transduction of SA and NO-induced stomatal closure.
基金Supported by The Breast Cancer Campaign and the Research Institute in Healthcare Sciences (Armesilla AL)The Wellcome Trust (Emerson M)
文摘Emerging evidence suggests that plasma membrane calcium ATPases (PMCAs) play a key role as regulators of calcium-triggered signal transduction pathways via interaction with partner proteins. PMCAs regulate these pathways by targeting specific proteins to cellular sub-domains where the levels of intracellular freecalcium are kept low by the calcium ejection properties of PMCAs. According to this model, PMCAs have been shown to interact functionally with the calcium-sensitive proteins neuronal nitric oxide synthase, calmodulindependent serine protein kinase, calcineurin and endothelial nitric oxidase synthase. Transgenic animals with altered expression of PMCAs are being used to evaluate the physiological significance of these interactions. To date, PMCA interactions with calcium-dependent partner proteins have been demonstrated to play a crucial role in the pathophysiology of the cardiovascular system via regulation of the nitric oxide and calcineurin/nuclear factor of activated T cells pathways. This new evidence suggests that PMCAs play a more sophisticated role than the mere ejection of calcium from the cells, by acting as modulators of signaling transduction pathways.
基金Hong Kong Research Grants Council (2465/05M)Hong KongUniversity Grants Committee (AOE/B-07/99)Hong Kong Baptist Univer-sity Matching Research Fund.
文摘Nitric oxide （NO） has been known as an important signal in plant antioxidative defense but its production and roles in water stress are less known. The present study investigated whether NO dependence on a NO synthase-like （NOS） activity is involved in the signaling of drought-induced protective responses in maize seedlings. NOS activity, rate of NO release and drought responses were analyzed when NO donor sodium nitroprusside （SNP）, NO scavenger c-PTIO （2-（4-carboxyphenyl）- 4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide） and NOS inhibitor L-NAME （NG-nitro-L-arginine methyl ester） were applied to both detached maize leaves and whole plants. Both NOS activity and the rate of NO release increased substantially under dehydration stress. The high NOS activity induced by c-PTIO as NO scavenger and NO accumulation inhibited by NOS inhibitor L-NAME in dehydration-treated maize seedlings indicated that most NO production under water deficit stress may be generated from NOS-like activity. After dehydration stress for 3 h, detached maize leaves pretreated with NO donor SNP maintained more water content than that of control leaves pretreated with water. This result was consistent with the decrease in the transpiration rate of SNP-treated leaves subjected to drought treatment for 3 h. Membrane permeability, a cell injury index, was lower in SNP-treated maize leaves under dehydration stress for 4 h when compared with the control leaves. Also, superoxide dismutase （SOD） activity of SNP combined drought treatment maize leaves was higher than that of drought treatment alone, indicating that exogenous NO treatment alleviated the water loss and oxidative damage of maize leaves under water deficit stress. When c-PTIO as a specific NO scavenger was applied, the effects of applied SNP were overridden. Treatment with L-NAME on leaves also led to higher membrane permeability, higher transpiration rate and lower SOD activities than those of control leaves, indicating that NOS-like activity was involved in the antioxidative defense under water stress. These results suggested that NO dependence on NOS-like activity serves as a signaling component in the induction of protective responses and is associated with drought tolerance in maize seedlings.
文摘Objective:: To study signal transduction pathway of nitric oxide inducing death of PC12 cells. Methods: Cell survival rate was measured with MTT assay, and caspase-3 activity with caspase-3 assay kits after PC12 cells were incubated with sodium nitroprusside (SNP), caspase-3 inhibitor Ⅱ plus SNP or p38 inhibitor-SB203580 plus SNP. Results: SNP induced death of PC12 cells in dose- and time-dependent manner and enhanced caspase-3 activity gradually. Both caspase-3 inhibitor Ⅱ and SB203580 reduced cell death, but SB203580 reduced caspase-3 activity significantly. Conclusions: NO may induce death of PC12 cells through activation of p38 and caspase-3.
基金Supported by the State Key Basic Research and Development Plan of China(2006CB100100)a grant from the Program for New Century Excellent Talents from the Ministry of Education of China to L.M. Fan.
文摘Nitric oxide （NO） plays important roles in diverse physiological processes in plants. NO can provoke both beneficial and harmful effects, which depend on the concentration and location of NO in plant cells. This review is focused on NO synthesis and the functions of NO in plant responses to abiotic environmental stresses. Abiotic stresses mostly induce NO production in plants. NO alleviates the harmfulness of reactive oxygen species, and reacts with other target molecules, and regulates the expression of stress responsive genes under various stress conditions.
基金This work was supported by the Natural National Science Foundation of China （Grant No. 30572331） the Natural Science Foundation of Zhejiang Province （Grant No. 302785）.
文摘Nitric oxide and reactive oxygen species are two important signal molecules that play key roles in plant defense responses. Nitric oxide generation and oxidative burst and accumulation of reactive oxygen species are the early reactions of Taxus chinensis suspension cells to fungal elicitor prepared from the cell walls of Penicillium citrinum. In order to investigate the relationship and/or interactions of ni- tric oxide and reactive oxygen species in the elici- tor-induced Taxol biosynthesis of T. chinensis sus- pension cells, we treated the cells with nitric oxide specific scavenger 2-4-carboxyphenyl-4,4,5,5-tetra- methylimidazoline-1-oxyl-3-oxide (cPITO), nitric ox- ide synthase inhibitor S,S′-1,3-phenylene-bis(1,2-eth- anediyl)-bis-isothiourea (PBITU), membrane NAD(P) H oxidase inhibitor diphenylene iodonium (DPI), su- peroxide dismutases (SOD) and catalase. The results show that pretreatment of T. chinensis cells with cPITO and DPI inhibited not only the elicitor-induced nitric oxide biosynthesis and oxidative burst, but also the elicitor-induced Taxol production, suggesting that both nitric oxide and reactive oxygen species are involved in elicitor-induced Taxol biosynthesis. Fur- thermore, pretreatment of the cells with cPITO and PBITU suppressed the elicitor-induced oxidative burst, indicating that the oxidative burst might be dependent on NO. Application of nitric oxide via its donor sodium nitroprusside (SNP) triggered Taxol biosynthesis of T. chinensis cells. The nitric ox-ide-induced Taxol production was suppressed by DPI, showing that the oxidative burst is involved in NO-triggered Taxol biosynthesis. However, nitric ox- ide and the fungal elicitor induced Taxol biosynthesis even though the accumulation of reactive oxygen species wass completely abolished in T. chinensis cells. Our data show that nitric oxide may mediate the elicitor-induced Taxol biosynthesis of T. chinensis suspension cells through both reactive oxygen spe- cies-dependent and -independent signal pathways. Moreover, the results of our work show that the elici- tor- and nitric oxide-induced Taxol biosynthesis is inhibited by catalase, indicating that H2O2 from the oxidative burst might be the signal molecule involved in induced Taxol production of T. chinensis cells.
基金supported by National Plan of High-Tech Research and Development(863-2-2-2-4).
文摘The depression of cardiac contractility induced by space microgravity is an important issue of aerospace medicine research, while its precise mechanism is still unknown. In the present study, we explored effects of simulated microgravity on nitric oxide (NO) level, inducible nitric oxide synthase (iNOS) expression and related regulative mechanism using electron spin resonance (ESR) spectroscopy, immunocytochemistry and in situ hybridization. We found a remarkable in-crease of NO level and up-regulation of iNOS and iNOS mRNA expression in rat cardiac myocytes under simulated microgravity. Staurosporine (a nonselective protein kinase inhibitor), calphostin C (a selective protein kinase C inhibitor), partially inhibited the effect of simulated microgravity. Thus regulative effect of simulated microgravity on iNOS expression is mediated at least partially via activation of protein kinase C. These results indicate that NO system in cardiac myocytes is sensi-tive to simulated microgravity and may play an important role in the depression of cardiac contrac-tility induced by simulated microgravity.
基金a grant from Doctor Point Foundation of Ministry of Education of China (No. 2004 0487060)
文摘To explore the roles of astrocytes in the epileptogenesis, astrocytes and neurons were isolated, purified and cultured in vitro from cerebral cortex of rats. The astrocytes were activated by ciliary neurotrophic factor (CNTF) and astrocytic conditioned medium (ACM) was collected to treat neurons for 4, 8 and 12 h. By using Western blot, the expression of calmodulin dependent protein kinase Ⅱ (CaMKⅡ), inducible nitric oxide synthase (iNOS) and adenylate cyclase (AC) was de- tected in neurons. The results showed that the expression of CaMKⅡ, iNOS and AC was increased significantly in the neurons treated with ACM from 4 h to 12 h (P<0.05), and that of iNOS and AC peaked at 8 h and 12 h respectively. It was suggested that there might be some epileptogenic factors in the ACM and such signal pathways as NOS-NO-cGMP, Ca2+?CaM-CaMKⅡ and AC-cAMP-PKA might take part in the signal transduction of epileptogenesis.
