體外長期氧化負荷對豚鼠心室肌細胞電壓依賴性鉀電流的影響.doc
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體外長期氧化負荷對豚鼠心室肌細胞電壓依賴性鉀電流的影響,本文共7頁 3913字摘要目的：研究豚鼠心室肌細胞在長期氧化負荷所致的細胞凋亡過程中延遲整流鉀電流(ik)和內(nèi)向整流鉀電流(ik1)的改變。方法：采用50 μmol/l h2o2 誘導(dǎo)（24 h）培養(yǎng)的新生大鼠心肌細胞凋亡，并采用此劑量體外處理分離的成年豚鼠心室肌細...
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體外長期氧化負荷對豚鼠心室肌細胞電壓依賴性鉀電流的影響
本文共7頁 3913字
摘要 目的：研究豚鼠心室肌細胞在長期氧化負荷所致的細胞凋亡過程中延遲整流鉀電流(Ik)和內(nèi)向整流鉀電流(Ik1)的改變。方法：采用50 μmol/L H2O2 誘導(dǎo)（24 h）培養(yǎng)的新生大鼠心肌細胞凋亡，并采用此劑量體外處理分離的成年豚鼠心室肌細胞24小時。以TUNEL法評價細胞凋亡，膜片鉗技術(shù)記錄電壓依賴性鉀電流。結(jié)果：50 μmol/L H2O2 (24 h)能夠明顯誘導(dǎo)培養(yǎng)新生大鼠心肌細胞凋亡，此劑量處理分離的豚鼠心肌細胞24小時后，電壓依賴性鉀電流(Ik, Ik1)密度下調(diào)。+40 mV 測定電壓下，對照組Ik電流密度為5.73±1.84pA/pF，50 μmol/L H2O2 組Ik電流密度為2.52±0.57pA/pF(n=8, P<0.01)； -120 mV和-40 mV測定電壓下，對照組Ik1電流密度為-59.7±11.9 pA/pF和5.73±1.84 pA/pF，50 μmol/L H2O2 組Ik1電流密度為-13.9±2.7 pA/pF(n=8, P<0.01)和2.52±0.57 pA/pF(n=8, P<0.05)，50 μmol/L H2O2處理24小時減弱 Ik1 的內(nèi)向整流特性。結(jié)論：豚鼠心室肌細胞在50 μmol/L H2O2處理24小時所致的細胞凋亡過程中，Ik, Ik1的電流密度均下降，而且Ik1的內(nèi)向整流特性減弱。
關(guān)鍵詞：過氧化氫，鉀，凋亡，心肌細胞
ABSTRACT AIM: To determine the changes of delayed rectifier K+ currents(Ik) and inward rectifier K+ currents(Ik1) in the ventricular myocytes of guinea pigs during the gradual apoptotic process by the chronic oxidant stress treatment. METHODS: 50 μmol/L H2O2 (24 h) was examined for inducing apoptosis in the cardiomyocytes culture of neonatal rats and was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h. Apoptosis was evaluated by using TUNEL methods and voltage-dependent K+ currents were recorded by using patch-clamp techniques. RESULTS: 50 μmol/L H2O2 (24 h) induced cell apoptosis significantly in the cardiomyocytes culture of neonatal rats. This concentration was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h and the voltage-dependent K+ currents densities (Ik, Ik1) were down-regulated. The densities of the delayed rectifier K+ currents(Ik) in 50 μmol/L H2O2 group were 2.52±0.57 pA/pF vs 5.73±1.84 pA/pF in the control group at +50 mV(n=8, P<0.01); The densities of the inward rectifier K+ currents(Ik1) in 50 μmol/L H2O2 group were -13.9±2.70 pA/pF,
2.52±0.57 pA/pF vs -59.7±11.9 pA/pF, 5.73±1.84 pA/pF in the control group at -120 mV (n=8, P<0.01) and –40 mV(n=8, P<0.05), respectively. The extent of inward rectifier property of Ik1 was weakened by 50 μmol/L H2O2 treatment. CONCLUSION: The densities of Ik, Ik1 in the cardiomyocytes of guinea pigs were down-regulated and the inward rectifier property of Ik1 was weakened during the gradual apoptotic process by 50 μmol/L H2O2 treatment for 24h.
KEY WORDS hydrogen peroxide; potassium; apoptosis; cardiac
myocytes
參考文獻:
1. Hughes FM Jr, Bortner CD, Purdy GD, Cidlowski JA. Intracellular K+ suppresses the activation of apoptosis in lymphocytes. J Biol Chem 1997; 272: 30567-76.
2. Yu SP, Yeh CH, Sensi SL, Gwag BJ, Canzoniero LM, Farhangrazi ZS et al. Mediation of neuronal apoptosis by enhancement of outward potassium current. Science 1997; 278: 114-7.
3. Yu SP, Yeh CH, Gottron F, Wang X, Grabb MC, Choi DW. Role of the outward delayed rectifier K+ current in ceramide-induced caspase activation and apoptosis in cultured cortical neurons. J Neuronchem 1999b; 73: 933-41.
4. Hubert h. Nietsch, Michael W. Roe, Jerome F. Fiekers, Ann L. Moore, and Steven D. Lidofsky. Activation of potassium and chloride channels by tumor necrosis factor α. Role in liver cell death. J Biol Chem 2000; 275: 20556-61.
5. Yu SP, Farhangrazi ZS, Ying HS, Yeh CH, Choi DW. Enhancement of outward potassium current may participate in beta-amyloid peptide-induced cortical neuronal death. Neurobiol Dis 1998; 5: 81-8.
本文共7頁 3913字
摘要 目的：研究豚鼠心室肌細胞在長期氧化負荷所致的細胞凋亡過程中延遲整流鉀電流(Ik)和內(nèi)向整流鉀電流(Ik1)的改變。方法：采用50 μmol/L H2O2 誘導(dǎo)（24 h）培養(yǎng)的新生大鼠心肌細胞凋亡，并采用此劑量體外處理分離的成年豚鼠心室肌細胞24小時。以TUNEL法評價細胞凋亡，膜片鉗技術(shù)記錄電壓依賴性鉀電流。結(jié)果：50 μmol/L H2O2 (24 h)能夠明顯誘導(dǎo)培養(yǎng)新生大鼠心肌細胞凋亡，此劑量處理分離的豚鼠心肌細胞24小時后，電壓依賴性鉀電流(Ik, Ik1)密度下調(diào)。+40 mV 測定電壓下，對照組Ik電流密度為5.73±1.84pA/pF，50 μmol/L H2O2 組Ik電流密度為2.52±0.57pA/pF(n=8, P<0.01)； -120 mV和-40 mV測定電壓下，對照組Ik1電流密度為-59.7±11.9 pA/pF和5.73±1.84 pA/pF，50 μmol/L H2O2 組Ik1電流密度為-13.9±2.7 pA/pF(n=8, P<0.01)和2.52±0.57 pA/pF(n=8, P<0.05)，50 μmol/L H2O2處理24小時減弱 Ik1 的內(nèi)向整流特性。結(jié)論：豚鼠心室肌細胞在50 μmol/L H2O2處理24小時所致的細胞凋亡過程中，Ik, Ik1的電流密度均下降，而且Ik1的內(nèi)向整流特性減弱。
關(guān)鍵詞：過氧化氫，鉀，凋亡，心肌細胞
ABSTRACT AIM: To determine the changes of delayed rectifier K+ currents(Ik) and inward rectifier K+ currents(Ik1) in the ventricular myocytes of guinea pigs during the gradual apoptotic process by the chronic oxidant stress treatment. METHODS: 50 μmol/L H2O2 (24 h) was examined for inducing apoptosis in the cardiomyocytes culture of neonatal rats and was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h. Apoptosis was evaluated by using TUNEL methods and voltage-dependent K+ currents were recorded by using patch-clamp techniques. RESULTS: 50 μmol/L H2O2 (24 h) induced cell apoptosis significantly in the cardiomyocytes culture of neonatal rats. This concentration was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h and the voltage-dependent K+ currents densities (Ik, Ik1) were down-regulated. The densities of the delayed rectifier K+ currents(Ik) in 50 μmol/L H2O2 group were 2.52±0.57 pA/pF vs 5.73±1.84 pA/pF in the control group at +50 mV(n=8, P<0.01); The densities of the inward rectifier K+ currents(Ik1) in 50 μmol/L H2O2 group were -13.9±2.70 pA/pF,
2.52±0.57 pA/pF vs -59.7±11.9 pA/pF, 5.73±1.84 pA/pF in the control group at -120 mV (n=8, P<0.01) and –40 mV(n=8, P<0.05), respectively. The extent of inward rectifier property of Ik1 was weakened by 50 μmol/L H2O2 treatment. CONCLUSION: The densities of Ik, Ik1 in the cardiomyocytes of guinea pigs were down-regulated and the inward rectifier property of Ik1 was weakened during the gradual apoptotic process by 50 μmol/L H2O2 treatment for 24h.
KEY WORDS hydrogen peroxide; potassium; apoptosis; cardiac
myocytes
參考文獻:
1. Hughes FM Jr, Bortner CD, Purdy GD, Cidlowski JA. Intracellular K+ suppresses the activation of apoptosis in lymphocytes. J Biol Chem 1997; 272: 30567-76.
2. Yu SP, Yeh CH, Sensi SL, Gwag BJ, Canzoniero LM, Farhangrazi ZS et al. Mediation of neuronal apoptosis by enhancement of outward potassium current. Science 1997; 278: 114-7.
3. Yu SP, Yeh CH, Gottron F, Wang X, Grabb MC, Choi DW. Role of the outward delayed rectifier K+ current in ceramide-induced caspase activation and apoptosis in cultured cortical neurons. J Neuronchem 1999b; 73: 933-41.
4. Hubert h. Nietsch, Michael W. Roe, Jerome F. Fiekers, Ann L. Moore, and Steven D. Lidofsky. Activation of potassium and chloride channels by tumor necrosis factor α. Role in liver cell death. J Biol Chem 2000; 275: 20556-61.
5. Yu SP, Farhangrazi ZS, Ying HS, Yeh CH, Choi DW. Enhancement of outward potassium current may participate in beta-amyloid peptide-induced cortical neuronal death. Neurobiol Dis 1998; 5: 81-8.
