2004Zhongguo yaolixue tongbaoRequires access

Effects of prostaglandin E_1 on hypoxia/reoxygenation apoptosis in cultured neonatal rat cardiomyocytes

Xiang Ma

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Abstract

AIMTo investigate the effects of prostaglandin E 1 on apoptosis induced by hypoxia/reoxygenation in cultured neonatal rat cardiomyocy tes. METHODSThe models of hypoxia/reoxygenation were made with t he first generation of cultured cardiomyocytes. Hypoxia/reoxygenation apoptosis in cultured neonatal rat cardiomyocytes was studied by agarose gel electrophores is and Tdt-mediated dUTP nick end labeling(TUNEL). Bcl-2 and bax mRNA were det ected by in situ hybridization. RESULTSThe results of DNA electr ophoresis in the H/R group showed the typical DNA ladder. And the DNA ladder decreased gradually corresponding to the increased dose of PGE 1. The TUNEL staining showed that the total number of apo ptotic cells in the H/R group was much biger than that in PGE 1(0 127 μmol·L -1 ) group. The results of in situ hybridization showed that the conten t of bcl-2 mRNA in H/R group was lower than control. And the content of bax mRN A showed a reverse result as bcl-2 mRNA. Compared with H/R group, the content o f bcl-2 mRNA was significantly higher after treatment with PGE 1(0 014 μmol ·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 ). But the content of bax mRNA in PGE 1(0 014 μmol·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 )groups was significantly lower than H/R group. CONCLUSI ONH/R injury can induce cardiomyocyte apoptosis. PGE 1 has obvious an ti-apoptotic effects on cardiomyocyte and the mechanisms are possibly by inhibi ting the expression of bax and increasing the expression of bcl-2.hein creaseddoseofPGE1 .TheTUNELstainingshowed thatthetotalnumberofapoptoticcellsintheH

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AIMTo investigate the effects of prostaglandin E 1 on apoptosis induced by hypoxia/reoxygenation in cultured neonatal rat cardiomyocy tes. METHODSThe models of hypoxia/reoxygenation were made with t he first generation of cultured cardiomyocytes. Hypoxia/reoxygenation apoptosis in cultured neonatal rat cardiomyocytes was studied by agarose gel electrophores is and Tdt-mediated dUTP nick end labeling(TUNEL). Bcl-2 and bax mRNA were det ected by in situ hybridization. RESULTSThe results of DNA electr ophoresis in the H/R group showed the typical DNA ladder. And the DNA ladder decreased gradually corresponding to the increased dose of PGE 1. The TUNEL staining showed that the total number of apo ptotic cells in the H/R group was much biger than that in PGE 1(0 127 μmol·L -1 ) group. The results of in situ hybridization showed that the conten t of bcl-2 mRNA in H/R group was lower than control. And the content of bax mRN A showed a reverse result as bcl-2 mRNA. Compared with H/R group, the content o f bcl-2 mRNA was significantly higher after treatment with PGE 1(0 014 μmol ·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 ). But the content of bax mRNA in PGE 1(0 014 μmol·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 )groups was significantly lower than H/R group. CONCLUSI ONH/R injury can induce cardiomyocyte apoptosis. PGE 1 has obvious an ti-apoptotic effects on cardiomyocyte and the mechanisms are possibly by inhibi ting the expression of bax and increasing the expression of bcl-2.hein creaseddoseofPGE1 .TheTUNELstainingshowed thatthetotalnumberofapoptoticcellsintheH

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Available abstract

AIMTo investigate the effects of prostaglandin E 1 on apoptosis induced by hypoxia/reoxygenation in cultured neonatal rat cardiomyocy tes. METHODSThe models of hypoxia/reoxygenation were made with t he first generation of cultured cardiomyocytes. Hypoxia/reoxygenation apoptosis in cultured neonatal rat cardiomyocytes was studied by agarose gel electrophores is and Tdt-mediated dUTP nick end labeling(TUNEL). Bcl-2 and bax mRNA were det ected by in situ hybridization. RESULTSThe results of DNA electr ophoresis in the H/R group showed the typical DNA ladder. And the DNA ladder decreased gradually corresponding to the increased dose of PGE 1. The TUNEL staining showed that the total number of apo ptotic cells in the H/R group was much biger than that in PGE 1(0 127 μmol·L -1 ) group. The results of in situ hybridization showed that the conten t of bcl-2 mRNA in H/R group was lower than control. And the content of bax mRN A showed a reverse result as bcl-2 mRNA. Compared with H/R group, the content o f bcl-2 mRNA was significantly higher after treatment with PGE 1(0 014 μmol ·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 ). But the content of bax mRNA in PGE 1(0 014 μmol·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 )groups was significantly lower than H/R group. CONCLUSI ONH/R injury can induce cardiomyocyte apoptosis. PGE 1 has obvious an ti-apoptotic effects on cardiomyocyte and the mechanisms are possibly by inhibi ting the expression of bax and increasing the expression of bcl-2.hein creaseddoseofPGE1 .TheTUNELstainingshowed thatthetotalnumberofapoptoticcellsintheH

Key concepts: Apoptosis, TUNEL assay, DNA fragmentation, Molecular biology, Messenger RNA, In situ hybridization, Hypoxia (environmental), Andrology

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