Purpose: To study the molecular mechanism of trabecular meshwork cells apoptosis induced by dexamethasone and the protection of pilocarpine.Methods: Determining mRNA expression with reverse transcription-polymerase ch...Purpose: To study the molecular mechanism of trabecular meshwork cells apoptosis induced by dexamethasone and the protection of pilocarpine.Methods: Determining mRNA expression with reverse transcription-polymerase chain reaction (RT-PCR), protein expression with Western blots and the percentage of apoptotic cells with fluorescent microscopy.Results: Dexamethasone up-regulated Fas proteins and affected Bax, caspase-8 and caspase-9 proteins in an action of first decrease then increase. Pre-treatment with pilocarpine decreased the four proteins expression, which were increased by dexamethasone. Pilocarpine self could decrease pro-apoptotic factors Bax, caspase-8 and caspase-9 proteins expression.Conclusion: Fas/FasL pathway participated in apoptotic process induced by dexamethasone in trabecular meshwork cells and the process was probably related with both caspase-8 and caspase-9 pathways. Pilocarpine protected the cells against apoptosis through down-regulating Fas, Bax, caspase-8 and caspase-9 proteins expression.展开更多
Purpose:To study whether muscarinic receptor agonists can protect cultured bovine trabecular meshwork cells against apoptosis induced by dexamethasone.Methods:The third to fifth passags of bovine trabecular meshwork c...Purpose:To study whether muscarinic receptor agonists can protect cultured bovine trabecular meshwork cells against apoptosis induced by dexamethasone.Methods:The third to fifth passags of bovine trabecular meshwork cells were grown to confluence and incubated for 1～14 days in growth media with dexamethasone or pretreatment of pilocarpine or carbachol.The cultures were evaluated for apoptosis by phase-contrast microscopy, fluorescence microscopy, DNA laddering and flow cytometric analysis.Results:Dexamethasone (0.24～0.96 mmol·L-1) induced apoptosis of trabecular mes-hwork cells in a dose and time-dependent manner.Before 0.48 mmol·L-1 dexametha-sone-treatment, 1.84 mmol·L-1 of pilocarpine or 2.74 mmol·L-1 of carbachol added could significantly reduce apoptotic percentage.Conclusion:Muscarinic receptor agonists can protect cultured bovine trabecular meshwork cells against apoptosis induced by dexamethasone. Eye Science 2004;20:42-47.展开更多
基金Supported by The National Nature Science Fund (No.79970782)The National Outstanding Youth Fund (No.39625022).
文摘Purpose: To study the molecular mechanism of trabecular meshwork cells apoptosis induced by dexamethasone and the protection of pilocarpine.Methods: Determining mRNA expression with reverse transcription-polymerase chain reaction (RT-PCR), protein expression with Western blots and the percentage of apoptotic cells with fluorescent microscopy.Results: Dexamethasone up-regulated Fas proteins and affected Bax, caspase-8 and caspase-9 proteins in an action of first decrease then increase. Pre-treatment with pilocarpine decreased the four proteins expression, which were increased by dexamethasone. Pilocarpine self could decrease pro-apoptotic factors Bax, caspase-8 and caspase-9 proteins expression.Conclusion: Fas/FasL pathway participated in apoptotic process induced by dexamethasone in trabecular meshwork cells and the process was probably related with both caspase-8 and caspase-9 pathways. Pilocarpine protected the cells against apoptosis through down-regulating Fas, Bax, caspase-8 and caspase-9 proteins expression.
文摘Purpose:To study whether muscarinic receptor agonists can protect cultured bovine trabecular meshwork cells against apoptosis induced by dexamethasone.Methods:The third to fifth passags of bovine trabecular meshwork cells were grown to confluence and incubated for 1～14 days in growth media with dexamethasone or pretreatment of pilocarpine or carbachol.The cultures were evaluated for apoptosis by phase-contrast microscopy, fluorescence microscopy, DNA laddering and flow cytometric analysis.Results:Dexamethasone (0.24～0.96 mmol·L-1) induced apoptosis of trabecular mes-hwork cells in a dose and time-dependent manner.Before 0.48 mmol·L-1 dexametha-sone-treatment, 1.84 mmol·L-1 of pilocarpine or 2.74 mmol·L-1 of carbachol added could significantly reduce apoptotic percentage.Conclusion:Muscarinic receptor agonists can protect cultured bovine trabecular meshwork cells against apoptosis induced by dexamethasone. Eye Science 2004;20:42-47.
