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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 protei
To investigate 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 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 protein 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 a nd caspase-9 protei