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2005•Journal of Sun Yat-sen UniversityRequires access

Protective Effect of Nicotine Against Apoptosis of Rat Cortical Neurons Induced by Colchicine

Xuelan Wang

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Abstract

[Objective]To investigate the effect of nicotine on rat cortical neurons induced by colchicine. [Methods] Pretrealment with different concentrations of nicotine (1, 10, 100)μmol/L for 2 h, the maximum effect reached by 10μmol/L nicotine pretreated 2 h before treatment colchicines. And Pretreatment different time (0.5, 2, 8) h with 10μmol/L nicotine. The changes in morphology of neurons treated nicotine or/and colchicines were observed with phase-contrast microscopy, and the rate of apoptosis were measured by Hoechsl33258 fluorescence staining and released lactate dehydrogenase (LDH) from the neurons. [Result] Nicotine antagonized neuron apoptosis induced by colchicines and reduced the apoptosis rate and LDH release. The effect reaches the peak level by 10μmol/L nicotine pretreated 2 h. [Conclusion] Nicotine can protect cortical neurons from apoptosis of induced by colchicine.

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[Objective]To investigate the effect of nicotine on rat cortical neurons induced by colchicine. [Methods] Pretrealment with different concentrations of nicotine (1, 10, 100)μmol/L for 2 h, the maximum effect reached by 10μmol/L nicotine pretreated 2 h before treatment colchicines. And Pretreatment different time (0.5, 2, 8) h with 10μmol/L nicotine. The changes in morphology of neurons treated nicotine or/and colchicines were observed with phase-contrast microscopy, and the rate of apoptosis were measured by Hoechsl33258 fluorescence staining and released lactate dehydrogenase (LDH) from the neurons. [Result] Nicotine antagonized neuron apoptosis induced by colchicines and reduced the apoptosis rate and LDH release. The effect reaches the peak level by 10μmol/L nicotine pretreated 2 h. [Conclusion] Nicotine can protect cortical neurons from apoptosis of induced by colchicine.

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Available abstract

[Objective]To investigate the effect of nicotine on rat cortical neurons induced by colchicine. [Methods] Pretrealment with different concentrations of nicotine (1, 10, 100)μmol/L for 2 h, the maximum effect reached by 10μmol/L nicotine pretreated 2 h before treatment colchicines. And Pretreatment different time (0.5, 2, 8) h with 10μmol/L nicotine. The changes in morphology of neurons treated nicotine or/and colchicines were observed with phase-contrast microscopy, and the rate of apoptosis were measured by Hoechsl33258 fluorescence staining and released lactate dehydrogenase (LDH) from the neurons. [Result] Nicotine antagonized neuron apoptosis induced by colchicines and reduced the apoptosis rate and LDH release. The effect reaches the peak level by 10μmol/L nicotine pretreated 2 h. [Conclusion] Nicotine can protect cortical neurons from apoptosis of induced by colchicine.

Key concepts: Colchicine, Nicotine, Apoptosis, Chemistry, Lactate dehydrogenase, Neuron, Pharmacology, Cortical neurons

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