【摘 要】
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Amyotrophic lateral sclerosis(ALS)is a common adult onset motor neuron(MN)disease leading to rapidly progressive degeneration of upper and lower MNs in the motor cortex,brain stem and spinal cord.Alth
【机 构】
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Department of Histology and Embryology,Weifang Medical University,Weifang,261053
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
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Amyotrophic lateral sclerosis(ALS)is a common adult onset motor neuron(MN)disease leading to rapidly progressive degeneration of upper and lower MNs in the motor cortex,brain stem and spinal cord.Although the etiology of most ALS cases remains unknown,researches show about 2%of patients are due to mutations in the gene of Cu/Zn superoxide dismutase(SOD1).And there is substantial evidence implicating oxidative stress as a central mechanism.Recently,much attention has been paid to the neuroprotective strategies for the treatment of ALS.Celastrol is a neuroprotective agent with antioxidant properties.The aim of the present study is to explore the antioxidant effects of celastrol against H2O2 induced insult in SOD1G93A transfected NSC-34 motor neuron-like cells,as well as the underlying mechanisms.The results showed pre-incubation of celastrol(50 nM)for 30 min prior to H2O2(10 μM)treatment for another 24 h significantly attenuated H2O2-induced SOD1G93A transfected NSC-34 cell death and reduced the levels of intracellular MDA.Real-time PCR showed the expressions of GCLC and GST were enhanced with pre-incubation of celastrol.Celastrol quickly induced ERK1/2 and Akt phosphorylation within 30 min and 1 h respectively.Pharmacological inhibitors of MEK(PD98059,10 μM),Akt(MK2206,10 μM)could abolish up-regulation of GCLC and GST induced by celastrol on mRNA levels.Taken together,we suggest that celastrol exerts a beneficial effect on anti-oxidative stress events in ALS which might be dependent on MEK/ERK,PI-3K/Akt cell signaling pathway activation.
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