Hydrogen sulfide suppresses the increase in reactive oxygen species in neurons induced by angiotensin II via ERK1/2 signal pathway |
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Authors: | MA Hong YU Hai-yun YU Yan CAO Dong-qing HUANG Ying JIN Hui-ming ZHU Yi-chun LU Ning |
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Institution: | Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China |
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Abstract: | AIM: To investigate the effect of hydrogen sulfide (H2S) on the reactive oxygen species (ROS) level in medullary neurons induced by angiotensin II (Ang II). METHODS: Primarily cultured rat medullary neurons were divided into 5 groups as follows: control group, Ang II group, sodium hydrosulfide(NaHS) group, NaHS with Ang II group, and PD98059 (an inhibitor of p-ERK1/2) with Ang II group. ROS production was measured with dihydroethidium (DHE) staining. The expression of p-ERK1/2 and ERK1/2 was determined by Western blotting. The activity of neurons was detected by CCK-8 assay. RESULTS: Ang II at concentration of 100 nmol/L significantly increased ROS level in the neurons, but the effect was inhibited by NaHS at concentrations of 50~200 μmol/L, while NaHS alone had no influence on the ROS level in neurons. Additionally, PD98059 also depressed the ROS level in neurons induced by Ang II. Furthermore, the enhanced expression of p-ERK1/2 in the neurons induced by Ang II was significantly reduced by NaHS. CONCLUSION: H2S remarkably inhibits the ROS level in the neurons induced by Ang II via activation of MAPK signal pathways, especially p-ERK1/2, indicating that H2S rescues neurons from oxidative stress through declining the enhanced expression of p-ERK1/2. |
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Keywords: | Hydrogen sulfide Angiotension II Neurons Reactive oxygen species |
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