期刊
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
卷 2016, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2016/2735347
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资金
- National Nature Science Foundation of China [81170237]
- National Science Foundation Fostering Talents in Basic Research of China [J1210041]
In the present study, we attempted to elucidate mechanisms for the regulation of intracellular calcium levels by H2S in primary rat medullary neurons. Our results showed that NaHS significantly increased the level of [Ca2+](i) in rat medullary neurons in a concentration-dependentmanner. L-Cysteine and SAM significantly raised the level of [Ca2+](i) in the medullary neurons while HA and/or AOAA produced a reversal effect. In addition, L-cysteine and SAM significantly increased but HA and/or AOAA decreased the production of H2S in the cultured neurons. The [Ca2+](i) elevation induced by H2S was significantly diminished by EGTA-Ca2+-free solutions, and this elevation was also reduced by nifedipine or nimodipine and mibefradil, suggesting the role of L-type and/or T-type Ca2+ channels. Moreover, the effect of H2S on [Ca2+](i) level in neurons was significantly attenuated by BAPTA-AM and thapsigargin, suggesting the source of Ca2+. Therefore, we concluded that both exogenous and endogenous H2S elevates [Ca2+](i) level in primarily cultured rat medullary neurons via both increasing calcium influx and mobilizing intracellular Ca2+ stores from ER.
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