Neuroprotective effects of hydrogen sulfide on sodium azide‑induced autophagic cell death in PC12 cells.
Neuroprotective effects of hydrogen sulfide on sodium azide‑induced autophagic cell death in PC12 cells.
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硫化氢对叠氮化钠诱导的 PC12 细胞自噬细胞死亡的神经保护作用
DOI：
10.3892/mmr.2017.7363
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发表时间：
2017-11
影响因子：
3.4
通讯作者：
Tao L
中科院分区：
文献类型：
--
作者：
Shan H;Chu Y;Chang P;Yang L;Wang Y;Zhu S;Zhang M;Tao L
叠氮化钠（NaN3）是一种具有迅速增长的商业重要性的化学品。它是非常急性毒性和抑制细胞色素氧化酶（COX）通过不可逆结合血红素辅因子。我们小组之前的一项研究表明，硫化氢（H2S）是已知的第三种内源性气体介质，对创伤性脑损伤（TBI）引起的神经元损伤具有保护作用。众所周知，创伤性脑损伤可降低COX活性，对中枢神经系统代谢产生不利影响。因此，在本研究中，我们假设H2S可能对NaN3毒性具有神经保护作用。目前的研究结果表明，NaN3处理诱导PC12细胞的非凋亡性细胞死亡，即自噬细胞死亡。内源性h2s生成酶，半胱硫氨酸-β-合成酶和3-巯基丙酮酸硫转移酶的表达在NaN3处理后呈剂量依赖性下降。H2S预处理显著减轻nan3诱导的细胞活力丧失和自噬细胞死亡，且呈剂量依赖性。目前的研究表明，基于h2s的策略在预防和/或治疗NaN3暴露后的神经元损伤方面具有未来的潜力。
Sodium azide (NaN3) is a chemical of rapidly growing commercial importance. It is very acutely toxic and inhibits cytochrome oxidase (COX) by binding irreversibly to the heme cofactor. A previous study from our group demonstrated that hydrogen sulfide (H2S), the third endogenous gaseous mediator identified, had protective effects against neuronal damage induced by traumatic brain injury (TBI). It is well-known that TBI can reduce the activity of COX and have detrimental effects on the central nervous system metabolism. Therefore, in the present study, it was hypothesized that H2S may provide neuroprotection against NaN3 toxicity. The current results revealed that NaN3 treatment induced non-apoptotic cell death, namely autophagic cell death, in PC12 cells. Expression of the endogenous H2S-producing enzymes, cystathionine-β-synthase and 3-mercaptopyruvate sulfurtransferase, decreased in a dose-dependent manner following NaN3 treatment. Pretreatment with H2S markedly attenuated the NaN3-induced cell viability loss and autophagic cell death in a dose-dependent manner. The present study suggests that H2S-based strategies may have future potential in the prevention and/or therapy of neuronal damage following NaN3 exposure.
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影响因子：
20.1
作者：
Calvert JW;Jha S;Gundewar S;Elrod JW;Ramachandran A;Pattillo CB;Kevil CG;Lefer DJ
通讯作者：
Lefer DJ
硫化氢在炎症病理学中的作用。
影响因子：
3.2
作者：
Bhatia M
通讯作者：
Bhatia M
影响因子：
4.2
作者：
Harris, LK;Black, RT;Phillips, LL
通讯作者：
Phillips, LL
影响因子：
3.5
作者：
Inomata, K;Tanaka, H
通讯作者：
Tanaka, H
影响因子：
2.7
作者：
Lutton, JD;Moonga, BS;Dempster, DW
通讯作者：
Dempster, DW