硫化氢钠
神经炎症
化学
胱硫醚β合酶
PI3K/AKT/mTOR通路
炎症
神经保护
下调和上调
信号转导
内分泌学
内科学
药理学
生物化学
生物
硫化氢
酶
医学
基因
有机化学
硫黄
半胱氨酸
作者
Xinrui Li,Peiquan Yu,Yinghua Yu,Ting Xu,Jiao Liu,Yuan Cheng,Xia Yang,Xiaoying Cui,Yin Chen,Yi Liu
标识
DOI:10.1016/j.intimp.2021.107545
摘要
Hyperglycemia-induced neuroinflammation promotes the progression of diabetic encephalopathy. Hydrogen sulfide (H2S) exerts anti-inflammatory and neuroprotective activities against neurodegenerative diseases. However, the effects of H2S on hyperglycemia-induced neuroinflammation has not been investigated in neurons. Herein, by using HT-22 neuronal cells, we found that high glucose decreased the levels of endogenous H2S and its catalytic enzyme, cystathionine-β-synthase (CBS). The administration of sodium hydrosulfide (NaHS, a H2S donor) or S-adenosylmethionine (SAMe, an allosteric activator of CBS) restored high glucose-induced downregulation of CBS and H2S levels. Importantly, H2S ameliorated high glucose-induced inflammation in HT-22 cells, evidenced by NaHS or SAMe inhibited the pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) expression in HT-22 cells exposed to high glucose. Furthermore, NaHS or SAMe restored the SIRT1 level and the phosphorylation of mTOR and NF-κB p65 disturbed by high glucose in HT-22 cells, suggesting H2S reversed high glucose-induced alteration of SIRT1-mTOR/NF-κB signaling pathway. Our results demonstrated that exogenous H2S treatment or enhancing endogenous H2S synthesis prevents the inflammatory processes in the neurons with the exposure of high glucose. Therefore, increasing the H2S level using NaHS or SAMe might shed light on the prophylactic treatment of diabetic encephalopathy.
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