Hydrogen Sulfide Inhibits Formaldehyde-Induced Senescence in HT-22 Cells via Upregulation of Leptin Signaling
Hydrogen Sulfide Inhibits Formaldehyde-Induced Senescence in HT-22 Cells via Upregulation of Leptin Signaling
复制标题
硫化氢通过上调瘦素信号传导抑制甲醛诱导的 HT-22 细胞衰老
DOI：
10.1007/s12017-019-08536-8
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发表时间：
2019-04
影响因子：
3.5
通讯作者：
Tang Xiao Qing
中科院分区：
文献类型：
--
作者：
Zhu Wei Wen;Ning Min;Peng Yi Zhu;Tang Yi Yun;Kang Xuan;Zhan Ke Bin;Zou Wei;Zhang Ping;Tang Xiao Qing
AbstractIt has been previously demonstrated that hydrogen sulfide (H2S) prevents formaldehyde (FA)-induced neurotoxicity. However, the exact mechanisms underlying this protection remain to be fully elucidated. Neuronal senescence is involved in FA-induced neurotoxicity. Leptin signaling has anti-aging function. The present work was to investigate the protection of H2S against FA-induced neuronal senescence and the mediatory role of leptin signaling. FA-exposed HT-22 cells were used as the vitro model of FA-induced neuronal senescence. The senescence-associated β-galactosidase (SA-β-Gal) positive cell was detected by β-galactosidase staining. The expressions of P16INK4a, P21CIP1, leptin, and lepRb (leptin receptor) were measured by western blot. The proliferation, viability, and apoptosis of cells were evaluated by Trypan blue exclusion assay, Cell Counting Kit-8 (CCK-8) assay, and Flow cytometry analysis, respectively. We found that H2S suppressed FA-induced senescence, as evidenced by the decrease in SA-β-Gal positive cells, the downregulations of P16INK4aand P21CIP1, as well as decrease in cell growth arrest, in HT-22 cells. Also, H2S upregulated the expressions of leptin and lepRb in FA-exposed HT-22 cells. Furthermore, leptin tA (a specific inhibitor of the leptin) abolished the protective effects of H2S on FA-induced senescence and neurotoxicity (as evidenced by the increase in cell viability and the decrease in cell apoptosis) in HT-22 cells. These results indicated that H2S prevents FA-induced neuronal senescence via upregulation of leptin signaling. Our findings offer a novel insight into the mechanisms underlying the protection of H2S against FA-induced neurotoxicity.Graphical AbstractFA upregulates the expressions of P16INK4aand P21CIP1via inhibiting leptin signaling, which in turn induces senescence in HT-22 cells; H2S downregulates the expressions of P16INK4aand P21CIP1via reversing FA-downregulated leptin signaling, which in turn prevents FA-induced senescence in HT-22 cells.
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影响因子：
3.8
作者：
Yu, Rui;Lai, Yongquan;Swenberg, James A.
通讯作者：
Swenberg, James A.
影响因子：
7.8
作者：
Mei Y;Jiang C;Wan Y;Lv J;Jia J;Wang X;Yang X;Tong Z
通讯作者：
Tong Z
影响因子：
3.5
作者：
J. Folch;Ignacio Pedrós;Iván Patraca;F. Sureda;F. Junyent;C. Beas‐Zárate;E. Verdaguer;M. Pallàs;C. Auladell;A. Camins
通讯作者：
J. Folch;Ignacio Pedrós;Iván Patraca;F. Sureda;F. Junyent;C. Beas‐Zárate;E. Verdaguer;M. Pallàs;C. Auladell;A. Camins
影响因子：
3.7
作者：
Ptak, Anna;Kolaczkowska, Elzbieta;Gregoraszczuk, Ewa L.
通讯作者：
Gregoraszczuk, Ewa L.
影响因子：
7.4
作者：
Pinto M;Moraes CT
通讯作者：
Moraes CT