Hydrogen ameliorates oxidative stress via PI3K-Akt signaling pathway in UVB-induced HaCaT cells.
Hydrogen ameliorates oxidative stress via PI3K-Akt signaling pathway in UVB-induced HaCaT cells.
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DOI：
10.3892/ijmm.2018.3550
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发表时间：
2018-06
影响因子：
5.4
通讯作者：
Bingxin Zhang;Zishen Zhao;Xiaoyin Meng;Hongguang Chen;Guojun Fu;K. Xie
中科院分区：
文献类型：
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作者：
Bingxin Zhang;Zishen Zhao;Xiaoyin Meng;Hongguang Chen;Guojun Fu;K. Xie
慢性紫外线（UV）照射诱导的氧化应激与皮肤损伤的发病机制有关。然而，核因子红细胞-2相关因子2（Nrf 2）途径是通过抑制氧化应激保护细胞免受UVB诱导的损伤的关键因素。此外，Nrf 2活化需要磷酸肌醇-3激酶（PI 3 K）/蛋白激酶B（AKT）途径的参与，其在各种细胞类型的存活中具有主要作用。分子氢对紫外线诱导的损伤具有保护作用，但其潜在机制仍然难以捉摸。本研究评估了氢气对UVB辐射引起的氧化应激损伤的保护作用，并研究了分子机制。在体外，收集UVB诱导的HaCaT细胞，通过荧光光谱法和ELISA法检测活性氧、8-异前列腺素F2α、丙二醛的含量;通过MTT法和乳酸脱氢酶法检测细胞活性和细胞毒性。结果表明，H2降低了HaCaT细胞活性氧、8-异前列腺素F2α和丙二醛的水平，促进了UVB照射诱导的HaCaT细胞PI 3 K、Akt、Nrf 2和血红素氧合酶-1的表达。值得注意的是，PI 3 K抑制部分逆转了氢对UVB诱导的HaCaT细胞的影响。因此，氢通过PI 3 K/Akt信号通路抑制Nrf 2/HO-1活化，有效地保护细胞免受UVB辐射诱导的氧化应激。
Chronic ultraviolet (UV) exposure-induced oxidative stress is associated with the pathogenesis of skin damage. However, the nuclear factor erythroid‑2‑related factor 2 (Nrf2) pathway is a critical factor in protecting cells against UVB‑induced injury through inhibiting oxidative stress. Furthermore, Nrf2 activation requires the involvement of the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT) pathway, which has a major role in survival of various cell types. Molecular hydrogen exerts protective effects on UV‑induced injury, but the underlying mechanisms have remained elusive. The present study assessed the protective effects of hydrogen against oxidative stress‑induced injury caused by UVB irradiation and investigated the molecular mechanisms. In vitro, UVB‑induced HaCaT cells were collected for the detection of reactive oxygen species, 8‑iso‑prostaglandin F2α, malondialdehyde via fluorescence spectrometry and ELISA; cell activity and cytotoxicity by MTT and lactate dehydrogenase assays, respectively. Additionally, the expression level of PI3K, Akt, Nrf2 and heme oxygenase‑1 (HO‑1) were investigated using western blot, etc. All of the results indicated that hydrogen decreased the levels of reactive oxygen species, 8‑iso‑prostaglandin F2α and malondialdehyde, and promoted the UVB exposure‑induced expression of PI3K, Akt, Nrf2 and heme oxygenase‑1 in HaCaT cells. Of note, PI3K inhibition partially reversed the effects of hydrogen on UVB‑induced HaCaT cells. Therefore, hydrogen effectively protects cells from UVB radiation‑induced oxidative stress by inhibiting Nrf2/HO‑1 activation through the PI3K/Akt signaling pathway.