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首页> 外文期刊>Photodiagnosis and Photodynamic Therapy >ALA-PDT suppressed the cell growth by Akt-/Erk-mTOR-p70 s6k pathway in human SZ95 sebocytes in vitro
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ALA-PDT suppressed the cell growth by Akt-/Erk-mTOR-p70 s6k pathway in human SZ95 sebocytes in vitro

机译：ALA-PDT通过体外Akt- / Erk-mTOR-p70 s6k途径抑制人SZ95皮脂细胞的细胞生长

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Background: Topical 5-aminolevulinic acid mediated photodynamic therapy (PDT) is known to be an effective method in treating acne vulgaris and other sebaceous gland-related diseases. The therapeutic mechanisms of ALA-PDT still remain undetermined. Our team has reported that ALA-PDT suppressed the cell growth in SZ95 sebocytes by mTOR-p70 S6K signaling. In this study, we aimed to investigate upstream of the mammalian target of rapamycin (mTOR) signaling cascade after ALA-PDT on cell growth of human SZ95 sebocytes.Material and methods: Human SZ95 sebocytes were treated with different concentration of 5-ALA PDT. Western blotting was used to detect and analyze the protein expression level of P-Akt (T308)/Akt, P-Akt (S473)/Akt, P-Erk/Erk, P-AMPK alpha (T172)/AMPK, P-AMPK alpha 1 (5485)/AMPK alpha 2 (S491)/AMPK, P-PRAS40/PRAS40, RagC. Meanwhile, mTOR pathway activator IGF-1 and mTORC1 inhibitor rapamycin were added to observe the interferences of P-p70 S6K/p70 S6K after ALA-PDT.Results: mTOR pathway inhibitor rapamycin decreased the level of P-p70 S6K reduced by ALA-PDT. Conversely, mTOR pathway activator IGF-1. ALA-PDT reduced the level of P-Akt (T308), P-Erk, P-AMPK alpha (T172), P-AMPK alpha 1 (S485)/AMPK alpha 2 (S491) and P-PRAS40, and no change was observed in the level of Rag C.Conclusion: ALA-PDT suppresses the cell growth in SZ95 cells through Akt-/Erk- mTOR -p70 s6k pathway rather than PRAS40-/RagC- mTOR pathway.
机译：背景：局部5-氨基乙酰丙酸介导的光动力疗法（PDT）是治疗寻常痤疮和其他皮脂腺相关疾病的有效方法。 ALA-PDT的治疗机制仍未确定。我们的团队报告说，ALA-PDT通过mTOR-p70 S6K信号传导抑制SZ95皮脂细胞的细胞生长。在这项研究中，我们旨在研究雷帕霉素（mTOR）信号转导的哺乳动物靶标上游对人SZ95皮脂细胞生长的影响。材料与方法：用不同浓度的5-ALA PDT处理人SZ95皮脂细胞。 Western印迹用于检测和分析P-Akt（T308）/ Akt，P-Akt（S473）/ Akt，P-Erk / Erk，P-AMPK alpha（T172）/ AMPK，P-AMPK的蛋白表达水平alpha 1（5485）/ AMPK alpha 2（S491）/ AMPK，P-PRAS40 / PRAS40，RagC。同时，加入mTOR通路激活剂IGF-1和mTORC1抑制剂雷帕霉素，观察ALA-PDT对P-p70 S6K / p70 S6K的干扰。结果：mTOR通路抑制剂雷帕霉素降低了ALA-PDT降低P-p70 S6K的水平。 。相反，mTOR途径激活剂IGF-1。 ALA-PDT降低了P-Akt（T308），P-Erk，P-AMPK alpha（T172），P-AMPK alpha 1（S485）/ AMPK alpha 2（S491）和P-PRAS40的水平，并且没有变化结论：ALA-PDT通过Akt- / Erk-mTOR -p70 s6k途径而非PRAS40- / RagC-mTOR途径抑制SZ95细胞的细胞生长。

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