Role of PI3K/Akt signaling in hydrogen sulfide-induced alteration in expression of collagen I and III in hepatic stellate cells / 中华肝脏病杂志
Chinese Journal of Hepatology
; (12): 430-433, 2014.
Article
em Zh
| WPRIM
| ID: wpr-314023
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of the PI3K/Akt signaling pathway in hydrogen sulfide-induced alterations in expression of collagen I and collagen III in hepatic stellate cells.</p><p><b>METHODS</b>In vitro cultured rat hepatic stellate cells (HSC-T6) were treated with hydrogen sulfide, or left untreated for use as controls, and divided into groups for treatment with different inhibitors for the various factors involved in the PI3K/Akt signaling pathway. Reverse transcription-PCR was used to measure Collagen I and collagen III mRNA expression. Western blotting was used to detect the protein expression of PI3K and p-Akt, which are upstream proteins of the PI3K/Akt pathway.</p><p><b>RESULTS</b>Compared with the untreated control cells, the hydrogen sulfide treated cells showed elevated expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F =14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt (F =23.522, P less than 0.05). Compared to the cells treated with hydrogen sulfide alone, the cells treated with the various inhibitors showed lower expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F=14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt protein (F =23.522, P less than 0.05).</p><p><b>CONCLUSION</b>Hydrogen sulfide can activate the PI3K/Akt pathway and elevate the expression of collagen I and collagen III in rat hepatic stellate cells.</p>
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Base de dados:
WPRIM
Assunto principal:
Farmacologia
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RNA Mensageiro
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Transdução de Sinais
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Células Cultivadas
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Fosfatidilinositol 3-Quinases
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Colágeno Tipo I
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Colágeno Tipo III
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Proteínas Proto-Oncogênicas c-akt
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Células Estreladas do Fígado
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Genética
Limite:
Animals
Idioma:
Zh
Revista:
Chinese Journal of Hepatology
Ano de publicação:
2014
Tipo de documento:
Article