High glucose/ox-LDL induced hepatic sinusoidal capillarization via αvβ5/FAK/ERK signaling pathway.

OBJECTIVE:The main purpose of this study is to explore the role of integrin αvβ5 in hepatic sinusoidal capillarization under high glucose/ox-LDL conditions. METHODS:Establish rat model of diabetic fatty liver disease. LSECs were extracted from tissue obtained from rats of control group, cultured and treated with media containing glucose (25 mM, 24 h)/ox-LDL (100 μg/ml, 24 h) in different inhibitors. The expression of integrin αvβ5, FAK, ERK, VN in LSECs were detected by RT-PCR and Western blot. Hematoxylin-eosin staining and gomori methenaminutese silver stain was used to observe the basement membrane histopathological features of the liver tissue. Immunohistochemical to detected the protein expression of integrin αvβ5 and VN in liver tissue. Using scanning electron microscopy to visualise the fenestration frequency and fenestration diameter. Protein expression of VN was also testified by immunofluorescence assay. RESULTS:CONCLUSIONS: Integrin αvβ5 which induces LSECs dysfunction, promoting hepatic sinusoidal capillarization regulates VN expression via ERK/FAK pathway under high glucose/ox-LDL, may be a potential target for prevention and treatment of T2DM with fatty liver disease.

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