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Effect of berberine on endoplasmic reticulum stress PERK apoptosis pathway in HK-2 cells by high fructose / 解放军医学杂志
Medical Journal of Chinese People's Liberation Army ; (12): 6-11, 2017.
Artículo en Chino | WPRIM | ID: wpr-618420
ABSTRACT
Objective To investigate the effect of berberine on endoplasmic reticulum stress PERK apoptosis pathway in HK-2 cells by high fructose.Methods HK-2 cells were grown in DMEM/F12, containing 10% fetal bovine serum (FBS) and divided randomly into four groups normal control group (Group C); Fructose group (Group F) it contains 25mmol/L fructose culture; Berberine group (Group B) 25mmol/L fructose + 10μmol/L berberine treatment group; TUDCA group (Group T)25mmol/L fructose +2μmol/L TUDCA culture group; Cells were collected after culturing 24h. The expression of glucose-regulated protein 78 (GRP78), CHOP protein and the phosphorylation levels of PERK, eIF2α were tested by Western blotting. The cell cycles were detected by flow cytometry and the apoptosis of cells were detected by TUNEL staining.ResultsWestern blotting showed that the expression of GRP78 and CHOP protein in group F was significantly higher than that in group C, and the levels of p-PERK and p-eIF2α in group F were significantly higher than those in group F. Compared with group F, GRP78, CHOP, p-PERK and p-eIF2α in group B and T were significantly lower (P0.05).Conclusion Persistent high fructose can activate the intracellular PERK pathway in HK-2 cells, causing endoplasmic reticulum stress. Berberine can inhibit the fructose-induced PERK and eIF2α phosphorylation, down-regulated the expression of GRP78, CHOP protein, thus by regulating PERK Pathways to alleviate cell cycle arrest and reduce cell apoptosis.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Medical Journal of Chinese People's Liberation Army Año: 2017 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Medical Journal of Chinese People's Liberation Army Año: 2017 Tipo del documento: Artículo