EUE active components geniposide and aucubin regulate palmitate-induced cell death.

Abstract

<p>Cells were treated with 500 µM palmitate in the presence or absence of 2.5, 5, or 10 µg/mL aucubin or geniposide for 24 hours. Cell viability (A) and caspase-3 activity (B) were analyzed. Immunoblotting was performed with antibody against active caspase-3, caspase-9, or β-actin (C). Cells were incubated with 500 µM palmitate in the presence or absence of 10 µg/mL aucubin or geniposide for 0, 6, 12, 24, or 48 hours. Cell viability (D) and caspase-3 (E) activity were analyzed. Cells were incubated with 500 µM palmitate in the presence or absence of 10 µg/mL aucubin or geniposide for 24 or 48 hours. Immunoblotting was performed with antibody against active caspase-3, caspase-9, or β-actin (F). Cells were incubated with 500 µM palmitate in the presence or absence of 10 µg/mL aucubin or geniposide for 24 hours and stained with Hoechst (G). Cells were incubated with 500 µM palmitate in the presence or absence of 10 µg/mL aucubin or geniposide for 24 or 48 hours. Immunoblotting was carried out with antibody against BAX, cathepsin B, LAMP-1, or tubulin (H). Cathepsin B activity in the medium was measured (I). Cells were incubated with 500 µM palmitate in the presence or absence of 10 µg/mL aucubin or geniposide for 24 hours. Immunostaining was performed with anti-LAMP-1 antibody and subsequently with anti-cathepsin B antibody. The degree of overlap in staining was quantified (J). ^*<i>p</i><0.05, significantly different from palmitate-treated condition Pal.; palmitate.</p