Salvianolic acid B inhibits autophagy and protects starving cardiac myocytes

• Published in: Acta pharmacologica Sinica Vol. 32; no. 1; pp. 38 - 44
• Main Authors: Han, Xiao, Liu, Jian-xun, Li, Xin-zhi
• Format: Journal Article
• Language: English
• Published: United States Nature Publishing Group 01.01.2011
• Subjects: Adenosine Triphosphate - metabolism; Animals; ATP含量; Autophagy - drug effects; Benzofurans - pharmacology; caspase; Cell Survival - drug effects; Cells, Cultured; Microtubule-Associated Proteins - metabolism; Myocytes, Cardiac - cytology; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Original; Rats; 丹酚酸B; 免疫印迹分析; 吞噬作用; 心肌细胞
• ISSN: 1671-4083; 1745-7254
• DOI: 10.1038/aps.2010.182

Aim： To investigate the protective or lethal role of autophagy and the effects of Salvianolic acid B （Sal B） on autophagy in starving myocytes. Methods： Cardiac myocytes were incubated under starvation conditions （GD） for 0, 1, 2, 3, and 6 h. Autophagic flux in starving cells was measured via chloroquine （3 pmol/L）. After myocytes were treated with Sal B （50 pmol/L） in the presence or absence of chloroquine （3 IJmol/L） under GD 3 h, the amount of LC3-11, the abundance of LC3-positive fluorescent dots in cells, cell viability and cellular ATP levels were determined using immunoblotting, immunofluorescence microscopy, MTT assay and luminometer, respectively. Moreover, electron microscopy （EM） and immunofluorescent duel labeling of LC3 and Caspase-8 were used to examine the characteristics of autophagy and apoptosis. Results： Immunoblot analysis showed that the amount of LC3-11 in starving cells increased in a time-dependent manner accompanied by increased LC3-positive fluorescence and decreased cell viability and ATP content. Sal B （50 pmol/L） inhibited the increase in LC3-1 reduced the abundance of LC3 immunofiuorescence and intensity of Caspase-8 fluorescence, and enhanced cellular viability and ATP levels in myocytes under GD 3 h, regardless of whether chloroquine was present. Conclusion： Autophagy induced by starvation for 3 h led to ceil injury. Sal B protected starving cells by blocking the early stage of autophagic flux and inhibiting apoptosis that occurred during autophagy.