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[Inhibitory effect of quercetin preconditioning on tunicamycin-induced apoptosis in macrophages and its mechanism.] [Article in Chinese]

YAO Shu-Tong, MIAO Cheng , LIU Qing-Hua, LI Yan-Yan, TIAN Hua, WANG Yun-Yun , MA Bian-Ying, FANG Yong-Qi ^*, QIN Shu-Cun^*

Institute of Atherosclerosis, Key Laboratory of Atherosclerosis in Universities of Shandong； College of Basic Medical Sciences； Department of Clinical Laboratory, Affiliated Hospital of Taishan Medical University； Grade 2008 of Biotechnology, Taishan Medical University, Taian 271000, China

Abstract

The purposes of the present study were to investigate the inhibitory effect of quercetin (QUE) preconditioning on endoplasmic reticulum stress (ERS) inducer tunicamycin (TM)-induced apoptosis in RAW264.7 macrophages and the underlying molecular mechanisms. RAW264.7 cells were pretreated with different concentrations (20, 40, and 80 μmol/L) of QUE for 30 min and then treated with TM (5 mg/L) for 12 h. Cell viability and apoptosis were determined using MTT assay and Annexin V-FITC apoptosis detection kit, respectively. The nuclear translocation of activating transcription factor 6 (ATF6) in cells was detected by immunofluorescence analysis and Western blot. Protein and mRNA expressions of C/EBP homologous protein (CHOP) and Bcl-2 were examined by Western blot and real-time PCR, respectively. The results showed that TM reduced cell viability and induced apoptosis in RAW264.7 macrophages. The cytotoxic effects of TM were significantly inhibited by QUE pretreatment at the concentrations of 40 and 80 μmol/L. Interestingly, we found that QUE also significantly suppressed the TM-induced translocation of ATF6, an ERS sensor, from the cytoplasm to the nucleus. In addition, exposure of RAW264.7 macrophages to TM resulted in a significant increase of the expression of CHOP, a transcription factor regulated by ATF6 under conditions of ERS, as well as a decrease of Bcl-2 at transcript and protein levels. QUE blocked these effects in a dose-dependent manner. These data indicate that QUE can protect RAW264.7 cells from TM-induced apoptosis and that the mechanism at least partially involves its ability to inhibit the ATF6-CHOP signaling pathway.

Key words: quercetin; endoplasmic reticulum stress; CHOP; tunicamycin; Macrophage; apoptosis

Received: 2012-05-04　　Accepted: 2012-06-19

Corresponding author: 方永奇,秦树存　　E-mail: yqfang@tsmc.edu.cn,shucunqin@hotmail.com

Citing This Article：

YAO Shu-Tong, MIAO Cheng , LIU Qing-Hua, LI Yan-Yan, TIAN Hua, WANG Yun-Yun , MA Bian-Ying, FANG Yong-Qi , QIN Shu-Cun. [Inhibitory effect of quercetin preconditioning on tunicamycin-induced apoptosis in macrophages and its mechanism.] [Article in Chinese]. Acta Physiol Sin 2013; 65 (1): 47-54 (in Chinese with English abstract).