Cardio-protective effects of salvianolic acid B on oxygen and glucose deprivation (OGD)-treated H9c2 cells. Issue 1 (4th December 2019)

• Record Type: Journal Article
• Authors: Yang, Bin; Zheng, Chunyan; Yu, Haichu; Zhang, Rui; Zhao, Cong; Cai, Shanglang
• Is Part Of: Artificial cells, nanomedicine, and biotechnology. Volume 47:Issue 1(2019)
• Page Start: 2274
• Page End: 2281
• Publication Date: 2019-12-04
• Subjects: Salvianolic acid B -- MEG3 -- MDM2/p53 -- AMPK; Artificial cells -- Periodicals; Nanotechnology -- Periodicals; Blood substitutes -- Periodicals; Tissue engineering -- Periodicals; Molecules -- Periodicals; Biotechnology -- Periodicals; 615.39
• DOI: 10.1080/21691401.2019.1621885
• Languages: English
• ISSNs: 2169-1401

Abstract

Abstract: The morphological feature of apoptosis is induced by oxygen and glucose deprivation (OGD) in cardiomyocytes H9c2 cells. Salvianolic acid B (Sal-B) has been studied in several pathological progresses, whereas it is still unclear whether maternally expressed gene 3 (MEG3) is an intermediate regulator during this progress. After pre-incubation with Sal-B and stimulation with OGD, viability and apoptosis of were examined in MEG3-overexpressed H9c2 cells. Cyclin D1, apoptosis-correlated proteins and regulators of signalling pathways were quantified with Western blot assay. MEG3 was detected by quantitative reverse transcription PCR (qRT-PCR). Sal-B was implicated in the enhancement of cell viability and suppression of apoptosis in OGD-treated H9c2 cells by repressing MEG3. In addition, MEG3 overexpression exerted an inhibitory effect on murine double minute 2 (MDM2) expression while aggrandized p53 expression in OGD-treated H9c2 cells which were pre-incubated with Sal-B. Furthermore, MEG3 overexpression abolished the up-regulative effect of Sal-B on phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) in OGD-treated H9c2 cells. These results indicated that cardio-protective function of Sal-B might be ascribed to its down-regulatory property on MEG3 expression which hence blocks p53 and triggers AMPK activation in OGD-treated cells.