Geniposide protects pancreatic β cells from high glucose‐mediated injury by activation of AMP‐activated protein kinase. (4th April 2017)

• Record Type: Journal Article
• Authors: Liu, Chunyan; Hao, Yanan; Yin, Fei; Zhang, Yonglan; Liu, Jianhui
• Is Part Of: Cell biology international. Volume 41:Number 5(2017)
• Page Start: 544
• Page End: 554
• Publication Date: 2017-04-04
• Subjects: 5′‐AMP‐activated protein kinase (AMPK) -- Bax -- Bcl‐2 -- Caspase‐3 -- geniposide -- glucose‐stimulated insulin secretion (GSIS); Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10758
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: Our previous works indicated that geniposide could regulate glucose‐stimulated insulin secretion (GSIS), and improved chronic high glucose‐induced dysfunctions in pancreatic β cells, but the molecular mechanisms remain largely unknown. In the present study, we investigated the role of 5′‐AMP‐activated protein kinase (AMPK) in high glucose induced cell injury and explored the associated molecular mechanisms in rat INS‐1 pancreatic β cells. Data suggested that geniposide obviously prevented the cell damage induced by high (25 mM) glucose in INS‐1 cells, which increased the protein levels of cell apoptosis‐associated enzymes, including heme oxygenase‐1 (HO‐1), and Bcl‐2, but apparently attenuated the protein level of Bax, an apoptotic protein. In addition, Compound C, an AMPK inhibitor, remarkably inhibited the effects of geniposide on the protein levels of HO‐1, Bcl‐2, and Bax, but AICAR, an AMPK activator, potentiated the role of geniposide on the protein levels of HO‐1, Bcl‐2, and Bax. More importantly, geniposide directly prevented the cleavage of caspase‐3 induced by high glucose, and this effect was also evidently prohibited by the pre‐incubation of compound C in high glucose‐treated INS‐1 cells. Furthermore, using the method of RNA interfere, we further proved that treatment with AMPK siRNA attenuated the effects of geniposide on the apoptosis‐associated proteins and cell viability. All these data suggest that AMPK plays a crucial role on geniposide antagonizing high glucose‐induced pancreatic β cells injury.