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. 2020 Apr:174:113785.
doi: 10.1016/j.bcp.2019.113785. Epub 2019 Dec 28.

Andrographolide promotes pancreatic duct cells differentiation into insulin-producing cells by targeting PDX-1

Shengmei Zhang  1 , Feirong Huang  1 , Wenjin Tian  1 , Jiashuang Lai  1 , Lixia Qian  1 , Wanjin Hong  2 , Haifeng Chen  3 , Liang-Cheng Li  4
Affiliations

Andrographolide promotes pancreatic duct cells differentiation into insulin-producing cells by targeting PDX-1

Shengmei Zhang et al. Biochem Pharmacol. 2020 Apr.

Abstract

Regeneration of β-cells by differentiation of pancreatic progenitor cells has the potential to fundamentally solve the problems of the loss of β-cell function and mass during disease progression in both type 1 or 2 diabetes. Therefore, discovery of novel differentiation inducers to promote islet regeneration is of great significance. Pancreatic and duodenal homeobox1 (PDX-1) is a key transcription factor that promotes the development and maturation of pancreatic β-cells. To screen potential novel small molecules for enhancing differentiation of PNAC-1 cells, a human pancreatic ductal cell lines into insulin-producing cells (IPCs), we developed a high-throughput screening method through fusing the PDX-1 promoter region with a luciferase reporter gene. We screened and identified that andrographolide named C1037 stimulates PDX-1 expression in both mRNA and protein level and significantly promotes PANC-1 cells differentiation into IPCs as compared with that of control cells. The therapeutic effect of C037 in Streptozotocin induced diabetic mouse model through differentiation of pancreatic ductal cells into insulin positive islets was also observed. Our study provides a novel method to screen compounds regulating the differentiation of pancreatic progenitor cells having the potential of enhancing islet regeneration for diabetes therapy.

Keywords: Andrographolide; Differentiation; Islet regeneration; PDX-1; Pancreatic duct cells.

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Conflict of interest statement

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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