Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Glycyrrhizinate attenuates exosome-induced endothelial cell proliferation and permeability through p38 pathway

Shun Xu , Aili Wang, Zaoli Shen, Yu Chen, Qing Jia

Department of Burn and Plastic Surgery, Seventh People's Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China;

For correspondence:- Shun Xu Email: Xushun2213@outlook.com

Accepted: 8 February 2023 Published: 31 March 2023

Citation: Xu S, Wang A, Shen Z, Chen Y, Jia Q. Glycyrrhizinate attenuates exosome-induced endothelial cell proliferation and permeability through p38 pathway. Trop J Pharm Res 2023; 22(3):517-523 doi: 10.4314/tjpr.v22i3.8

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the mechanism of action involved in the treatment of severe burn injury with glycyrrhizinate (DG).

Methods: Exosomes were purified from sera of patients with burn injury using an ultra-high-speed centrifuge, and verified by western blot. Cell proliferation and permeability were assessed using cell counting kit (CCK)-8, transepithelial-transendothelial electrical resistance (TEER), and Fluorescein Isothiocyanate (FITC) dextran assays, while immunoblotting was used for assay of the levels of p38, occluding, and zonula occludens 1 (ZO-1).

Results: Serum-derived exosomes (serum-exo) significantly suppressed cell proliferation while causing hyperpermeability in HUVECs (p < 0.001). Furthermore, DG alleviated the hyperpermeability and inhibition of cell proliferation caused by serum-exo (p < 0.001). In addition, the upregulation of p-P38 induced by serum-exo decreased upon DG treatment. Interestingly, the effect of DG was blocked by anisomycin, a specific p38 activator, indicating that p38 signaling pathway may contribute to the function of DG.

Conclusion: Glycyrrhizinate attenuates serum-exo-induced cell proliferation and permeability alteration via p38 signaling pathway, thereby making it a potential agent for the management of severe burn injury.

Keywords: Burn wound, Exosomes, Glycyrrhizinate, Permeability, Proliferation