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Original Research Article | OPEN ACCESS

Procyanidin A1 acts as an antioxidant stressor in gestational diabetes

Mengni Zhu, Liping Liu

Department of Obstetrics and Gynecology, The Sixth Hospital of Wuhan, Wuhan, Hubei Province 430000, China;

For correspondence:-  Liping Liu   Email: liuliping3051001@163.com   Tel:+8618062441008

Accepted: 30 August 2023        Published: 30 September 2023

Citation: Zhu M, Liu L. Procyanidin A1 acts as an antioxidant stressor in gestational diabetes. Trop J Pharm Res 2023; 22(9):1863-1869 doi: 10.4314/tjpr.v22i9.13

© 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 evaluate the mechanism and effect of Procyanidin A1 (PCA1) in gestational diabetes mellitus (GDM).
Methods: Human trophoblast cell line HTR-8/Svneo was treated with 25 mM glucose for 24 h, and the effect of PCA1 on HTR-8/SVneo cell viability and proliferation was determined by CCK-8 assay and EdU proliferation kit. The expression of BAX, Bcl-2, cleaved Caspase-3 and cleaved caspase-9 was determined by western blotting. Cell apoptosis was assessed by Annexin V-FITC/ PI staining. Cellular generation of reactive oxygen species (ROS) was determined by ROS assay kit while superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) were determined by the corresponding assay kits. The effect of PCA1 on Nrf2/HO-1 pathway was evaluated by determining the expression of Keap1, Nfr2, and HO-1.
Results: Procyanidin A1 (PCA1) increased the viability of high glucose (HG) -induced HTR-8/SVneo cells and promoted cell proliferation. Furthermore, PCA1 significantly inhibited HG-induced BAX, cleaved caspase-3, and cleaved caspase-9 expression, resulting in further reduction in HG-induced cell apoptosis. High glucose (HG) induced a significant increase in intracellular ROS levels, and this HG-induced oxidative stress was inhibited by PCA1. Furthermore, PCA1 activated Nrf2/HO-1 pathway and this was responsible for its proliferative, anti-apoptosis and anti-oxidative effects.
Conclusion: Procyanidin A1 promotes proliferation, and inhibits apoptosis and oxidative stress induced by high glucose in trophoblast cells by activating Nrf2/HO-1 signaling pathway. Therefore, it is a potential drug for the treatment of GDM.

Keywords: Procyanidin A1, Antioxidant, Gestational diabetes, Trophoblast damage

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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