GLPwatch

Exendin-4 attenuates inflammation-mediated endothelial cell apoptosis in varicose veins through inhibiting the MAPK-JNK signaling pathway.

J Recept Signal Transduct Res · 2020

Last updated 2026-09-22

In a lab study, researchers treated cells with a substance called LPS, which caused cell death. When they added Exendin-4 to the cells, it reduced inflammation, oxidative stress, and energy stress, leading to less cell death. Exendin-4 worked by blocking the MAPK-JNK signaling pathway.

AI summary of the abstract below.

JournalJ Recept Signal Transduct Res, 2020
Citations3
Relative citation ratio0.26
NIH percentile16
Molecules —

Abstract

Inflammation response has been found to be associated with endothelial cell death in the progression of varicose veins. Exendin-4 is able to reduce inflammation and thus attenuate cell apoptosis. The aim of our study is to explore the influence of Exendin-4 on LPS-treated endothelial cells. Cells were treated with LPS. Exendin-4 was added into the medium of cells. Western blots, qPCR, and ELISA were used to analyze the role of Exendin-4 in LPS-mediated cell death. We found that LPS treatment caused significantly cell death. Whereas this trend could be attenuated by Exendin-4. After treatment with Exendin-4, inflammation factors upregulation and oxidative stress activation were significantly repressed, an effect that was followed by a drop in the levels of glucose production and lactic acid generation. At the molecular levels, Exendin-4 treatment inhibited the activity of MAPK-JNK signaling pathway in the presence of LPS treatment. LPS causes cell apoptosis through inducing inflammation response, oxidative stress and energy stress. Exendin-4 treatment enhances cell survival, reduces inflammation, and improves energy stress through inhibiting the MAPK-JNK signaling pathway.

Verbatim abstract via PubMed 32338116 ↗