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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 2026-05-28

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 ratio0.27
NIH percentile17
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 ↗