Open AccessGambogic acid prevents angiotensin II‑induced abdominal aortic aneurysm through inflammatory and oxidative stress dependent targeting the PI3K/Akt/mTOR and NF‑κB signaling pathways
Author(s) -
Qiang Liu,
Shan Peng,
Haibin Li
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.9720
Subject(s) - gambogic acid , protein kinase b , pi3k/akt/mtor pathway , oxidative stress , angiotensin ii , proinflammatory cytokine , chemistry , signal transduction , pharmacology , biology , biochemistry , immunology , apoptosis , inflammation , receptor
Gamboge is the dry resin secreted by Garcinia hanbaryi Hook.f, with the function of promoting blood circulation and anti‑cancer effects, detoxification, hemostasis and killing insects. It is also used for the treatment of cancer, brain edema and other diseases. Gambogic acid is the main effective constituent of Gamboge. The present study tested the hypothesis that the effect of Gambogic acid prevents angiotensin II‑induced abdominal aortic aneurysm (AAA), and explored its underlying mechanism. It was demonstrated that gambogic acid significantly inhibited AAA incidence rate, and reduced edge leading aortic diameter and aortic wall thickness in AAA mice. Gambogic acid treatment markedly decreased the levels of proinflammatory cytokines and oxidative stress factors, and transforming growth factor‑β (TGF‑β) and matrix metalloproteinase (MMP)‑2 and MMP‑9 protein expression in AAA mice. Furthermore, Gambogic acid decreased expression of phosphatidylinositol 3‑kinase (PI3K), and phosphorylation of protein kinase B (Akt), mechanistic target of rapamycin (mTOR) and p70‑S6 kinase 1. It also suppressed nuclear factor (NF)‑κB protein expression in AAA mice. The findings of the present study indicated that Gambogic acid prevents angiotensin II‑induced AAA through inflammatory and oxidative stress‑dependent targeting of the PI3K/Akt/mTOR and NF‑κB signaling pathways.