Monotropein alleviates H2O2‑induced inflammation, oxidative stress and apoptosis via NF‑κB/AP‑1 signaling.
Feng Jiang, Xiao-Rong Xu, Wei-Ming Li, Kun Xia, Le-Feng Wang, Xin-Chun Yang
Author Information
Feng Jiang: Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Xiao-Rong Xu: Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Wei-Ming Li: Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Kun Xia: Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Le-Feng Wang: Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Xin-Chun Yang: Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Aging is a major risk factor in cardiovascular disease (CVD). Oxidative stress and inflammation are involved in the pathogenesis of CVD, and are closely associated with senescent vascular endothelial cells. Monotropein (Mtp) exerts various bioactive roles, including anti‑inflammatory and antioxidative effects. The aim of the present study was to investigate the function of Mtp in senescent endothelial cells. An MTT assay was performed to evaluate the influence of Mtp on H2O2‑stimulated human umbilical vein endothelial cells (HUVECs). Senescent cells were assessed by determining the expression of senescence‑associated β‑galactosidase, high mobility group AT‑hook 1 and DNA damage marker γ‑H2A.X variant histone. Malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH‑Px) and proinflammatory cytokine concentrations were estimated using assay kits to evaluate the levels of oxidative stress and inflammation in HUVECs. The TUNEL assay was performed to identify apoptotic cells. Furthermore, the expression levels of endothelial cell adhesion factors, NF‑κB, activator protein‑1 (AP‑1) and apoptotic proteins were determined via western blotting. Mtp enhanced HUVEC viability following H2O2 stimulation. H2O2‑mediated increases in MDA, proinflammatory cytokine and endothelial cell adhesion factor levels were decreased by Mtp treatment, whereas Mtp reversed H2O2‑mediated downregulation of SOD and GSH‑Px activity. Furthermore, Mtp inhibited cell apoptosis, NF‑κB activation and AP‑1 expression in H2O2‑stimulated HUVECs; however, NF‑κB activator counteracted the anti‑inflammatory, antioxidative and antiapoptotic effects of Mtp. The present study indicated that Mtp ameliorated H2O2‑induced inflammation and oxidative stress potentially by regulating NF‑κB/AP‑1.
