ArticleMolecular medicine reports2020
Monotropein alleviates H2O2‑induced inflammation, oxidative stress and apoptosis via NF‑κB/AP‑1 signaling.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 89 citations in OpenAlex.
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- Monotropein represses the proliferation and angiogenesis via the AKT/NF-κB pathway in lung cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Monotropein attenuates renal cell carcinoma cell progression and M2 macrophage polarization by weakening NF-κB.International urology and nephrology · 2025Article
- Occupational Exposure to Disinfectants and Risk of Incident Cardiovascular Disease among US Nurses: The Nurses' Health Study II.Environmental health perspectives · 2025Article
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- Monotropein inhibits MMP9-mediated cardiac oxidative stress, inflammation, matrix degradation and apoptosis in a mouse and cell line models of septic cardiac injury.Molecular biology reports · 2025Article
- Monotropein resists atherosclerosis by reducing inflammation, oxidative stress, and abnormal proliferation and migration of vascular smooth muscle cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
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- Current Perspectives on the NF-κB Signaling Axis as a Potential Pharmacological Target in Cardiorenal Syndrome.Drug design, development and therapy · 2025Review
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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