ArticleMolecular medicine reports2016
Tormentic acid inhibits H2O2-induced oxidative stress and inflammation in rat vascular smooth muscle cells via inhibition of the NF-κB signaling pathway.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- Recent Advances in ROS-Sensitive Nano-Formulations for Atherosclerosis Applications.Pharmaceutics · 2021Review
- The Occurrence and Biological Activity of Tormentic Acid-A Review.Molecules (Basel, Switzerland) · 2021Review
- Neuroprotective effect of tormentic acid against memory impairment and neuro‑inflammation in an Alzheimer's disease mouse model.Molecular medicine reports · 2020Article
- Mangiferin Rich Products fromMolecules (Basel, Switzerland) · 2020Article
- An Evaluation of the Antibacterial Properties of Tormentic Acid Congener and Extracts FromAdvances in pharmacological and pharmaceutical sciences · 2020Article
- Crosstalk between the Akt/mTORC1 and NF-κB signaling pathways promotes hypoxia-induced pulmonary hypertension by increasing DPP4 expression in PASMCs.Acta pharmacologica Sinica · 2019Article
- Cyclic Stretching Exacerbates Tendinitis by Enhancing NLRP3 Inflammasome Activity via F-Actin Depolymerization.Inflammation · 2018Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tormentic acid (TA) is a triterpene isolated from the stem bark of the plant Vochysia divergens and has been reported to exhibit anticancer, anti‑inflammatory and anti‑atherogenic properties. However, the functions of TA in hydrogen peroxide (H2O2)‑induced oxidative stress and inflammation in rat vascular smooth muscle cells (RVSMCs) remain unclear. Therefore, the present study aimed to investigate whether TA suppressed H2O2‑induced oxidative stress and inflammation in RVSMCs, and to determine its molecular mechanisms. The present study demonstrated that TA inhibited reactive oxygen species (ROS) generation, induced H2O2 in RVSMCs, and inhibited H2O2-induced expression of inducible nitric oxide synthase (iNOS) and NADPH oxidase (NOX) in RVSMCs. In addition, TA significantly decreased the production of tumor necrosis factor‑α (TNF‑α), interleukin 6 (IL‑6) and IL‑1β. Furthermore, TA pretreatment prevented nuclear factor‑κB (NF‑κB) subunit p65 phosphorylation and NF‑κB inhibitor α (IκBα) degradation induced by H2O2 in RVSMCs. TA is, therefore, suggested to inhibit H2O2-induced oxidative stress and inflammation in RVSMCs via inhibition of the NF‑κB signaling pathway. TA may have potential as a pharmacological agent in the prevention or treatment of atherosclerosis.
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