ArticleThe journal of venomous animals and toxins including tropical diseases2017
Articular inflammation induced by an enzymatically-inactive Lys49 phospholipase A
Article in The journal of venomous animals and toxins including tropical diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Inhibition of PLA2G4E/cPLA2 promotes survival of random skin flaps by alleviating Lysosomal membrane permeabilization-Induced necroptosis.Autophagy · 2022Article
- Secreted Phospholipases AInternational journal of biological sciences · 2022Review
- Article
- Highly bioavailable curcumin powder suppresses articular cartilage damage in rats with mono-iodoacetate (MIA)-induced osteoarthritis.Food science and biotechnology · 2020Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundArthritis is a set of inflammatory conditions that induce aching, stiffness, swelling, pain and may cause functional disability with severe consequences to the patient's lives. These are multi-mediated pathologies that cannot be effectively protected and/or treated. Therefore, the aim of this study was to establish a new model of acute arthritis, using a Lys49-PLA
methodsThe articular inflammation was induced by MT-II (10 μg/joint) injection into the left tibio-tarsal or femoral-tibial
resultsPlasma extravasation in the knee joints was observed 5 and 15 min after MT-II (10 μg/joint) injection. MT-II also induced a polymorphonuclear cell influx into the femoral-tibial-patellar joints observed 8 h after its injection, a period that coincided with the peak of the hyperalgesic effect. Hyperalgesia was inhibited by the pretreatment of the animals with cyclooxygenase inhibitor indomethacin, with type-2 cyclooxygenase inhibitor celecoxib, with AACOCF
conclusionThese results demonstrated the multi-mediated characteristic of the articular inflammation induced by MT-II, which demonstrates its relevance as a model for arthritis mechanisms and treatment evaluation.
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Registered trials
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