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ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Ethnopharmacology
Volume 15 - 2024 |
doi: 10.3389/fphar.2024.1471542
This article is part of the Research Topic The Vascular System: Effects of Traditional Medicines and Mechanism of Action View all articles
Neuroprotective effect of Bouvardia ternifolia (Cav.) Schltdl via inhibition of TLR4/NF-B, Caspase-3/Bax/Bcl-2 pathways in ischemia\reperfusion injury in rats
Provisionally accepted- 1 2 Centro de Desarrollo de Productos Bióticos, Instituto Politécnico Nacional, Yautepec, Mexico
- 2 Centro de Investigaciones Biomédicas del Sur, Instituto Mexicano del Seguro Social, Xochitepec, Mexico
- 3 Laboratorio de Metabolismo I, Departamento de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Ciudad de México, Mexico, Mexico
Bouvardia terniflora dichloromethane extract decreased oxidant stress markers, altered the redox environment, and activated antioxidant enzymes, protecting neurons against damage induced by ischemia/reperfusion. It reduced the expression of inflammatory markers associated with the NF-κB pathway, apoptosis, and glial activation while modulating the production of proteins such as COX-2, iNOS, nNOS, NF-κB, and TLR4. In the BCCAO/reperfusion model, the mechanism of action by which the compounds present in the dichloromethane extract intervene involves different signaling pathways. Initially, they prevented the activation of iNOS and nNOS proteins, leading to decreased production of reactive oxygen and nitrogen species, lipid peroxidation, and the activation of antioxidant enzymes such as catalase and superoxide dismutase. The reduction in oxidant stress decreased expression of proteins and genes involved in apoptosis, such as Bax, Bcl-2, and caspase-3. Additionally, the compounds in the extract acted by inhibiting the TLR4 receptor, impeding the translocation of the transcription factor NF-κB to the nucleus and, consequently, inhibiting inflammatory mediators like IL-1β, IL-6, TNF-α, and COX-2. Moreover, the compounds in the dichloromethane extract attenuated the activation of microglia and astrocytes, as reflected in the reduced expression of glial activation genes such as GFAP and AiF1.
Keywords: oxidant stress1, cerebral ischemia2, glial activation3, inducible nitric oxide synthase4, neuronal nitric oxide5
Received: 27 Jul 2024; Accepted: 09 Sep 2024.
Copyright: © 2024 Zapata-Lopera, Trejo-Tapia, CANO-EUROPA, Rodríguez-Hernández, Franco-Rojas, Herrera-Ruiz and Jimenez-Ferrer. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Enrique Jimenez-Ferrer, Centro de Investigaciones Biomédicas del Sur, Instituto Mexicano del Seguro Social, Xochitepec, Mexico
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