Activation of the NLRP3 inflammasome complex in the brains of rats exposed to high-altitude hypoxia (3153 m a.s.l.)

• Autores: Calderon, Roger, Dávila, Roberto, Ramos-Gonzalez, Mariella, Lira Mejia, Boris
• Formato: artículo
• Fecha de Publicación: 2024
• Institución: Universidad Peruana Cayetano Heredia
• Repositorio: Revistas - Universidad Peruana Cayetano Heredia
• Lenguaje: español
• OAI Identifier: oai:revistas.upch.edu.pe:article/7447
• Enlace del recurso: https://revistas.upch.edu.pe/index.php/STV/article/view/7447
• Nivel de acceso: acceso abierto

Exposure to high-altitude hypobaric hypoxia provides a useful pathophysiological model for studying the brain's response to reduced oxygen availability. In this study, gene expression was analyzed in different brain regions (hypothalamus, striatum, hippocampus, and cerebral cortex) of rats exposed to 3153 m a.s.l., focusing on markers of inflammation and cellular adaptation: NLRP3, IL-1β, and HIF-1α. For the samples obtained from each brain region, three consecutive procedures were performed following the manufacturer's instructions: total RNA extraction, reverse transcription to complementary DNA (cDNA), and quantification by real-time PCR (qPCR). Findings showed limited induction of NLRP3, whereas IL-1β and HIF-1α were markedly overexpressed. These results suggest that cerebral hypoxia triggers a sustained inflammatory response during the 28-day exposure period, accompanied by HIF-1α-mediated transcriptional adaptation, a key regulator of homeostasis under hypoxic conditions. The increase in IL-1β indicates a neuroinflammatory microenvironment capable of inducing neuronal damage, while HIF-1α acts as a modulator of proinflammatory and cell survival genes. Overall, the results demonstrate that high-altitude hypoxia not only impairs brain function but also activates inflammatory and adaptive pathways potentially involved in the initiation of neurodegenerative processes.