Anti-Inflammatory Effect of Beta-Caryophyllene Mediated by the Involvement of TRPV1, BDNF and trkB in the Rat Cerebral Cortex after Hypoperfusion/Reperfusion
| Autor: | Maria Pina Serra, Marianna Boi, Antonella Carta, Elisabetta Murru, Gianfranca Carta, Sebastiano Banni, Marina Quartu |
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| Jazyk: | angličtina |
| Rok vydání: | 2022 |
| Předmět: |
Cerebral Cortex
Inflammation Male Polycyclic Sesquiterpenes Brain-Derived Neurotrophic Factor Organic Chemistry Anti-Inflammatory Agents TRPV Cation Channels beta-caryophyllene neuroinflammation acute bilateral common carotid artery occlusion TRPV1 BDNF trkB GFAP Iba1 Western blot immunohistochemistry General Medicine Catalysis Brain Ischemia Rats Computer Science Applications Inorganic Chemistry nervous system Reperfusion Injury Reperfusion Animals Receptor trkB Rats Wistar Physical and Theoretical Chemistry Molecular Biology Spectroscopy |
| Zdroj: | International Journal of Molecular Sciences; Volume 23; Issue 7; Pages: 3633 |
| ISSN: | 1422-0067 |
| DOI: | 10.3390/ijms23073633 |
| Popis: | We have previously shown that bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R) is a model to study early hypoperfusion/reperfusion-induced changes in biomarkers of the tissue physiological response to oxidative stress and inflammation. Thus in this study, we investigate with immunochemical assays if a single dose of beta-caryophyllene (BCP), administered before the BCCAO/R, can modulate the TRPV1, BDNF, and trkB receptor in the brain cortex; the glial markers GFAP and Iba1 were also examined. Frontal and temporal-occipital cortical regions were analyzed in two groups of male rats, sham-operated and submitted to BCCAO/R. Six hours before surgery, one group was gavage fed a dose of BCP (40 mg/per rat in 300 μL of sunflower oil), the other was pre-treated with the vehicle alone. Western blot analysis showed that, in the frontal cortex of vehicle-treated rats, the BCCAO/R caused a TRPV1 decrease, an increment of trkB and GFAP, no change in BDNF and Iba1. The BCP treatment caused a decrease of BDNF and an increase of trkB levels in both sham and BCCAO/R conditions while inducing opposite changes in the case of TRPV1, whose levels became higher in BCCAO/R and lower in sham conditions. Present results highlight the role of BCP in modulating early events of the cerebral inflammation triggered by the BCCAO/R through the regulation of TRPV1 and the BDNF-trkB system. |
| Databáze: | OpenAIRE |
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