A.R. Ramos-Molina , A.R. Tejeda-Martínez , J.M. Viveros-Paredes , V. Chaparro-Huerta , M.F. Urmeneta-Ortíz , L.J. Ramírez-Jirano , M.E. Flores-Soto
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Although the precise pathogenesis of PD remains unclear, several studies demonstrate that oxidative stress, inflammation, low levels of antioxidants, and the presence of biomolecules that generate reactive oxygen species can disrupt the blood–brain barrier (BBB) as an essential feature of the disease.</div></div><div><h3>Aims</h3><div>This study aimed to test whether agonism to cannabinoid receptor type 2 (CB2) through the administration of β-caryophyllene (BCP) could correct BBB permeability in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) parkinsonism induction model.</div></div><div><h3>Methods</h3><div>We conducted a molecular assessment of proteins (immunochemistry and western blot), BBB permeability, and related biomarkers of PD (lipid peroxidation) in the MPTP mouse model of the disease.</div></div><div><h3>Results</h3><div>Expression of zonula occludens (ZO-1) and occludin tight junction (TJ) proteins was dampened in the striatum and substantia nigra pars compacta of mice, while lipid peroxidation and BBB permeability increased in the striatum in the MPTP-treated group, and these effects were reversed under BCP administration. This phytocannabinoid was able to restore protein expression and immunoreactivity of tyrosine hydroxylase (TH), ionized calcium-binding adapter molecule 1 (Iba-1), and glial fibrillary acidic protein (GFAP), as well as nuclear factor-erythroid 2-related factor (NRF2) translocation to the nucleus, and NADPH quinone oxidase 1 (NQO1) expression in mice treated with MPTP.</div></div><div><h3>Conclusion</h3><div>These results highlight the role of CB2 as a therapeutic target for PD, suggesting that its activation may ameliorate PD-related BBB disruption and oxidative stress, reducing the selective death of dopaminergic neurons.</div></div>","PeriodicalId":19300,"journal":{"name":"Neurologia","volume":"40 2","pages":"Pages 191-203"},"PeriodicalIF":2.9000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Beta-caryophyllene inhibits the permeability of the blood–brain barrier in MPTP-induced parkinsonism\",\"authors\":\"A.R. 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Beta-caryophyllene inhibits the permeability of the blood–brain barrier in MPTP-induced parkinsonism
Introduction
Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder worldwide. Although the precise pathogenesis of PD remains unclear, several studies demonstrate that oxidative stress, inflammation, low levels of antioxidants, and the presence of biomolecules that generate reactive oxygen species can disrupt the blood–brain barrier (BBB) as an essential feature of the disease.
Aims
This study aimed to test whether agonism to cannabinoid receptor type 2 (CB2) through the administration of β-caryophyllene (BCP) could correct BBB permeability in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) parkinsonism induction model.
Methods
We conducted a molecular assessment of proteins (immunochemistry and western blot), BBB permeability, and related biomarkers of PD (lipid peroxidation) in the MPTP mouse model of the disease.
Results
Expression of zonula occludens (ZO-1) and occludin tight junction (TJ) proteins was dampened in the striatum and substantia nigra pars compacta of mice, while lipid peroxidation and BBB permeability increased in the striatum in the MPTP-treated group, and these effects were reversed under BCP administration. This phytocannabinoid was able to restore protein expression and immunoreactivity of tyrosine hydroxylase (TH), ionized calcium-binding adapter molecule 1 (Iba-1), and glial fibrillary acidic protein (GFAP), as well as nuclear factor-erythroid 2-related factor (NRF2) translocation to the nucleus, and NADPH quinone oxidase 1 (NQO1) expression in mice treated with MPTP.
Conclusion
These results highlight the role of CB2 as a therapeutic target for PD, suggesting that its activation may ameliorate PD-related BBB disruption and oxidative stress, reducing the selective death of dopaminergic neurons.
期刊介绍:
Neurología es la revista oficial de la Sociedad Española de Neurología y publica, desde 1986 contribuciones científicas en el campo de la neurología clínica y experimental. Los contenidos de Neurología abarcan desde la neuroepidemiología, la clínica neurológica, la gestión y asistencia neurológica y la terapéutica, a la investigación básica en neurociencias aplicada a la neurología. Las áreas temáticas de la revistas incluyen la neurologia infantil, la neuropsicología, la neurorehabilitación y la neurogeriatría. Los artículos publicados en Neurología siguen un proceso de revisión por doble ciego a fin de que los trabajos sean seleccionados atendiendo a su calidad, originalidad e interés y así estén sometidos a un proceso de mejora. El formato de artículos incluye Editoriales, Originales, Revisiones y Cartas al Editor, Neurología es el vehículo de información científica de reconocida calidad en profesionales interesados en la neurología que utilizan el español, como demuestra su inclusión en los más prestigiosos y selectivos índices bibliográficos del mundo.