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Photobiomodulation Inhibits Ischemia-Induced Brain Endothelial Senescence via Endothelial Nitric Oxide Synthase.
Feng, Yu; Huang, Zhihai; Ma, Xiaohui; Zong, Xuemei; Tesic, Vesna; Ding, Baojin; Wu, Celeste Yin-Chieh; Lee, Reggie Hui-Chao; Zhang, Quanguang.
Afiliación
  • Feng Y; Institute for Cerebrovascular and Neuroregeneration Research, Shreveport, LA 71103, USA.
  • Huang Z; Department of Neurology, Louisiana State University Health, Shreveport, LA 71103, USA.
  • Ma X; Institute for Cerebrovascular and Neuroregeneration Research, Shreveport, LA 71103, USA.
  • Zong X; Department of Neurology, Louisiana State University Health, Shreveport, LA 71103, USA.
  • Tesic V; Department of Neurology, Louisiana State University Health, Shreveport, LA 71103, USA.
  • Ding B; Institute for Cerebrovascular and Neuroregeneration Research, Shreveport, LA 71103, USA.
  • Wu CY; Department of Neurology, Louisiana State University Health, Shreveport, LA 71103, USA.
  • Lee RH; Institute for Cerebrovascular and Neuroregeneration Research, Shreveport, LA 71103, USA.
  • Zhang Q; Department of Neurology, Louisiana State University Health, Shreveport, LA 71103, USA.
Antioxidants (Basel) ; 13(6)2024 May 23.
Article en En | MEDLINE | ID: mdl-38929072
ABSTRACT
Recent research suggests that photobiomodulation therapy (PBMT) positively impacts the vascular function associated with various cerebrovascular diseases. Nevertheless, the specific mechanisms by which PBMT improves vascular function remain ambiguous. Since endothelial nitric oxide synthase (eNOS) is crucial in regulating vascular function following cerebral ischemia, we investigated whether eNOS is a key element controlling cerebrovascular function and the senescence of vascular endothelial cells following PBMT treatment. Both rat photothrombotic (PT) stroke and in vitro oxygen-glucose deprivation (OGD)-induced vascular endothelial injury models were utilized. We demonstrated that treatment with PBMT (808 nm, 350 mW/cm2, 2 min/day) for 7 days significantly reduced PT-stroke-induced vascular permeability. Additionally, PBMT inhibited the levels of endothelial senescence markers (senescence green and p21) and antiangiogenic factor (endostatin), while increasing the phospho-eNOS (Ser1177) in the peri-infarct region following PT stroke. In vitro study further indicated that OGD increased p21, endostatin, and DNA damage (γH2AX) levels in the brain endothelial cell line, but they were reversed by PBMT. Intriguingly, the beneficial effects of PBMT were attenuated by a NOS inhibitor. In summary, these findings provide novel insights into the role of eNOS in PBMT-mediated protection against cerebrovascular senescence and endothelial dysfunction following ischemia. The use of PBMT as a therapeutic is a promising strategy to improve endothelial function in cerebrovascular disease.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Antioxidants (Basel) Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Antioxidants (Basel) Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza