1. Academic Validation
  2. Improvement of cerebral ischemia-reperfusion injury by L-3-n-butylphthalide through promoting angiogenesis

Improvement of cerebral ischemia-reperfusion injury by L-3-n-butylphthalide through promoting angiogenesis

  • Exp Brain Res. 2021 Jan;239(1):341-350. doi: 10.1007/s00221-020-05978-6.
Ying Huang 1 Lishou Pan 2 Ting Wu 3
Affiliations

Affiliations

  • 1 Department of Pharmacy, The People's Hospital of Yichun City, Yichun, 336000, People's Republic of China.
  • 2 Department of Neurology, The People's Hospital of Yichun City, Yichun, 336000, People's Republic of China.
  • 3 Department of Pharmacy, The People's Hospital of Yichun City, Yichun, 336000, People's Republic of China. [email protected].
Abstract

Cerebral ischemia/reperfusion (I/R) injury may lead to a poor prognosis for ischemic stroke patients after reperfusion therapy, and currently, lacks effective therapeutic intervention. This study aimed to investigate the effects of L-3-n-butylphthalide (L-NBP) on cerebral I/R injury in rats. Rat models of cerebral I/R injury were established using the middle cerebral artery occlusion/refusion (MACO/R) surgery and were administrated intragastrically with L-NBP or vehicle. We found that L-NBP attenuated the histological damages and reduced the brain hematoma in MACO/R rats. L-NBP also significantly improved the neurological function, alleviated the brain edema, and reduced the permeability of blood-brain barrier of MACO/R rats. Moreover, we detected that L-NBP considerably facilitated microvessel formation in the lesion area of brain in MACO/R rats. Finally, we found that L-NBP significantly increased the protein and mRNA expression levels of Nrf2, HIF-1α, and VEGF in the brain of MACO/R rats. In conclusion, our results demonstrated that L-NBP exerted significant beneficial effects on cerebral I/R injury in rats through promoting angiogenesis, which may be associated with the activation of Nrf2/HIF-1α/VEGF signaling pathway. Our results suggested that L-NBP could be a potential therapeutic drug for cerebral I/R injury.

Keywords

Angiogenesis; Cerebral ischemia/reperfusion injury; L-3-n-butylphthalide; Neurological function.

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