Intracranial Cerebrovascular Occlusive Disease

Harrigan, Mark R.; Deveikis, John P.

doi:10.1007/978-1-61779-946-4_19

Cited by 1 publication

(1 citation statement)

References 195 publications

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“…MCAO is the most common cause of ischemic stroke, accounting for more than 50% of intracranial vascular lesions. 25 The MCAO model was established by the method of thread embolism, which was widely used in clinical and experimental research. 26 The core of the treatment of cerebral ischemia lies in the protection of neuronal injury and vascular recanalization.…”

Section: Discussionmentioning

confidence: 99%

Butylphthalide protects against ischemia-reperfusion injury in rats via reducing neuron ferroptosis and oxidative stress

Sun

Peili

et al. 2023

Journal of Investigative Medicine

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Local ischemia in the cerebra leads to vascular injury and necrosis. Ferroptosis is involved in the pathophysiological process of many diseases and widely exists when ischemia-reperfusion injury occurs in many organs. The aim of this study was to evaluate the effect of Butylphthalide (NBP) on middle cerebral artery occlusion (MCAO) rats model-caused neuron injury. Sprague Dawley Rats were randomly allocated to receive sham and MCAO operation. NBP low-dose (40 mg/kg b.w), and high-dose (80 mg/kg b.w) were administrated in MACO rats. Results showed NBP improves infarct volume, attenuates neuronal apoptosis in the brain tissue of MCAO rats. The tumor necrosis factor (TNF-α), IL-6, and malondialdehyde (MDA) levels decreased after NBP administration, while the activity of superoxide dismutase (SOD) and the ratio of GSH/GSSG in MACO rats increased. MACO caused non-heme iron accumulation in the brain tissue and Perl’s staining confirmed NBP attenuates ferroptosis in MACO rats. The protein expressions of SCL7A11 and glutathione peroxidase 4 (GPX4) decreased following MCAO, and NBP treatment subsequently increased the expression of SCL7A11 and GPX4. In vitro analysis in cortical neuron cells indicated that the GPX4 inhibitor reverses the inhibition of ferroptosis by NBP, which suggested that the SCL7A11/GPX4 pathway majorly contributed to the NBP ferroptosis protection effect.

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Section: Discussionmentioning

confidence: 99%