Quassin ameliorates acute cerebral infarction with attenuation of NF-κB signaling and neuroinflammation.

Acute cerebral infarction is a severe cerebrovascular disease characterized by neuronal injury, oxidative stress, and neuroinflammatory activation. Quassin is a bioactive quassinoid isolated from Quassia amara with reported antioxidant and anti-inflammatory activities; however, its protective effects against cerebral ischemic injury and the underlying mechanisms remain to be further clarified. In this study, middle cerebral artery occlusion/reperfusion rat models and oxygen-glucose deprivation/reoxygenation models in bEnd.3 brain microvascular endothelial cells were established to evaluate the neuroprotective effects of Quassin. Neurological deficit scoring and hematoxylin-eosin staining were used to assess neurological dysfunction and brain histopathological injury. Cell viability was detected using the Cell Counting Kit-8 assay. Inflammatory cytokines were measured by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, intracellular reactive oxygen species were detected by DCFH-DA staining and flow cytometry, and nuclear factor kappa B pathway activation was analyzed by immunohistochemistry and Western blotting. Quassin markedly improved neurological deficits, alleviated brain histopathological damage, and restored cell viability after ischemic injury. Moreover, quassin reduced reactive oxygen species accumulation and decreased the expression of interleukin-1 beta, interleukin-6, tumor necrosis factor alpha, and inducible nitric oxide synthase. At the molecular level, quassin reduced the phosphorylation of IκBα and p65, consistent with attenuated NF-κB signaling activation. The nuclear factor kappa B inhibitor pyrrolidine dithiocarbamate further supported the involvement of this pathway. These findings suggest that the protective effects of quassin against cerebral ischemic injury are associated with reduced oxidative stress, neuroinflammation, and NF-κB signaling activation.