Abstract
Objective: The aim of the study was to investigate the effect of Dilong on cerebral infarction (CI) in a rat model. Methods: The neurological function of rats was evaluated with the mNSS. The expression of neurotrophic factors was determined using immunohistochemical method and western blotting. Hematoxylin-eosin (H&E) staining was arranged to observe the histopathologic changes. The infarct volume of brain in rats was arranged through TTC stain. Apoptosis was investigated by terminal dUTP nick end labeling (TUNEL) staining. The expressions of oxidative stress markers and pro-inflammatory cytokines were examined using ELISA assay. Results: Rats with CI manifested neurological impairment, elevated BDNF and NGF expression, augmented infarct area, enhanced neuronal apoptosis, increased antioxidant enzyme activities, decreased malondialdehyde (MDA) content in brain tissues, and accelerated production of inflammatory cytokines. With the treatment of Dilong, the neurological impairment, neuronal apoptosis, oxidative damage and inflammatory injury were all attenuated. Conclusion: Dilong could ameliorate CI in rats by anti-oxidant and antiinflammatory effects.
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