The present investigation evaluates the protective effect of
Ginkgetin aglycone (GA) against
ischemic stroke-induced neuronal injury.
Ischemic stroke was produced by the
middle cerebral artery occlusion (MCAO) model and animals were a group that received GA 100 and 200 mg/kg, i.p. five days before the induction of MCAO. The effect of GA against
stroke was determined by estimating the neurological deficit score and brain water content was also observed. Moreover
terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay was done for determining the neuronal apoptosis and Western blot assay also performed for estimating the expression of several
proteins. Results of the study suggest that the neurological deficit score and brain water content was found to be lower in the GA treated group than the
ischemia/reperfusion (I/R) group of rats. Moreover the number of TUNEL positive cells was found to be lower in the GA treated group than in the I/R group of rats. There was a significant (p < 0.01) decrease in the oxidative stress parameters and
cytokine in the tissue homogenate of the GA treated group compared to the I/R group of rats. Further treatment with GA attenuates altered expression of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K),
protein kinase B (Akt),
B-cell lymphoma 2 (Bcl-2),
signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa light chain enhancer of activated B cells (NF-B),
toll-like receptor 4 (TLR-4),
Janus kinase 2 (JAK-2) and sirtuin-1 (SIRT-1)
protein in the brain tissues of
stroke rats. In conclusion, data of the report reveal that treatment with
Ginkgetin aglycone protects the neuronal injury against
stroke in rats by reducing oxidative stress and
inflammation.