Present study aimed to assess effect of pre-treatment with Mucuna pruriens seed
extract and its bioactive molecule(s) on NMDAR and Tau protein gene expression in
cerebral ischemic rodent model. Methanol extract of M. pruriens seeds was
characterized by HPLC, and β-sitosterol was isolated by flash chromatography. In
vivo studies to observe the effect of pre-treatment (28 days) with methanol extract of
M. pruriens seed and β-sitosterol on the unilateral cerebral ischemic rat model.
Cerebral ischemia induced by left common carotid artery occlusion (LCCAO) for
75 min (on day 29) followed by reperfusion for 12 h. Rats (n = 48) divided into four
groups. GroupI (control,Untreated + LCCAO)-No pre-treatment + cerebral ischemia;
GroupII(β-sitosterol + Sham)-pre-treatment with β-sitosterol, 10 mg/kg/day + sham-
operated; GroupIII(β-sitosterol + LCCAO)-pre-treatment with β-sitosterol, 10 mg/kg/
day + cerebral ischemia; GroupIV(methanol extract + LCCAO)-pre-treatment with
methanol extract of M. pruriens seeds, 50 mg/kg/day + cerebral ischemia.
Neurological deficit score was assessed just before sacrifice. Experimental animals
were sacrificed after 12 h reperfusion. Brain histopathology was performed. Gene
expression of NMDAR and Tau protein of left cerebral hemisphere (occluded side) was
performed by RT-PCR. Results revealed that the neurological deficit score was lower
in groups III and IV compared to group I. NMDAR and tau protein mRNA expression in
left cerebral hemisphere were upregulated in Group I, downregulated in groups III and
IV. Histopathology of left cerebral hemisphere (occluded side) in Group I showed
features of ischemic brain damage. Groups III and IV, left cerebral hemisphere showed
less ischemic damage compared GroupI. Right cerebral hemisphere showed no areas
of ischemia-induced brain changes. Pre-treatment with β-sitosterol and methanol
extract of M. pruriens seeds may reduce ischemic brain injury following unilateral
common carotid artery occlusion in rats.
