Effect of chlorophyll and aqueous extracts of Bacopa monniera and Valeriana wallichii on ischaemia and reperfusion-induced cerebral injury in mice.

Bilateral carotid artery occlusion followed by reperfusion produced significant cerebral infarction and impaired short-term memory, motor co-ordination and lateral push response. Individual pretreatments with chlorophyll and aqueous extracts of B. monniera and V. wallichii markedly attenuated ischaemia-reperfusion induced cerebral injury in terms of decreased infarct size, increase in short-term memory, motor in coordination and lateral push response. The results suggest that chlorophyll and aqueous extracts of B. monniera and V. wallichii prevent ischaemia-reperfusion induced cerebral injury with comparable potency.

Remote ischaemic preconditioning and prevention of cerebral injury.

Bilateral carotid artery occlusion of 10 min followed by reperfusion for 24 hr was employed in present study to produce ischaemia and reperfusion induced cerebral injury in mice. Cerebral infarct size was measured using triphenyltetrazolium chloride staining. Short-term memory was evaluated using elevated plus maze. Inclined beam walking test was employed to assess motor incoordination. Bilateral carotid artery occlusion followed by reperfusion produced cerebral infarction and impaired short-term memory, motor co-ordination and lateral push response. A preceding episode of mesenteric artery occlusion for 15 min and reperfusion of 15 min (remote mesenteric ischaemic preconditioning) prevented markedly ischaemia-reperfusion-induced cerebral injury measured in terms of infarct size, loss of short-term memory, motor coordination and lateral push response. Glibenclamide (5 mg/kg, iv) a KATP channel blocker and caffeine (7 mg/kg, iv) an adenosine receptor blocker attenuated the neuroprotective effect of remote mesenteric ischaemic preconditioning. It may be concluded that neuroprotective effect of remote mesenteric ischaemic preconditioning may be due to activation of adenosine receptors and consequent activation of KATP channels in mice.