Planta Med 2008; 74 - PA119
DOI: 10.1055/s-0028-1084117

Evaluation of neuroprotective effect of Slimaluma in cerebral ischemia reperfusion injury in rats

R Rajendran 1, NS Vyawahare 2, UN Harle 2, DB Ambikar 2, RA Khandare 2, MR Gadkari 2
  • 1Green Chem, Domlur, Bangalore, 560071, India
  • 2AISSMS College of Pharmacy, Kennedy Road, Pune, 411001, India

Oxidative stress is one of the primary factors that exacerbate the damage by ischemia reperfusion injury [1] causing behavioral and cognitive deficit [2]. Several studies have demonstrated that neuroprotective agents are used to prevent this oxidative stress due to the reperfusion injury [3]. Slimaluma (SL), a branded product and an enriched phytochemical composition developed from Caralluma fimbriata (CF) of family Asclepiadaceae [4] which is a traditionally claimed neuroprotective agent was evaluated against the ischemia reperfusion injury. Eighteen male wistar rats were equally divided into 3 groups' (viz. sham operated control; control and SL-500mg/kg) and treated for 14 days. On the 14th day, 60 minute after the last dose all the rats except sham operated were subjected to 30min bilateral common carotid artery occlusion (BCCAO) followed by 45min reperfusion. Thereafter rectal temperature was measured and then all rats were sacrificed for the biochemical estimations. Data was analysed using the student t test [2,5,6] wherein the vehicle treated control data was compared with sham operated control and SL treated was compared with control rats. Control rats showed a significant increase in the body temperature where as a significant reduction was observed with the SL pretreated rats, thereby indicating the neuroprotection [3]. Biochemical investigations revealed a significant increase in the lipid peroxidation in control rats whereas SL pretreatment showed a significant reduction. On the other hand glutathione content was significantly reduced due to the ischemia and increased with the pretreatment of SL-500 thereby validated biochemical basis of neuroprotection by SL- against the reperfusion induced neurodegeneration [2, 3]. Catalase activity was unaffected with SL [6]. In summary SL-500 protected the rats from ischemia reperfusion injury; the action is mediated by the modulation of lipid peroxidation and glutathione content.

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