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A pinboard by
sarun koirala

young faculty, after completing MD, B.P. Koirala Institute of Health sciences

PINBOARD SUMMARY

its neuroscience and behavior and anatomy of brain research

Introduction: A stroke is a medical emergency and can cause permanent neurological damage.The more extensive the area of brain affected, the more functions that are likely to be lost.

Objectives: To access and compare neurological deficits after 60 min of reperfusion after induction of stroke and 14 days after treatment with ashwagandha i .p. in different groups and to see infract area in brain using 2,3,5 Triphenyltetrazolium chloride (TTC) stain.

Materials and Methods: 21 Male wistar albino rats weighing 200–220gm, 7 in each group were randomly allocated to form 3 groups. Control group was made with only skin incision in neck region (Group A0), Experimental group with unilateral internal carotid artery ligation and Group with unilateral internal carotid artery ligation and treatment with ashwaganda 10 mg/kg i. p. for 14 days. Commercially available Withania somnifera (ashwagandha) root extract (Vitamin world. Inc. NY, USA) was used as intra peritoneal route. After 14 days of i.p injection, neurological deficits tests was assessed, animal were anesthetized and sacrificed. The brain was removed, cut in coronal section of 2mm thickness, immersed in TTC (Sigma Aldrich, Merck Group Germany) solution and incubated at 37 0C for 20 min. Images of brain section was captured using Nikkon DSC 501 model digital camera and the infract area was calculated using KLONK Image Measurement Software, USA. Inferential analysis was done by t- test to see the significant level at p< 0.05 with 95% confidence interval and ANOVA, Post Hoc test was applied to compare between different groups.

          Results: There was red stained area in normal brain tissue indicating normal activity of mitochondrial enzyme activity- succinate dehydrogenase which caused conversion of 2,3,5 TTC to formazen, a tetrazolium salt.
          The white infarct area (unstained) was formed because of increased level of free oxygen radicals and reduced activity of succinate dehydrogenase enzyme after hypoxic ischemia caused by artery ligation. Area of infarct in the ashwagandha treated group  as compared to non- treatment group after 14days was seen significant.
          There was significant differences in area of infract between Withania somnifera (ashwagandha) treated group and non-medicated group p= 0.017. Latency of fall off time in Rotarod test was seen significant (p= 0.000) in between the group while  no significant difference was seen in grip strength test.