The Evaluation Effect of Palmatin on Improvmnt of Learning and Memory, Antioxidant Capacity and Necrosis Cell Death on Hippocampus Following Brain Ischemia Reperfusion

Abstract

Introduction: Palmatine is a protoberbene of the alkaloids group with antioxidant activities in various animal models. Recent studies have shown that palmatine prevents gentamicin-induced apoptosis in kidney tissue with antioxidant effects. Brain ischemia-reperfusion can cause irreversible damage especially in the area of the hippocampus. The aim of the study was to evaluate the effect of Palmatine on cognitive function, antioxidant activity and neuronal cell death following brain ischemia-reperfusion in male rats.

Methods: 21 male wistar rats were divided into three groups. 1- Sham group, 2- Ischemia group due to obstruction of both normal carotid arteries for 20 minutes, and 3- Treatment group in which palmatine injection at a dose of 100 mg / kg was performed intraperitoneally at the beginning of the reperfusion period and again after 24 and 48 hours. Spatial memory test was evaluated by Morris water maze. The brains were removed for antioxidant enzyme evaluation and Nissl staining to assess necrosis neuronal death within the hippocampal CA1 area.

Results: The results showed that the rate of learning in treatment group improved versus the ischemia group (P<0.05). Moreover, the attendance of animals in the target circle in the probe test, in the treatment groups was significantly higher than the Ischemia group which indicates an improvement in memory performance (P<0.05). Palmatine could significantly reduce necrosis cell death (P<0.05) in CA1 area of hippocampus. Also palmatine could significantly reduce MDA and increase SOD concentration (P<0.05).

Conclusion: The findings showed that treatment with Palmatine significantly ameliorated hippocampal injury and spatial learning and memory impairments after brain ischemic. These protective effects of Palmatine appear to be mediated by many mechanisms such as necrosis and apoptosis cell death by suppression of free radicals formation.