Volume 32, Issue 214 (11-2022)
J Mazandaran Univ Med Sci 2022, 32(214): 43-54 |
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Shiri E, Bigdeli M R, Eidi A, Mortazavi S P. Effect of Saponin on Cerebral Edema Rate in
An Animal Model of Stroke. J Mazandaran Univ Med Sci 2022; 32 (214) :43-54
URL: http://jmums.mazums.ac.ir/article-1-18385-en.html
URL: http://jmums.mazums.ac.ir/article-1-18385-en.html
Abstract: (1562 Views)
Background and purpose: Oxidative stress and neuroinflammation are the main causes of cerebral ischemia. Saponin with steroid or triterpenoid compounds with a sugar part has strong antioxidant and anti-inflammatory properties. The aim of this study was to evaluate the effect of saponin on cerebral edema, Bax gene expression level, and ischemic neurological defects.
Materials and methods: In this experimental study, 24 male Wistar rats were divided into three groups: sham, stroke, and stroke+saponin. Rats in the stroke+saponin group received intravenous injection of saponin (3mg/kg) 30 minutes before cerebral ischemia. Each group was divided into two subgroups: brain edema (n=5) and gene expression level investigation (n=3). Cerebral ischemia was induced by middle cerebral artery occlusion model. After 24 hrs, we investigated neurological deficits resulting from ischemia (Kruskal-Wallis test), the degree of brain edema, and Bax gene expression levels in the cortex, piriform cortex-amygdala, striatum, and hippocampus (one-way ANOVA).
Results: Findings indicated a significant decrease in the score of neurological defects resulting from ischemia, the amount of cerebral edema, and the level of Bax gene expression in stroke+saponin group (P<0.05).
Conclusion: This study showed that saponin pretreatment in rats with ischemia-reperfusion injury can be effective in reducing the damage caused by cerebral ischemia.
Materials and methods: In this experimental study, 24 male Wistar rats were divided into three groups: sham, stroke, and stroke+saponin. Rats in the stroke+saponin group received intravenous injection of saponin (3mg/kg) 30 minutes before cerebral ischemia. Each group was divided into two subgroups: brain edema (n=5) and gene expression level investigation (n=3). Cerebral ischemia was induced by middle cerebral artery occlusion model. After 24 hrs, we investigated neurological deficits resulting from ischemia (Kruskal-Wallis test), the degree of brain edema, and Bax gene expression levels in the cortex, piriform cortex-amygdala, striatum, and hippocampus (one-way ANOVA).
Results: Findings indicated a significant decrease in the score of neurological defects resulting from ischemia, the amount of cerebral edema, and the level of Bax gene expression in stroke+saponin group (P<0.05).
Conclusion: This study showed that saponin pretreatment in rats with ischemia-reperfusion injury can be effective in reducing the damage caused by cerebral ischemia.
Type of Study: Research(Original) |
Subject:
physiology
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