Protective effects of rehmannia Yinzi on ischemic injury induced by reperfusion in rats
Author(s): Zhou Jinghui
Pages: 116-118,136
Year: 2017 Issue: 2
Journal: Journal of Navy Medicine
Keyword: Rehmannia Yinzi; Cerebral ischemia-reperfusion injury; Protective effect;
Abstract: Objective To explore the protective effects of rehmannia Yinzi on ischemic injury induced by reperfusion in rats.Methods Seventy-two clean-grade Wistar rats with a body weight of 260-280 g were randomly divided into 4 groups:group A,group B,the model group and the normal control group,each consisting of 18 animals.For the animals of group A,rehmannia Yinzi liquid was given by gavage at a dose of 36 g/kg following development of the model,and for animals of group B,nimodipine was given also by gavage at a dose of 12.5 mg/kg.The animals of the model group received physiological saline by gavage following development of the model,and the animals of the control group received normal feed.In the animals of the former 3 groups,bilateral common carotid artery was clipped to develop the ischemia model,and then,blood reperfusion was performed to induce ischemic injury.Three weeks after gavage of rehmannia Yinzi,the levels of superoxide dismutase(SOD) and malondiadehyde(MDA) were detected in the brain tissue.Morris water maze experiment and platform-jump experiment were performed to detect the learning and memory capacity of the rats,and the area of infarction was measured as well.Results SOD level [(93.42 ± 18.78) kU/g prot] in the model group was obviously lower than that of the normal control group [(158.36 ±22.32) kU/g prot],but MDA level [(6.35 ±2.04) μmol/g prot] was significantly higher than that of the control group,[(2.63 ± 1.86) μmol/g prot],and statistical significance could be noticed,when comparisons were made between the 2 groups(P ＜ 0.05).The animal model was successfully developed.The SOD levels of group A [(135.34 ± 20.12) kU/g prot] and group B [(132.78 ± 19.56) kU/g prot] were significantly higher than those of the model group,and the MDA levels of group A [(3.46 ± 1.75) μmol/g prot] and group B [(3.82 ± 1.82) μmo]/g prot] were significantly lower than those of the model group.Statistical significance could also be noted,when comparisons were made between the 2 groups (P ＜ 0.05).The rate of learning and memory errors,as well as latency were all significantly lower than those of the model group,and the latency of group A and group B were significantly shorter than that of the model group.Statistical significance could be found,when comparisons were made between the 2 groups(P ＜ 0.05).The areas of cerebral infarction in group A and group B were significantly smaller than that of the model group,and the area of cerebral infarction in group A was significantly smaller than that in group B,also with statistical significance(P ＜ 0.05).Conclusion Rehmannia Yinzi liquid could improve blood circulation in the damaged brain tissues,reduce the area of infarction,improve energy metabolism in the damaged brain,enhance suppressed nerve cells,repair nerve function defect,and also help to protect the damaged neurons.
Pages: 116-118,136
Year: 2017 Issue: 2
Journal: Journal of Navy Medicine
Keyword: Rehmannia Yinzi; Cerebral ischemia-reperfusion injury; Protective effect;
Abstract: Objective To explore the protective effects of rehmannia Yinzi on ischemic injury induced by reperfusion in rats.Methods Seventy-two clean-grade Wistar rats with a body weight of 260-280 g were randomly divided into 4 groups:group A,group B,the model group and the normal control group,each consisting of 18 animals.For the animals of group A,rehmannia Yinzi liquid was given by gavage at a dose of 36 g/kg following development of the model,and for animals of group B,nimodipine was given also by gavage at a dose of 12.5 mg/kg.The animals of the model group received physiological saline by gavage following development of the model,and the animals of the control group received normal feed.In the animals of the former 3 groups,bilateral common carotid artery was clipped to develop the ischemia model,and then,blood reperfusion was performed to induce ischemic injury.Three weeks after gavage of rehmannia Yinzi,the levels of superoxide dismutase(SOD) and malondiadehyde(MDA) were detected in the brain tissue.Morris water maze experiment and platform-jump experiment were performed to detect the learning and memory capacity of the rats,and the area of infarction was measured as well.Results SOD level [(93.42 ± 18.78) kU/g prot] in the model group was obviously lower than that of the normal control group [(158.36 ±22.32) kU/g prot],but MDA level [(6.35 ±2.04) μmol/g prot] was significantly higher than that of the control group,[(2.63 ± 1.86) μmol/g prot],and statistical significance could be noticed,when comparisons were made between the 2 groups(P ＜ 0.05).The animal model was successfully developed.The SOD levels of group A [(135.34 ± 20.12) kU/g prot] and group B [(132.78 ± 19.56) kU/g prot] were significantly higher than those of the model group,and the MDA levels of group A [(3.46 ± 1.75) μmol/g prot] and group B [(3.82 ± 1.82) μmo]/g prot] were significantly lower than those of the model group.Statistical significance could also be noted,when comparisons were made between the 2 groups (P ＜ 0.05).The rate of learning and memory errors,as well as latency were all significantly lower than those of the model group,and the latency of group A and group B were significantly shorter than that of the model group.Statistical significance could be found,when comparisons were made between the 2 groups(P ＜ 0.05).The areas of cerebral infarction in group A and group B were significantly smaller than that of the model group,and the area of cerebral infarction in group A was significantly smaller than that in group B,also with statistical significance(P ＜ 0.05).Conclusion Rehmannia Yinzi liquid could improve blood circulation in the damaged brain tissues,reduce the area of infarction,improve energy metabolism in the damaged brain,enhance suppressed nerve cells,repair nerve function defect,and also help to protect the damaged neurons.
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