医学
神经保护
糖尿病
氧化应激
链脲佐菌素
内科学
冲程(发动机)
缺血
内分泌学
缺血预处理
梗塞
心脏病学
心肌梗塞
机械工程
工程类
作者
Jens P. Goetze,Jakob Albrethsen
标识
DOI:10.1016/j.regpep.2014.04.002
摘要
Ischemic preconditioning (IPreC) can render the brain more tolerant to a subsequent potential lethal ischemic injury. Hyperglycemia has been shown to increase the size of ischemic stroke and worsen the clinical outcome following a stroke, thus exacerbating oxidative stress. Adropin has a significant association with cardiovascular disease, especially with diabetes. In this study, we aimed to evaluate the role of the IPreC due to modulating the expression of adropin and oxidative damage markers against stroke by induced transient middle cerebral artery occlusion (MCAo) in streptozotocin (STZ)-induced diabetic rats.72 male Spraque Dawley rats were allocated to 8 groups. In order to evaluate alterations of anti/oxidative status and adropin level, we induced transient MCAo seven days after STZ-induced diabetes. Also we performed IPreC 72 h before transient MCAo to assess whether IPreC could have a neuroprotective effect against ischemia-reperfusion injury.The general characteristics of STZ-treated rats (STZ) included reduced body weight and elevated blood glucose levels compared to non-diabetic ones. Ischemic preconditioning before cerebral ischemia significantly reduced infarction size compared with the other groups [IPreC + MCAo (27 ± 11 mm3) vs. MCAo (109 ± 17 mm3) p < 0.001; STZ + IPreC + MCAo (38 ± 10 mm3) vs. STZ + MCAo (165 ± 45 mm3) p < 0.001, respectively]. The mean total antioxidant status level in IPreC groups was higher than other groups (p ≤ 0.05). Moreover, IPreC considerably decreased mean adropin levels compared with other groups (p ≤ 0.05).The study results supported the neuroprotective effects of ischemic preconditioning in MCA infarcts correlated with the level of oxidative damage markers and adropin.
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