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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Protocatechuic Acid Prevents Early Hour Ischemic Reperfusion Brain Damage by Restoring Imbalance of Neuronal Cell Death and Survival Proteins
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Protocatechuic Acid Prevents Early Hour Ischemic Reperfusion Brain Damage by Restoring Imbalance of Neuronal Cell Death and Survival Proteins

机译：Protocatechuic acid通过恢复神经细胞死亡和生存蛋白的不平衡来防止早期缺血再灌注脑损伤

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Objective: To investigate the neuroprotective effect of protocatechuic acid (PCA) on cell death/survival protein imbalance in a rat model of middle cerebral artery occlusion and reperfusion. Methods: Focal ischemia was induced by middle cerebral artery occlusion in adult male Wistar rats and confirmed by measuring infarction of brain by 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Rats were treated with vehicle or PCA at 10, 30 or 50 mg/kg dose intraperitoneally and subjected to neurological deficits or beam walk assessment at 24 h of reperfusion. Effective dose of PCA (50 mg/kg) was administered at 1, 2 and 3 h time point of post-ictus ischemia. Cellular damage and nuclear condensation was observed by haematoxylin and eosin (H and E) staining and Hoechst 33342 staining respectively. Additionally, immunohistochemical expression of caspase 3 and cAMP-response element binding protein (CREB) and their mRNA's were observed. Results: PCA at 30 and 50 mg/kg significantly improved behavioural performance and reduced infarction. Maximum neuroprotective effect of PCA (50 mg/kg) was found at 1 h (early hours) post-ictus ischemia along with reduction in cellular damage and nuclear condensation. PCA increased CREB protein and it's mRNA, while suppressed caspase-3 protein and mRNA at 1 h of reperfusion injury. Conclusion: PCA exhibit the potential to prevent early hour (1h) reperfusion injury restoring balance of survival and death protein may offer a cost effective adjuvant therapy in stroke.
机译：目的：探讨原儿茶酸（PCA）对大鼠大脑中动脉闭塞再灌注模型细胞死亡/存活蛋白失衡的保护作用。方法：用成年雄性Wistar大鼠大脑中动脉闭塞诱导局灶性脑缺血，并用2,3,5-三苯基四氮唑（TTC）染色法检测脑梗塞。给大鼠腹腔注射10、30或50 mg/kg剂量的溶媒或PCA，并在再灌注24小时进行神经功能缺损或束流行走评估。在发作后缺血的1、2和3 h时间点给予有效剂量的PCA（50 mg/kg）。苏木精-伊红（H和E）染色和Hoechst 33342染色分别观察细胞损伤和核浓缩。此外，还观察了半胱天冬酶3和cAMP反应元件结合蛋白（CREB）及其mRNA的免疫组化表达。结果：30和50 mg/kg的PCA显著改善行为表现，减少梗死。PCA（50 mg/kg）的最大神经保护作用出现在缺血发作后1小时（早期），同时细胞损伤和核浓缩减少。在再灌注损伤1h，PCA增加CREB蛋白及其mRNA，同时抑制caspase-3蛋白和mRNA。结论：PCA具有预防早期（1h）再灌注损伤的潜力，恢复生存和死亡蛋白的平衡可能为脑卒中提供一种经济有效的辅助治疗。

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