PDF(Pubmed)
Abstract：
OBJECTIVE: Reduction of cerebral ischemia-reperfusion injury (IRI)/re-oxygenation injury, is defined as the paradoxical exacerbation of the cellular dysfunction and death, following restoration of the blood flow to previously ischemic tissues. The re-establishment of blood flow is essential to salvage the ischemic tissues. As a result, the treatment of IRI with novel therapies, which have fewer side effects, are of great importance. Therefore, this study aimed to investigate the effects of curcumin nanoparticle (CN) pre-treatment on the cerebral I/R rat model.
METHODS: In this experimental study, CN was administered to rats orally five days before the bilateral common carotid artery occlusion (BCCAO) and continued for three days. The intensity of oxidative stress, the activities of antioxidant enzymes, glutathione (GSH) content, the activity of mitochondrial enzymes, including succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and lactate dehydrogenase (LDH), curcumin bioavailability, pERK/ERK expression ratio and TFEB protein were studied. Data analysis was performed using Graphpad Prism V.8 software, one-way analysis of variance (ANOVA) with the statistical package for the social sciences (SPSS V.26 software).
RESULTS: Cerebral IRI-damage significantly increased the oxidative stress (P=0.0008) and decreased the activity of the antioxidant enzymes including catalase (CAT) (P<0.001), super oxide dismutase (SOD) (P<0.001), reduced GSH (P<0.001), mitochondrial enzymes, pERK/ERK expression ratio (P=0.002) and TEFB protein (P=0.005) in rats\' brains. In addition, the pre-treatment of the rats with CN resulted in a decrease in the reactive oxygen species (ROS), and an increase in the activities of antioxidants and mitochondrial enzymes. This in turn up-regulated the pERK/ERK expression ratio and TEFB expression.
CONCLUSIONS: CN has neuroprotective effects on the cerebral IRI condition due to its antioxidant properties and is able to overexpress the pERK and TFEB proteins; thus, it can be considered as a suitable treatment option during and after the incidence of stroke.
METHODS: In this experimental study, CN was administered to rats orally five days before the bilateral common carotid artery occlusion (BCCAO) and continued for three days. The intensity of oxidative stress, the activities of antioxidant enzymes, glutathione (GSH) content, the activity of mitochondrial enzymes, including succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and lactate dehydrogenase (LDH), curcumin bioavailability, pERK/ERK expression ratio and TFEB protein were studied. Data analysis was performed using Graphpad Prism V.8 software, one-way analysis of variance (ANOVA) with the statistical package for the social sciences (SPSS V.26 software).
RESULTS: Cerebral IRI-damage significantly increased the oxidative stress (P=0.0008) and decreased the activity of the antioxidant enzymes including catalase (CAT) (P<0.001), super oxide dismutase (SOD) (P<0.001), reduced GSH (P<0.001), mitochondrial enzymes, pERK/ERK expression ratio (P=0.002) and TEFB protein (P=0.005) in rats\' brains. In addition, the pre-treatment of the rats with CN resulted in a decrease in the reactive oxygen species (ROS), and an increase in the activities of antioxidants and mitochondrial enzymes. This in turn up-regulated the pERK/ERK expression ratio and TEFB expression.
CONCLUSIONS: CN has neuroprotective effects on the cerebral IRI condition due to its antioxidant properties and is able to overexpress the pERK and TFEB proteins; thus, it can be considered as a suitable treatment option during and after the incidence of stroke.
摘要：
目的：减轻脑缺血再灌注损伤（IRI）/复氧损伤，被定义为细胞功能障碍和死亡的矛盾恶化，恢复先前缺血组织的血流。血流的重建对于挽救缺血组织至关重要。因此,用新疗法治疗IRI，副作用较少，非常重要。因此,本研究旨在探讨姜黄素纳米粒(CN)预处理对脑I/R大鼠模型的影响。
方法：在本实验研究中，在双侧颈总动脉闭塞（BCCAO）之前五天，将CN口服给药至大鼠，并持续三天。氧化应激的强度，抗氧化酶的活性，谷胱甘肽（GSH）含量，线粒体酶的活性，包括琥珀酸脱氢酶（SDH），苹果酸脱氢酶（MDH）和乳酸脱氢酶（LDH），姜黄素生物利用度，研究了pERK/ERK表达率和TFEB蛋白。使用GraphpadPrismV.8软件进行数据分析，使用社会科学统计软件包（SPSSV.26软件）进行单向方差分析（ANOVA）。
结果：大脑IRI损伤显著增加了氧化应激（P=0.0008），并降低了包括过氧化氢酶（CAT）在内的抗氧化酶的活性（P<0.001）。超氧化物歧化酶(SOD)(P<0.001),GSH降低（P<0.001），线粒体酶，大鼠脑中pERK/ERK表达比率(P=0.002)和TEFB蛋白(P=0.005)。此外,用CN预处理大鼠导致活性氧（ROS）减少，抗氧化剂和线粒体酶的活性增加。这反过来上调了pERK/ERK表达比率和TEFB表达。
结论：CN由于其抗氧化特性而对大脑IRI状况具有神经保护作用，并且能够过表达pERK和TFEB蛋白；因此，它可以被认为是中风发生期间和之后的合适治疗选择。
方法：在本实验研究中，在双侧颈总动脉闭塞（BCCAO）之前五天，将CN口服给药至大鼠，并持续三天。氧化应激的强度，抗氧化酶的活性，谷胱甘肽（GSH）含量，线粒体酶的活性，包括琥珀酸脱氢酶（SDH），苹果酸脱氢酶（MDH）和乳酸脱氢酶（LDH），姜黄素生物利用度，研究了pERK/ERK表达率和TFEB蛋白。使用GraphpadPrismV.8软件进行数据分析，使用社会科学统计软件包（SPSSV.26软件）进行单向方差分析（ANOVA）。
结果：大脑IRI损伤显著增加了氧化应激（P=0.0008），并降低了包括过氧化氢酶（CAT）在内的抗氧化酶的活性（P<0.001）。超氧化物歧化酶(SOD)(P<0.001),GSH降低（P<0.001），线粒体酶，大鼠脑中pERK/ERK表达比率(P=0.002)和TEFB蛋白(P=0.005)。此外,用CN预处理大鼠导致活性氧（ROS）减少，抗氧化剂和线粒体酶的活性增加。这反过来上调了pERK/ERK表达比率和TEFB表达。
结论：CN由于其抗氧化特性而对大脑IRI状况具有神经保护作用，并且能够过表达pERK和TFEB蛋白；因此，它可以被认为是中风发生期间和之后的合适治疗选择。
