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脑缺血再灌注中的类黄酮及其对作为信号通路活性的激酶的影响。

Flavonoids in Brain Ischemia-Reperfusion and their Effect on Kinases as Signaling Pathway Activity.

作者信息

Danis Esra Gulsum, Mogulkoc Rasim, Baltaci Abdulkerim Kasim

机构信息

Department of Physiology, Medical School, Selcuk University, Konya, Turkey.

出版信息

CNS Neurol Disord Drug Targets. 2025 Apr 30. doi: 10.2174/0118715273374176250414051135.

DOI:10.2174/0118715273374176250414051135
PMID:40325527
Abstract

Brain ischemia-reperfusion injury (CIRI) refers to brain ischemia that leads to cellular dysfunction and cell death after a certain period, and ischemic damage is rescued by providing blood supply and reperfusion. And then, reperfusion includes components such as ion imbalance, mitochondrial dysfunction, oxidative stress, neuroinflammation, Ca2+ overload, and apoptosis, which do not cause tissue damage. Autophagy also occurs in CIRI due to oxygen deficiency, and autophagy has been shown to protect cells from ischemic injury. Flavonoids are a class of essential and diversified secondary plant metabolites found in different concentrations in leaves, flowers, roots, and fruits. Various studies have shown that flavonoids have healing qualifications such as anti-inflammatory, antimutagenic, anticarcinogenic, and antimicrobial. We aim to determine how flavonoids may affect signaling pathways and kinases in rats with CIRI. The results show that the activity of JAK2/STAT3, NF-κB, RhoA/ROCK, JNK-p38, and cAMKII signaling pathways increases under CIRI, and the PI3K/Akt/mTOR signaling pathway is suppressed. Studies using various flavonoids (kaempferol, chrysin, naringin, naringenin, quercetin, wogonin) have shown a neuroprotective effect by reversing the situation in signaling pathways during CIRI damage.

摘要

脑缺血再灌注损伤(CIRI)是指脑缺血一段时间后导致细胞功能障碍和细胞死亡,而通过恢复血液供应和再灌注可挽救缺血损伤。然后,再灌注包括离子失衡、线粒体功能障碍、氧化应激、神经炎症、Ca2+超载和细胞凋亡等成分,这些成分不会导致组织损伤。由于缺氧,自噬也会在CIRI中发生,并且自噬已被证明可保护细胞免受缺血损伤。黄酮类化合物是一类重要且多样的次生植物代谢产物,在叶片、花朵、根和果实中以不同浓度存在。各种研究表明,黄酮类化合物具有抗炎、抗诱变、抗癌和抗菌等治疗特性。我们旨在确定黄酮类化合物如何影响CIRI大鼠的信号通路和激酶。结果表明,在CIRI条件下,JAK2/STAT3、NF-κB、RhoA/ROCK、JNK-p38和cAMKII信号通路的活性增加,而PI3K/Akt/mTOR信号通路受到抑制。使用各种黄酮类化合物(山奈酚、白杨素、柚皮苷、柚皮素、槲皮素、汉黄芩素)的研究表明,通过逆转CIRI损伤期间信号通路的情况可产生神经保护作用。

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