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Molecules, Vol. 28, Pages 1747: Pharmacological Modulations of Nrf2 and Therapeutic Implications in Aneurysmal Subarachnoid Hemorrhage
un Mo An aneurysmal subarachnoid hemorrhage (aSAH) is a subtype of stroke with high morbidity and mortality. The main causes of a poor prognosis include early brain injury (EBI) and delayed vasospasm, both of which play a significant role in the pathophysiological process. As an important mechanism of EBI and delayed vasospasm, oxidative stress plays an important role in the pathogenesis of aSAH by producing reactive oxygen species (ROS) through the mitochondria, hemoglobin, or enzymatic pathways in the early stages of aSAH. As a result, antioxidant therapy, which primarily targets the Nrf2-related pathway, can be empl...
Source: Molecules - February 12, 2023 Category: Chemistry Authors: Qia Zhang Jianmin Zhang Jun Mo Tags: Review Source Type: research

Astragaloside IV attenuates ferroptosis after subarachnoid hemorrhage via Nrf2/HO-1 signaling pathway
Subarachnoid hemorrhage (SAH) is a severe type of stroke featuring exceptionally high rate of morbidity and mortality due to the lack of effective management. Ferroptosis can be defined as a novel iron-dependent programmed cell death in contrast to classical apoptosis and necrosis. Astragaloside IV (AS-IV) is an active ingredient extracted from Astragalus membranaceus with established therapeutic effect on CNS diseases. However, the exact role of ferroptosis in Astragaloside IV-mediated neuroprotection after SAH is yet to be demonstrated. In the present study, the SAH model of SD male rats with endovascular perforation was...
Source: Frontiers in Pharmacology - August 19, 2022 Category: Drugs & Pharmacology Source Type: research

Thioredoxin 1 regulates the pentose phosphate pathway via ATM phosphorylation after experimental subarachnoid hemorrhage in rats
Brain Res Bull. 2022 May 16;185:162-173. doi: 10.1016/j.brainresbull.2022.05.008. Online ahead of print.ABSTRACTSubarachnoid hemorrhage (SAH), a type of hemorrhagic stroke, is a neurological emergency with high morbidity and mortality. Early brain injury (EBI) after SAH is the leading cause of poor prognosis in SAH patients. TRX system is a NADPH-dependent antioxidant system which is composed of thioredoxin reductase (TRXR), thioredoxin (TRX). The pentose phosphate pathway (PPP), a pathway through which glucose can be metabolized, is a major source of NADPH. Thioredoxin 1 (TRX1) is a member of thioredoxin system mainly loc...
Source: Brain Research Bulletin - May 19, 2022 Category: Neurology Authors: Xiaodong Wang Zongqi Wang Jie Wu Lingling Wang Xiang Li Haitao Shen Haiying Li Jianguo Xu Wen Li Gang Chen Source Type: research

The Mfn1- βIIPKC Interaction Regulates Mitochondrial Dysfunction via Sirt3 Following Experimental Subarachnoid Hemorrhage
AbstractNeuronal injury following subarachnoid hemorrhage (SAH) has been shown to be associated with mitochondrial dysfunction and oxidative stress. βIIPKC, a subtype of protein kinase C (PKC), accumulates on the mitochondrial outer membrane and phosphorylates mitofusin 1 (Mfn1) at serine 86. Here, we investigated the role of Mfn1-βIIPKC interaction in brain damage and neurological function in both in vivo and in vitro experimental SAH models. The expression of βIIPKC protein and the interaction of Mfn1-βIIPKC were found to be increased after OxyHb treatment in primary cultured cortical neurons and were also observed i...
Source: Translational Stroke Research - February 22, 2022 Category: Neurology Source Type: research

Fucoxanthin Mitigates Subarachnoid Hemorrhage-Induced Oxidative Damage via Sirtuin 1-Dependent Pathway
AbstractOxidative stress is a key component of the pathological cascade in subarachnoid hemorrhage (SAH). Fucoxanthin (Fx) possesses a strong antioxidant property and has shown neuroprotective effects in acute brain injuries such as ischemic stroke and traumatic brain injury. Here, we investigated the beneficial effects of Fx against SAH-induced oxidative insults and the possible molecular mechanisms. Our data showed that Fx could significantly inhibit SAH-induced reactive oxygen species production and lipid peroxidation, and restore the impairment of endogenous antioxidant enzymes activities. In addition, Fx supplementati...
Source: Molecular Neurobiology - October 7, 2020 Category: Neurology Source Type: research

Cryptotanshinone Attenuates Oxygen-Glucose Deprivation/ Recovery-Induced Injury in an in vitro Model of Neurovascular Unit
Conclusions Despite the above limitations, we indicate that the protective mechanism of CTs against OGD/R damage might exert via inhibiting neuron apoptosis and attenuating BBB disruption. Furthermore, we also clarified that CTs inhibited neuronal apoptosis possibly by blocking the activation of MAPK signaling pathways, and CTs alleviating BBB disruption may associated with the regulation of TJPs and MMP-9 in our experiment. Accordingly, CTs will represent a novel and potent candidate for the treatment of CIRI in the future. Ethics Statement This study was carried out in accordance with the recommendations of China�...
Source: Frontiers in Neurology - April 17, 2019 Category: Neurology Source Type: research