Wu-zhu-yu Decoction reduces early brain injury following subarachnoid hemorrhage in vivo and in vitro by activating the Nrf2 antioxidant system via SIRT6 targeting

Xu, Min; Yue, Qiyu; He, Ziyang; Ling, Xiaoyang; Wang, Wenhua; Gong, Mingjie

doi:10.1016/j.jep.2023.117335

Cited by 2 publications

(1 citation statement)

References 43 publications

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“…Research has shown that reducing oxidative stress can alleviate early brain damage [ 93 ]. Rat experiments have shown that traditional Chinese medicine Wu zhu yu reaction (WZYD) activates the Nrf2/heme oxygenase-1 (HO-1) signaling pathway through sirtuin 6 (SIRT6) mediated deacetylation of histone H3 lysine 56 (H3K56), inhibits oxidative stress, and can alleviate cerebral hemorrhage and edema after SAH, thereby alleviating EBI after SAH [ 94 ]. Another animal experiment showed that the mitochondrial-targeted antioxidant peptide elamipretide (also known as SS31) reduces lipid peroxidation, increases antioxidant enzyme activity, reverses mitochondrial dysfunction; and reduces blood-brain barrier damage, brain edema, and cell apoptosis after SAH, thereby improving neurological function damage by activating the Nrf2 signaling pathway [ 95 ].…”

Section: Potential Mechanisms Of Early Brain Injurymentioning

confidence: 99%

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Kang,

Tian,

Zhang

et al. 2024

Chin Neurosurg Jl

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Spontaneous subarachnoid hemorrhage (SAH), mainly caused by ruptured intracranial aneurysms, is a serious acute cerebrovascular disease. Early brain injury (EBI) is all brain injury occurring within 72 h after SAH, mainly including increased intracranial pressure, decreased cerebral blood flow, disruption of the blood-brain barrier, brain edema, oxidative stress, and neuroinflammation. It activates cell death pathways, leading to neuronal and glial cell death, and is significantly associated with poor prognosis. Ferroptosis is characterized by iron-dependent accumulation of lipid peroxides and is involved in the process of neuron and glial cell death in early brain injury. This paper reviews the research progress of ferroptosis in early brain injury after subarachnoid hemorrhage and provides new ideas for future research.

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Section: Potential Mechanisms Of Early Brain Injurymentioning

confidence: 99%

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Kang,

Tian,

Zhang

et al. 2024

Chin Neurosurg Jl

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Xinglou Chengqi Decoction Protects against Cerebral Ischemia/Reperfusion Injury by Inhibiting Ferroptosis via SLC7A11/GPX4 Signaling

Liu,

Yue,

Zhang

et al. 2024

Advanced Biology

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Xinglou Chengqi decoction (XLCQD) is a Chinese formula that offers benefits in ischemic stroke. However, the underlying mechanism of the effects of XLCQD‐mediated anti‐ischemic stroke effects remains obscure. This study investigates the ferroptosis mechanism of XLCQD against cerebral ischemia/reperfusion (I/R) injury using rat models of middle cerebral artery occlusion/reperfusion (MCAO/R). Ferroptosis differs from traditional cell death pathways and is linked to oxidative stress‐induced lipid peroxidation and glutathione (GSH) depletion, which is essential to the development of ischemic stroke. In this study, it is shown that XLCQD improves brain infarction, neurological dysfunction, and histopathological changes caused by MCAO/R exposure, and improving I/R‐induced oxidative damage through inhibition of ferroptosis via (Solute Carrier Family 7 Member 11) SLC7A11/ (glutathione peroxidase 4) GPX4 pathway. Interestingly, it is found that XLCQD‐mediated protection in I/R is reversed by the silence of SLC7A11. XLCQD intervention significantly promotes GSH content and suppresses Reactive Oxygen Species(ROS), iron accumulation, as well as Malondialdehyde (MDA) generation, are markedly abrogated when SLC7A11 is knockdown by SLC7A11‐shRNA transfection, indicating that SLC7A11 is the main target of XLCQD to further trigger intracellular events. In conclusion, XLCQD attenuates in vivo cerebral I/R injury by reducing ferroptosis via the SLC7A11/GPX4 pathway.

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Wu-zhu-yu Decoction reduces early brain injury following subarachnoid hemorrhage in vivo and in vitro by activating the Nrf2 antioxidant system via SIRT6 targeting

Cited by 2 publications

References 43 publications

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Xinglou Chengqi Decoction Protects against Cerebral Ischemia/Reperfusion Injury by Inhibiting Ferroptosis via SLC7A11/GPX4 Signaling

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