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Condition: Hemorrhagic Stroke
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Total 120 results found since Jan 2013.
HMGB1/TLR4 induces autophagy and promotes neuroinflammation after intracerebral hemorrhage
CONCLUSIONS: During the acute phase of ICH, the HMGB1/TLR4/MyD88 axis acts via autophagy to promote inflammation.PMID:35820449 | DOI:10.1016/j.brainres.2022.148003
Source: Brain Research - July 12, 2022 Category: Neurology Authors: Chunyan Lei Yongyu Li Xiaoyan Zhu Haijiang Li Xiaolong Chang Source Type: research
CDK5 Mediates Proinflammatory Effects of Microglia through Activated DRP1 Phosphorylation in Rat Model of Intracerebral Hemorrhage
CONCLUSION: CDK5 may regulate DRP1 by direct phosphorylation in microglia and further induce microglia secreting proinflammation factor.PMID:35795154 | PMC:PMC9252704 | DOI:10.1155/2022/1919064
Source: Disease Markers - July 7, 2022 Category: Laboratory Medicine Authors: Mingqing He Xiaoyan Wang Zheng Liu Qiyuan Cui Ying Chen Wenqing Geng Jinzhou Zhu Jiabing Shen Source Type: research
Hemorrhage-Induced Sphingosine Kinase 1 Contributes to Ferroptosis-Mediated Secondary Brain Injury in Intracerebral Hemorrhage
In this study, transcriptional changes in ICH patients were assessed by microarray data, exposing Sphk1 as a highly upregulated gene during ICH. Furthermore, Sphk1 chemical inhibitors and siRNA were used to inhibit ICH-induced Sphk1 upregulation in in vivo and in vitro models, showing that Sphk1 inhibition after protects against ferroptosis and attenuates secondary brain injury and cell death. Mechanistically, this study unveiled that sphingosine kinase 1/sphingosine 1-phosphate/extracellular-regulated protein kinases/phosphorylated extracellular-regulated protein kinases (Sphk1/S1p/ERK/p-ERK) pathway is responsible for re...
Source: Molecular Neurobiology - February 26, 2022 Category: Neurology 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
Activation of RAR α Receptor Attenuates Neuroinflammation After SAH via Promoting M1-to-M2 Phenotypic Polarization of Microglia and Regulating Mafb/Msr1/PI3K-Akt/NF-κB Pathway
ConclusionActivation of the RARα receptor attenuated neuroinflammation by promoting M1-to-M2 phenotypic polarization in microglia and regulating the Mafb/Msr1/PI3K-Akt/NF-κB pathway. RARα might serve as a potential target for SAH therapy.
Source: Frontiers in Immunology - February 14, 2022 Category: Allergy & Immunology Source Type: research
c-Abl Tyrosine Kinase-Mediated Neuronal Apoptosis in Subarachnoid Hemorrhage by Modulating the LRP-1-Dependent Akt/GSK3 β Survival Pathway
AbstractAccumulating evidence suggests that neuronal apoptosis plays a critical role in early brain injury (EBI) after subarachnoid hemorrhage (SAH), and the inhibition of apoptosis can induce neuroprotective effects in SAH animal models. c-Abl has been reported to promote neuronal apoptosis in Alzheimer ’s disease and cerebral ischemia, but its role in SAH had not been illuminated until now. In the present study, the effect of c-Abl on neuronal apoptosis induced by SAH was investigated. c-Abl protein levels and neuronal apoptosis were markedly increased 24 h after SAH, and the inhibition of endo genous c-Abl reduced ne...
Source: Journal of Molecular Neuroscience - November 22, 2021 Category: Neuroscience Source Type: research
Kisspeptin-54 attenuates oxidative stress and neuronal apoptosis in early brain injury after subarachnoid hemorrhage in rats via GPR54/ARRB2/AKT/GSK3 β signaling pathway
In conclusion, our results suggested that administration of KP54 attenuated oxidative stress, neuronal apoptosis and neurobehavioral impairments through GPR54/ARRB2/AKT/GSK3β signaling pathway after SAH in rat. Thus, KP54 may provide an effective treatment strategy for SAH patients.PMID:33989759 | DOI:10.1016/j.freeradbiomed.2021.05.012
Source: Free Radical Biology and Medicine - May 14, 2021 Category: Biology Authors: Yi Huang Yong Guo Lei Huang Yuanjian Fang Dujuan Li Rui Liu Qin Lu Reng Ren Lihui Tang Lifei Lian Yongmei Hu Jiping Tang Gao Chen John H Zhang Source Type: research
Dihydrolipoic acid enhances autophagy and alleviates neurological deficits after subarachnoid hemorrhage in rats
In this study, we investigated the role of dihydrolipoic acid (DHLA) on enhancing autophagy and alleviating neurological deficits after SAH. SAH was induced by endovascular perforation in male Sprague-Dawley rats. DHLA (30 mg/kg) was administered intraperitoneally 1 h (h) after SAH. Small interfering ribonucleic acid (siRNA) for lysosome-associated membrane protein-1 (LAMP1) was administered through intracerebroventricular (i.c.v) route 48 h before SAH induction. SAH grading score, neurological score, immunofluorescence staining, Fluoro-Jade C (FJC) staining, and Western blot were examined. DHLA treatment increased autopha...
Source: Experimental Neurology - May 11, 2021 Category: Neurology Authors: Keren Zhou Budbazar Enkhjargal Jun Mo Tongyu Zhang Qiquan Zhu Pei Wu Cesar Reis Jiping Tang John H Zhang Jianmin Zhang Source Type: research
BYHWD Alleviates Inflammatory Response by NIK-Mediated Repression of the Noncanonical NF- κB Pathway During ICH Recovery
Intracerebral hemorrhage (ICH) is a life-threatening type of stroke that lacks effective treatments. The inflammatory response following ICH is a vital response that affects brain repair and organism recovery. The nuclear factor κB (NF-κB) signaling pathway is considered one of the most important inflammatory response pathways and one of its response pathways, the noncanonical NF-κB signaling pathway, is known to be associated with persistent effect and chronic inflammation. NF-κB–inducing kinase (NIK) via the noncanonical NF-κB signaling plays a key role in controlling inflammation. Here, we investigated potential ...
Source: Frontiers in Pharmacology - May 7, 2021 Category: Drugs & Pharmacology Source Type: research
Transforming growth factor ‑β1 functions as a competitive endogenous RNA that ameliorates intracranial hemorrhage injury by sponging microRNA‑93‑5p
Mol Med Rep. 2021 Jul;24(1):499. doi: 10.3892/mmr.2021.12138. Epub 2021 May 6.ABSTRACTIntracerebral hemorrhage (ICH) has the highest mortality rate of all stroke subtypes but an effective treatment has yet to be clinically implemented. Transforming growth factor‑β1 (TGF‑β1) has been reported to modulate microglia‑mediated neuroinflammation after ICH and promote functional recovery; however, the underlying mechanisms remain unclear. Non‑coding RNAs such as microRNAs (miRNAs) and competitive endogenous RNAs (ceRNAs) have surfaced as critical regulators in human disease. A known miR‑93 target, nuclear factor eryth...
Source: Molecular Medicine - May 6, 2021 Category: Molecular Biology Authors: Han Wang Xianming Cao Xiaoqing Wen Dongling Li Yetong Ouyang Bing Bao Yuqin Zhong Zhengfang Qin Min Yin Zhiying Chen Xiaoping Yin Source Type: research
