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Condition: Ischemic Stroke

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Total 193 results found since Jan 2013.

Protective Effects of ShcA Protein Silencing for Photothrombotic Cerebral Infarction
This study suggests that the regulation of ShcA protein expression can be a therapeutic target for reducing brain damage with mitochondrial dysfunction caused by thrombotic infarction.
Source: Translational Stroke Research - September 6, 2021 Category: Neurology Source Type: research

Hypothermia Promotes Mitochondrial Elongation In Cardiac Cells Via Inhibition Of Drp1
In conclusion hypothermia promoted elongation of cardiac mitochondria via reduced pDrp1S616 abundance which was also associated with suppression of cellular oxygen consumption. Silencing of TRPV1 in H9c2 cardiomyocytes reproduced the morphological and respirometric phenotype of hypothermia. This report demonstrates a novel mechanism of cold-induced inhibition of mitochondrial fission.PMID:34331901 | DOI:10.1016/j.cryobiol.2021.07.013
Source: Cryobiology - July 31, 2021 Category: Biology Authors: David Taylor Juliana Germano Yang Song Hanane Hadj-Moussa Stefanie Marek-Iannucci Raeesa Dhanji Jon Sin Lawrence S C Czer Kenneth B Storey Roberta A Gottlieb Source Type: research

Tetramethylpyrazine Preserves the Integrity of Blood-Brain Barrier Associated With Upregulation of MCPIP1 in a Murine Model of Focal Ischemic Stroke
Tetramethylpyrazine (TMP), a prominent ingredient of Chinese herb Ligusticum chuanxiong Hort, is known to suppress neuroinflammation and protect blood-brain barrier (BBB) integrity. We investigated whether monocyte chemotactic protein-induced protein 1 (MCPIP1, also known as Regnase-1), a newly identified zinc-finger protein, plays a role in TMP-mediated anti-inflammation and neuroprotection. Male C57BL/6 mice were subjected to focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) for 2 h, followed by reperfusion for 24 h. TMP (25 mg/kg or 50 mg/kg) or vehicle was administered intraperitoneally 12Â...
Source: Frontiers in Pharmacology - July 28, 2021 Category: Drugs & Pharmacology Source Type: research

Long non-coding RNA MIAT impairs neurological function in ischemic stroke via up-regulating microRNA-874-3p-targeted IL1B
CONCLUSION: Shortly, this study figures out that MIAT impairs neurological function in IS via up-regulating miR-874-3p-targeted IL1B.PMID:34265390 | DOI:10.1016/j.brainresbull.2021.07.005
Source: Brain Research Bulletin - July 15, 2021 Category: Neurology Authors: Shuai Zhang Yue Zhang Na Wang Yu Wang Huan Nie Yueyue Zhang Huiying Han Shan Wang Wenjuan Liu Chunrui Bo Source Type: research

Long noncoding RNA Meg3 mediates ferroptosis induced by oxygen and glucose deprivation combined with hyperglycemia in rat brain microvascular endothelial cells, through modulating the p53/GPX4 axis
In this study, rat brain microvascular endothelial cells (RBMVECs) were exposed to 6 h of oxygen and glucose deprivation (OGD), and subsequent reperfusionvia incubating cells with glucose of various high concentrations for 24 h to imitateinvitro diabetic brain ischemic injury. It was shown that the marker events of ferroptosis and increasedMeg3 expression occurred after the injury induced by OGD combined with hyperglycemia. However, all ferroptotic events were reversed with the treatment ofMeg3-siRNA. Moreover, in this in vitro model, p53 was also characterized as a downstream target ofMeg3. Furthermore, p53 knockdown prot...
Source: European Journal of Histochemistry - July 2, 2021 Category: Biomedical Science Authors: Cheng Chen, Yan Huang, Pingping Xia, Fan Zhang, Longyan Li, E Wang, Qulian Guo, Zhi Ye Source Type: research

Melatonin protects against focal cerebral ischemia-reperfusion injury in diabetic mice by ameliorating mitochondrial impairments: involvement of the Akt-SIRT3-SOD2 signaling pathway
Aging (Albany NY). 2021 Jun 11;13. doi: 10.18632/aging.203137. Online ahead of print.ABSTRACTDiabetic patients are more vulnerable to cerebral ischemia-reperfusion (CIR) injury and have a worse prognosis and higher mortality after ischemic stroke than non-diabetic counterparts. Melatonin can exert neuroprotective effects against CIR injury in nondiabetic animal models. However, its effects on diabetic CIR injury and the underlying mechanisms remain unclarified. Herein, we found that melatonin administration improved neurological deficit, cerebral infarct volume, brain edema, and cell viability, reduced mitochondrial swelli...
Source: Aging - June 12, 2021 Category: Biomedical Science Authors: Lian Liu Quan Cao Wenwei Gao Bingyu Li Zhongyuan Xia Bo Zhao Source Type: research

SIRT1/PGC-1 α signaling activation by mangiferin attenuates cerebral hypoxia/reoxygenation injury in neuroblastoma cells
This study is designed to investigate the protective effect of MGF treatment in the setting of cerebral IRI and to elucidate the potential mechanisms. We first evaluated the toxicity of MGF and chose the safe concentrations for the following experiments. MGF exerted obvious neuroprotection against hypoxia/reoxygenation (HR)-induced injury, indicated by restored cell viability and cell morphology, decreased lactate dehydrogenase (LDH) release and reactive oxygen species generation. MGF also restored the protein expressions of SIRT1, PGC-1α, Nrf2, NQO1, HO-1, NRF1, UCP2, and Bcl2 down-regulated by HR treatment. However, SIR...
Source: European Journal of Pharmacology - June 11, 2021 Category: Drugs & Pharmacology Authors: Mengfan Chen Zheng Wang Wenying Zhou Chenxi Lu Ting Ji Wenwen Yang Zhenxiao Jin Ye Tian Wangrui Lei Songdi Wu Qi Fu Zhen Wu Xue Wu Mengzhen Han Minfeng Fang Yang Yang Source Type: research

Galectin-1 Contributes to Vascular Remodeling and Blood Flow Recovery After Cerebral Ischemia in Mice
AbstractGalectin-1 is found in the vasculature and has been confirmed to promote angiogenesis in several cancer models. Furthermore, galectin-1 has been demonstrated to improve the recovery of cerebral ischemia. However, whether vascular remodeling contributes to this improvement is still unknown. In the present study, photochemical cerebral ischemia was induced in both galectin-1-treated (2  μg/day,i.c.v, 3  days) and galectin-1 knockout mice. Laser speckle imaging and immunofluorescent staining demonstrated that circulation and vascular remodeling in the ischemic cortex were improved by galectin-1 treatment but disrup...
Source: Translational Stroke Research - May 10, 2021 Category: Neurology Source Type: research

FABP4 alleviates endoplasmic reticulum stress-mediated ischemia-reperfusion injury in PC12 cells via regulation of PPAR γ.
FABP4 alleviates endoplasmic reticulum stress-mediated ischemia-reperfusion injury in PC12 cells via regulation of PPARγ. Exp Ther Med. 2021 Mar;21(3):181 Authors: Yang XL, Mi JH, Dong Q Abstract Ischemic stroke is a life-threatening complication with a high rate of morbidity. Circulating fatty acid binding protein 4 (FABP4) has been reported to be associated with the outcome of acute ischemic stroke. The present study aimed to illustrate the function of FABP4 in ischemic stroke. PC12 cells exposed to oxygen glucose deprivation/reoxygenation (OGD/R) were used to mimic ischemia-reperfusion (I/R) injury...
Source: Experimental and Therapeutic Medicine - January 27, 2021 Category: General Medicine Tags: Exp Ther Med Source Type: research

The AMPAR antagonist perampanel protects the neurovascular unit against traumatic injury via regulating Sirt3.
CONCLUSION: Our results indicate that the noncompetitive AMPAR antagonist perampanel protects the NVU system and reduces brain damage after TBI via activating the Sirt3 cascades. PMID: 33421349 [PubMed - as supplied by publisher]
Source: CNS Neuroscience and Therapeutics - January 9, 2021 Category: Neuroscience Authors: Chen T, Liu WB, Qian X, Xie KL, Wang YH Tags: CNS Neurosci Ther Source Type: research

Electroacupuncture Alleviates Cerebral Ischemia/Reperfusion Injury in Rats by Histone H4 Lysine 16 Acetylation-Mediated Autophagy
Conclusions: EA treatment inhibited the H4K16ac process, facilitated autophagy, and alleviated I/R injury. These findings suggested that regulating histone H4 lysine 16 acetylation-mediated autophagy may be a key mechanism of EA at Du20 and Du26 to treat I/R.
Source: Frontiers in Psychiatry - December 18, 2020 Category: Psychiatry Source Type: research