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您的检索式：作者名="Kenneth Elkin"
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| 1 | Normobaric oxygen therapy attenuates hyperglycolysis in ischemic stroke显示文摘Normobaric oxygen therapy has gained attention as a simple and convenient means of achieving neuroprotection against the pathogenic cascade initiated by acute ischemic stroke.The mechanisms underlying the neuroprotective efficacy of normobaric oxygen therapy,however,have not been fully elucidated.It is hypothesized that cerebral hyperglycolysis is involved in the neuroprotection of normobaric oxygen therapy against ischemic stroke.In this study,Sprague-Dawley rats were subjected to either 2-hour middle cerebral artery occlusion followed by 3-or 24-hour reperfusion or to a permanent middle cerebral artery occlusion event.At 2 hours after the onset of ischemia,all rats received either 95%oxygen normobaric oxygen therapy for 3 hours or room air.Compared with room air,normobaric oxygen therapy significantly reduced the infarct volume,neurological deficits,and reactive oxygen species and increased the production of adenosine triphosphate in ischemic rats.These changes were associated with reduced transcriptional and translational levels of the hyperglycolytic enzymes glucose transporter 1 and 3,phosphofructokinase 1,and lactate dehydrogenase.In addition,normobaric oxygen therapy significantly reduced adenosine monophosphate-activated protein kinase mRNA expression and phosphorylated adenosine monophosphate-activated protein kinase protein expression.These findings suggest that normobaric oxygen therapy can reduce hyperglycolysis through modulating the adenosine monophosphate-activated protein kinase signaling pathway and alleviating oxidative injury,thereby exhibiting neuroprotective effects in ischemic stroke.This study was approved by the Institutional Animal Investigation Committee of Capital Medical University(approval No.AEEI-2018-033)on August 13,2018. | Zhe Cheng Feng-Wu Li Christopher R.Stone Kenneth Elkin Chang-Ya Peng Redina Bardhi Xiao-Kun Geng Yu-Chuan Ding | 2021 | Neural Regeneration Research2021，16，6： | 1 |
| 2 | Human Serum-derived Extracellular Vesicles Protect A549 from PM_(2.5)-induced Cell Apoptosis显示文摘Objective Epidemiological studies reveal that exposure to fine particulate matter(aerodynamic diameter≤2.5μm,PM_(2.5))increases the morbidity and mortality of respiratory diseases.Emerging evidence suggests that human circulating extracellular vesicles(EVs)may offer protective effects against injury caused by particulate matter.Currently,however,whether EVs attenuate PM_(2.5)-induced A549 cell apoptosis is unknown.Methods EVs were isolated from the serum of healthy subjects,quantified via nanoparticle tracking analysis,and qualified by the marker protein CD63.PM_(2.5)-exposed(50μg/mL)A549 cells were pretreated with 10μg/mL EVs for 24 h.Cell viability,cell apoptosis,and AKT activation were assessed via Cell Counting Kit-8,flow cytometry,and Western blot,respectively.A rescue experiment was also performed using MK2206,an AKT inhibitor.Results PM_(2.5)exposure caused a 100%in crease in cell apoptosis.EVs treatme nt reduced cell apoptosis by 10%,promoted cell survival,and inhibited the PM_(2.5)-induced upregulation of Bax/Bcl2 and cleaved caspase 3/caspase 3 in PM_(2.5)-exposed A549 cells.Moreover,EVs treatment reversed PM_(2.5)-induced reductions in p-AKT^(Thr308)and p-AKT^(Ser473).A KT inhibition attenuated the anti-apoptotic effect of EVs treatment on PM_(2.5)-exposed A549 cells.Conclusions EVs treatment promotes cell survival and attenuates PM_(2.5)-induced cell apoptosis via AKT phosphorylation.Human serum-derived EVs may be an efficacious novel therapeutic strategy in PM_(2.5)-induced lung injury. | ZHOU Qiu Lian BAI Yu Zheng GAO Juan DUAN Yi LYU Yi Cheng GUAN Long Fei ELKIN Kenneth XIE Yu Ling JIAO Zheng WANG Hong Yun | 2021 | Biomedical and Environmental Sciences2021，34，1： | 0 |
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