کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8960736 | 1646430 | 2018 | 52 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
l-Cysteine suppresses hypoxia-ischemia injury in neonatal mice by reducing glial activation, promoting autophagic flux and mediating synaptic modification via H2S formation
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کلمات کلیدی
RT-PCRPSD-95STAT3RIPAPFAPMSFHBSSCBSDAPITTCAOAALC3-IImTORGFAPCD86H2S3-MSTcluster of differentiation 86MDAphenylmethane-sulfonyl fluoride3-mercaptopyruvate sulfurtransferase - 3-merkaptopyruvate sulfurransferase4,6-diamidino-2-phenylindole - 4،6-دیامیدین-2-فنیلینولd-amino acid oxidase - D-آمینو اسید اکسیدازHanks balanced salt solution - Hanks محلول نمک را تعویض می کندIba-1 - IBA-1ROS - ROSAutophagy - اتوفاژیaminooxyacetic acid - اسید aminooxyaceticinterleukin - اینترلوکینtumor necrosis factor-α - تومور نکروز عامل αDAO - دائوCNS - دستگاه عصبی مرکزیpostnatal day - روز پس از زایمانradioimmunoprecipitation assay - سنجش radioimmunoprecipitationHydrogen sulfide - سولفید هیدروژنCystathionine β synthase - سیستاتینین بتا سنتازcentral nervous system - سیستم عصبی مرکزیSynaptophysin - سیناپتوفیزینSyn - سینتTNF-α - فاکتور نکروز توموری آلفاGlial activation - فعال سازی گلیالmalondialdehyde - مالون دی آلدهیدsignal transducer and activator of transcription 3 - مبدل سیگنال و فعال کننده رونویسی 3ionized calcium binding adaptor molecule-1 - مولکول-1 متصل کننده کلسیم یونیزه شدهBehavioral deficits - نقص رفتاریNORT - نورتmammalian target of rapamycin - هدف پستانداران رپامایسینSynapse - همایه یا سیناپسhypoxic-ischemic - هیپوکسیک-ایسکمیکreverse transcription–polymerase chain reaction - واکنش زنجیره ای رونویسی-پلیمراز معکوسNovel Object Recognition task - وظیفه شناسایی شیء رمانparaformaldehyde - پارافرمالدهیدGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالpostsynaptic density protein 95 - پروتئین چگالی Postynaptic 95Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We previously reported that l-Cysteine, an H2S donor, significantly alleviated brain injury after hypoxia-ischemic (HI) injury in neonatal mice. However, the mechanisms underlying this neuroprotective effect of l-Cysteine against HI insult remain unknown. In the present study, we tested the hypothesis that the protective effects of l-Cysteine are associated with glial responses and autophagy, and l-Cysteine attenuates synaptic injury as well as behavioral deficits resulting from HI. Consistent with our previous findings, we found that treatment with l-Cysteine after HI reduced early brain injury, improved behavioral deficits and synaptic damage, effects which were associated with an up-regulation of synaptophysin and postsynaptic density protein 95 expression in the lesioned cortex. l-Cysteine attenuated the accumulation of CD11b+/CD45high cells, activation of microglia and astrocytes and diminished HI-induced increases in reactive oxygen species and malondialdehyde within the lesioned cortex. In addition, l-Cysteine increased microtubule associated protein 1 light chain 3-II and Beclin1 expression, decreased p62 expression and phosphor-mammalian target of rapamycin and phosphor-signal transducer and activator of transcription 3. Further support for a critical role of l-Cysteine was revealed from results demonstrating that treatment with an inhibitor of the H2S-producing enzyme, amino-oxyacetic acid, reversed the beneficial effects of l-Cysteine described above. These results demonstrate that l-Cysteine effectively alleviates HI injury and improves behavioral outcomes by inhibiting reactive glial responses and synaptic damage and an accompanying triggering of autophagic flux. Accordingly, l-Cysteine may provide a new a therapeutic approach for the treatment of HI via the formation of H2S.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain, Behavior, and Immunity - Volume 73, October 2018, Pages 222-234
Journal: Brain, Behavior, and Immunity - Volume 73, October 2018, Pages 222-234
نویسندگان
Danqing Xin, Xili Chu, Xuemei Bai, Weiwei Ma, Hongtao Yuan, Jie Qiu, Changxing Liu, Tong Li, Xin Zhou, Wenqiang Chen, Dexiang Liu, Zhen Wang,