کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5735017 | 1612899 | 2018 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nrf2 inhibits NLRP3 inflammasome activation through regulating Trx1/TXNIP complex in cerebral ischemia reperfusion injury
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کلمات کلیدی
TBHQQuantitative reverse transcriptase-PCRNrf2tert-butylhydroquinoneqRT-PCRTTCTXNIPMCAONLRP3MCAO/RDMSO - DMSOI/R - I / RTrx1 - TRX1inflammation - التهاب( توروم) middle cerebral artery occlusion/reperfusion - انسداد / عود مجدد شریان مغزی میانیmiddle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیIschemia reperfusion - ایسکمی reperfusionTriphenyltetrazolium chloride - ترفتhenyltetrazolium chlorideantioxidant response element - عنصر پاسخ آنتی اکسیدانnuclear factor erythroid 2-related factor 2 - فاکتور هسته ای عامل erythroid 2 مرتبط 2ARE - هستندThioredoxin interacting protein - پروتئین متصل به تیورودکسینnod-like receptor protein 3 - پروتئین گیرنده مانند گربه 3
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The nod-like receptor protein 3 (NLRP3) inflammasome has a critical role in inflammation damage in ischemic injury, and the activation of the inflammasome is closely related to the interaction with thioredoxin interacting protein (TXNIP), which dissociates from the thioredoxin1 (Trx1)/TXNIP complex under oxidative stress. However, the negative regulator of NLRP3 inflammasome activation has not been fully investigated. Nuclear factor erythroid 2-related factor 2 (Nrf2) takes on a critical part in the antioxidant stress system, that controls the driven genes of antioxidant response element (ARE). Activate Nrf2 could inhibit the activation of NLRP3 inflammasome in acute liver injury and severe lupus nephritis. We aimed to explore the protective effect of Nrf2 in inhibiting the NLPR3 inflammasome formulation through the Trx1/TXNIP complex in cerebral ischemia reperfusion (cerebral I/R) injury. Middle cerebral artery occlusion/reperfusion (MCAO/R) model was used to imitate ischemic insult. Nrf2 was activated by tert-butylhydroquinone (tBHQ) intraperitoneally (i.p.) injection (16.7 mg/kg), Nrf2,Trx1 and NLRP3 siRNAs were infused into the left paracele (12 μl per rat), protein and mRNA levels were assessed by Western blot, qRT-PCR. ELISA was used for IL-1β and IL-18 activity measurements. After upregulating Nrf2, the expression of TXNIP in cytoplasm, NLRP3 inflammasome, and downstream factors caspase-1, IL-18, and IL-1β were significantly reduced, and Nrf2 knockdown yielded the opposite results. Trx1 knockdown produced the same effect of Nrf2 inhibition and the protective effect of Nrf2 was mostly abolished. Our results suggested that Nrf2 acted as a protective regulator against NLRP3 inflammasome activation by regulating the Trx1/TXNIP complex, which could possibly represent an innovative insight into the treatment of ischemia and reperfusion injury.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Behavioural Brain Research - Volume 336, 15 January 2018, Pages 32-39
Journal: Behavioural Brain Research - Volume 336, 15 January 2018, Pages 32-39
نویسندگان
Yanghao Hou, Yueting Wang, Qi He, Lingyu Li, Hui Xie, Yong Zhao, Jing Zhao,