FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4282935429> ?p ?o ?g. }

• W4282935429 abstract "Abstract Background Neuronal pyroptosis and neuroinflammation with excess microglial activation are widely involved in the early pathological process of ischemic stroke. Repetitive transcranial magnetic stimulation (rTMS), as a non-invasive neuromodulatory technique, has recently been reported to be anti-inflammatory and regulate microglial function. However, few studies have elucidated the role and mechanism of rTMS underlying regulating neuronal pyroptosis and microglial polarization. Methods We evaluated the motor function in middle cerebral artery occlusion/reperfusion (MCAO/r) injury mice after 1-week intermittent theta-burst rTMS (iTBS) treatment in the early phase with or without depletion of microglia by colony-stimulating factor 1 receptor (CSF1R) inhibitor treatment, respectively. We further explored the morphological and molecular biological alterations associated with neuronal pyroptosis and microglial polarization via Nissl, EdU, TTC, TUNEL staining, electron microscopy, multiplex cytokine bioassays, western blot assays, immunofluorescence staining and RNA sequencing. Results ITBS significantly protected against cerebral ischemia/reperfusion (I/R) injury-induced locomotor deficits and neuronal damage, which probably relied on the regulation of innate immune and inflammatory responses, as evidenced by RNA sequencing analysis. The peak of pyroptosis was confirmed to be later than that of apoptosis during the early phase of stroke, and pyroptosis was mainly located and more severe in the peri-infarcted area compared with apoptosis. Multiplex cytokine bioassays showed that iTBS significantly ameliorated the high levels of IL-1β, IL-17A, TNF-α, IFN-γ in MCAO/r group and elevated the level of IL-10. ITBS inhibited the expression of neuronal pyroptosis-associated proteins (i.e., Caspase1, IL-1β, IL-18, ASC, GSDMD, NLRP1) in the peri-infarcted area rather than at the border of infarcted core. KEGG enrichment analysis and further studies demonstrated that iTBS significantly shifted the microglial M1/M2 phenotype balance by curbing proinflammatory M1 activation (Iba1 + /CD86 + ) and enhancing the anti-inflammatory M2 activation (Iba1 + /CD206 + ) in peri-infarcted area via inhibiting TLR4/NFκB/NLRP3 signaling pathway. Depletion of microglia using CSF1R inhibitor (PLX3397) eliminated the motor functional improvements after iTBS treatment. Conclusions rTMS could alleviate cerebral I/R injury induced locomotor deficits and neuronal pyroptosis by modulating the microglial polarization. It is expected that these data will provide novel insights into the mechanisms of rTMS protecting against cerebral I/R injury and potential targets underlying neuronal pyroptosis in the early phase of stroke." @default.
• W4282935429 created "2022-06-16" @default.
• W4282935429 creator A5013267722 @default.
• W4282935429 creator A5029237111 @default.
• W4282935429 creator A5031813114 @default.
• W4282935429 creator A5039740996 @default.
• W4282935429 creator A5042232968 @default.
• W4282935429 creator A5052413239 @default.
• W4282935429 creator A5055055894 @default.
• W4282935429 creator A5063481044 @default.
• W4282935429 creator A5064406915 @default.
• W4282935429 creator A5074273728 @default.
• W4282935429 creator A5079060559 @default.
• W4282935429 creator A5083896582 @default.
• W4282935429 date "2022-06-11" @default.
• W4282935429 modified "2023-10-16" @default.
• W4282935429 title "Intermittent theta-burst stimulation improves motor function by inhibiting neuronal pyroptosis and regulating microglial polarization via TLR4/NFκB/NLRP3 signaling pathway in cerebral ischemic mice" @default.
• W4282935429 cites W1541679432 @default.
• W4282935429 cites W1586581625 @default.
• W4282935429 cites W1768846296 @default.
• W4282935429 cites W1966634013 @default.
• W4282935429 cites W1966928838 @default.
• W4282935429 cites W1979561481 @default.
• W4282935429 cites W1992745167 @default.
• W4282935429 cites W2003605139 @default.
• W4282935429 cites W2037772830 @default.
• W4282935429 cites W2046848104 @default.
• W4282935429 cites W2049201207 @default.
• W4282935429 cites W2102278945 @default.
• W4282935429 cites W2103327450 @default.
• W4282935429 cites W2123060905 @default.
• W4282935429 cites W2124287371 @default.
• W4282935429 cites W2131271579 @default.
• W4282935429 cites W2134526812 @default.
• W4282935429 cites W2134729461 @default.
• W4282935429 cites W2138773756 @default.
• W4282935429 cites W2141458291 @default.
• W4282935429 cites W2169083957 @default.
• W4282935429 cites W2191679689 @default.
• W4282935429 cites W2220638769 @default.
• W4282935429 cites W2280175773 @default.
• W4282935429 cites W2331173984 @default.
• W4282935429 cites W236978204 @default.
• W4282935429 cites W2424408772 @default.
• W4282935429 cites W2443048158 @default.
• W4282935429 cites W2486445835 @default.
• W4282935429 cites W2560541542 @default.
• W4282935429 cites W2590458460 @default.
• W4282935429 cites W2618544227 @default.
• W4282935429 cites W2759752365 @default.
• W4282935429 cites W2763683189 @default.
• W4282935429 cites W2769599719 @default.
• W4282935429 cites W2789018622 @default.
• W4282935429 cites W2888957013 @default.
• W4282935429 cites W2898326983 @default.
• W4282935429 cites W2902742106 @default.
• W4282935429 cites W2905172994 @default.
• W4282935429 cites W2939367805 @default.
• W4282935429 cites W2944065915 @default.
• W4282935429 cites W2947791363 @default.
• W4282935429 cites W2955686537 @default.
• W4282935429 cites W2963134140 @default.
• W4282935429 cites W2972382635 @default.
• W4282935429 cites W2997901555 @default.
• W4282935429 cites W3000146621 @default.
• W4282935429 cites W3003770712 @default.
• W4282935429 cites W3004609274 @default.
• W4282935429 cites W3021384307 @default.
• W4282935429 cites W3025982218 @default.
• W4282935429 cites W3026606390 @default.
• W4282935429 cites W3048341541 @default.
• W4282935429 cites W3083125992 @default.
• W4282935429 cites W3083450776 @default.
• W4282935429 cites W3085239696 @default.
• W4282935429 cites W3092842545 @default.
• W4282935429 cites W3120573399 @default.
• W4282935429 cites W3150928114 @default.
• W4282935429 cites W3189698361 @default.
• W4282935429 cites W3217169429 @default.
• W4282935429 cites W4200262064 @default.
• W4282935429 doi "https://doi.org/10.1186/s12974-022-02501-2" @default.
• W4282935429 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35690810" @default.
• W4282935429 hasPublicationYear "2022" @default.
• W4282935429 type Work @default.
• W4282935429 citedByCount "36" @default.
• W4282935429 countsByYear W42829354292022 @default.
• W4282935429 countsByYear W42829354292023 @default.
• W4282935429 crossrefType "journal-article" @default.
• W4282935429 hasAuthorship W4282935429A5013267722 @default.
• W4282935429 hasAuthorship W4282935429A5029237111 @default.
• W4282935429 hasAuthorship W4282935429A5031813114 @default.
• W4282935429 hasAuthorship W4282935429A5039740996 @default.
• W4282935429 hasAuthorship W4282935429A5042232968 @default.
• W4282935429 hasAuthorship W4282935429A5052413239 @default.
• W4282935429 hasAuthorship W4282935429A5055055894 @default.
• W4282935429 hasAuthorship W4282935429A5063481044 @default.
• W4282935429 hasAuthorship W4282935429A5064406915 @default.
• W4282935429 hasAuthorship W4282935429A5074273728 @default.
• W4282935429 hasAuthorship W4282935429A5079060559 @default.
• W4282935429 hasAuthorship W4282935429A5083896582 @default.

• next