{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T15:51:42Z","timestamp":1792165902548,"version":"4.4.0"},"reference-count":26,"publisher":"Wiley","license":[{"start":{"date-parts":[[2023,2,25]],"date-time":"2023-02-25T00:00:00Z","timestamp":1677283200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Changsha Science & Technology Bureau","award":["kq2004154"],"award-info":[{"award-number":["kq2004154"]}]},{"name":"Changsha Science & Technology Bureau","award":["2020JJ8017"],"award-info":[{"award-number":["2020JJ8017"]}]},{"DOI":"10.13039\/501100004735","name":"Natural Science Foundation of Hunan Province","doi-asserted-by":"publisher","award":["kq2004154"],"award-info":[{"award-number":["kq2004154"]}],"id":[{"id":"10.13039\/501100004735","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004735","name":"Natural Science Foundation of Hunan Province","doi-asserted-by":"publisher","award":["2020JJ8017"],"award-info":[{"award-number":["2020JJ8017"]}],"id":[{"id":"10.13039\/501100004735","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2023,2,25]]},"abstract":"<jats:p>Ischemic stroke is a kind of central nervous disease characterized by high morbidity, high mortality, and high disability. Inflammation and autophagy play important roles in cerebral ischemia\/reperfusion (CI\/R) injury. The present study characterizes the effects of TLR4 activation on inflammation and autophagy in CI\/R injury. An in vivo CI\/R rat injury model and an in vitro hypoxia\/reoxygenation (H\/R) SH-SY5Y cell model were established. Brain infarction size, neurological function, cell apoptosis, inflammatory mediators\u2019 levels, and gene expression were measured. Infarction, neurological dysfunction, and neural cell apoptosis were induced in CI\/R rats or in H\/R-induced cells. The expression levels of NLRP3, TLR4, LC3, TNF-\u03b1, interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-18 (IL-18) clearly increased in I\/R rats or in H\/R-induced cells, while TLR4 knockdown significantly suppressed NLRP3, TLR4, LC3, TNF-\u03b1, and interleukin-1\/6\/18 (IL-1\/6\/18) in H\/R-induced cells, as well as cell apoptosis. These data indicate that TLR4 upregulation induced CI\/R injury via stimulating NLRP3 inflammasome and autophagy. Therefore, TLR4, is a potential therapeutic target to improve management of ischemic stroke.<\/jats:p>","DOI":"10.1155\/2023\/9335166","type":"journal-article","created":{"date-parts":[[2023,2,25]],"date-time":"2023-02-25T16:05:08Z","timestamp":1677341108000},"page":"1-9","source":"Crossref","is-referenced-by-count":31,"title":["TLR4 Enhances Cerebral Ischemia\/Reperfusion Injury via Regulating NLRP3 Inflammasome and Autophagy"],"prefix":"10.1155","volume":"2023","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3930-5541","authenticated-orcid":true,"given":"Li","family":"Mao","sequence":"first","affiliation":[{"name":"Department of Basic Medicine, Changsha Health Vocational College, Changsha, 410600 Hunan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Da-Hua","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Neurology, Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, Changsha, 410006 Hunan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo-Huang","family":"Hu","sequence":"additional","affiliation":[{"name":"The Affiliated Changsha Hospital of Hunan Normal University, Changsha, 410006 Hunan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6865-5386","authenticated-orcid":true,"given":"Jian-Hu","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Neurology, Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, Changsha, 410006 Hunan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.4103\/1673-5374.247465"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.1007\/s10072-017-2938-1"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1177\/1756286418794184"},{"key":"4","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopha.2020.109860"},{"key":"5","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbi.2020.12.009"},{"key":"6","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2020.591803"},{"key":"7","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2021.657478"},{"key":"8","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20133328"},{"issue":"9","key":"9","doi-asserted-by":"crossref","first-page":"1677","DOI":"10.1038\/jcbfm.2012.88","article-title":"Inflammatory cytokines in experimental and human stroke","volume":"32","author":"K. 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