{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T11:31:14Z","timestamp":1789471874914,"version":"build-2803163510"},"reference-count":30,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,6,24]],"date-time":"2019-06-24T00:00:00Z","timestamp":1561334400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Scientific and Technological Project of Shiyan City of Hubei Province","award":["18Y10"],"award-info":[{"award-number":["18Y10"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Parkinson's disease (PD) is neurodegenerative dyskinesia characterized by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Although neuroinflammation is one of the pathological features of PD, its mechanism of promoting PD is still not fully understood. Recently, the microRNA (miR) is considered to play a critical regulatory role in inflammatory responses. In this study, we examined the anti\u2010inflammatory activity, antineuronal injury, and the underlying target of miR\u2010190 with MPTP\u2010induced PD mouse model and BV2 cells. The results showed that miR\u2010190 is downregulated in lipopolysaccharide (LPS)\u2010induced BV2 cells; however, when the miR\u2010190 overexpressed, the expression of proinflammatory mediators, such as iNOS, IL\u20106, TNF\u2010\u03b1, and TGF\u2010\u03b21, were inhibited and the anti\u2010inflammatory mediator such IL\u201010 was increased. In addition, we predicted the potential target of miR\u2010190 to be Nlrp3 and verified by luciferase reporter assay. The results also showed that Nlrp3 was upregulated in LPS\u2010induced BV2 cells, whereas knockdown of Nlrp3 inhibited the LPS\u2010induced inflammatory response in BV2 cells. Furthermore, upregulation of miR\u2010190 or knockdown of Nlrp3 inhibited LPS\u2010induced apoptosis in BV2 cells. However, the apoptosis inhibition effect of miR\u2010190 was abrogated by overexpression of Nlrp3. Finally, upregulation of miR\u2010190 inhibited the activation of microglial cells and inflammation and attenuated the tyrosine hydroxylase loss in SNpc in MPTP\u2010induced PD mice. In conclusion, we demonstrated that miR\u2010190 alleviates neuronal damage and inhibits inflammation via negatively regulating the expression and activation of Nlrp3 in MPTP\u2010induced PD mouse model.<\/jats:p>","DOI":"10.1002\/jcp.28907","type":"journal-article","created":{"date-parts":[[2019,6,24]],"date-time":"2019-06-24T10:46:59Z","timestamp":1561373219000},"page":"23379-23387","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":75,"title":["MicroRNA\u2010190 alleviates neuronal damage and inhibits neuroinflammation via Nlrp3 in MPTP\u2010induced Parkinson's disease mouse model"],"prefix":"10.1002","volume":"234","author":[{"given":"Qiang","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Neurology Taihe Hospital, Hubei University of Medicine Shiyan P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Songlin","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Neurology Taihe Hospital, Hubei University of Medicine Shiyan P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5342-5377","authenticated-orcid":false,"given":"Jun","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Neurology Taihe Hospital, Hubei University of Medicine Shiyan P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongxia","family":"Cai","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, Taihe Hospital Hubei University of Medicine Shiyan P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Neurology Taihe Hospital, Hubei University of Medicine Shiyan P.R. 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