{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T20:14:50Z","timestamp":1783455290520,"version":"3.55.0"},"reference-count":27,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2020,5,31]],"date-time":"2020-05-31T00:00:00Z","timestamp":1590883200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Parkinson's disease (PD) is a neurodegenerative disease which results in damage in neuronal cells. Insulin\u2010like growth factor (IGF)\u20101 was previously reported to play a role of neuroprotection in some diseases. Nitric oxide (NO) can also regulate neuronal cells. However, the mechanisms underlying IGF\u20101 and NO in PD still need to be elucidated. In present study, we explored the interaction between IGF\u20101 and inducible Nitric\u2010Oxide Synthase (iNOS) in PD progression. We firstly constructed PD models by methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP) or MPP<jats:sup>+<\/jats:sup> treatment. Then RT\u2010qPCR revealed that IGF\u20101 expression was downregulated while iNOS expression was upregulated in MPTP model. Moreover, IGF\u20101 elevation or iNOS depletion enhanced cell viability and blocked cell apoptosis. Rescue assay disclosed iNOS overexpression reversed the effect on viability and apoptosis mediated by IGF\u20101 upregulation. Furthermore, IGF\u20101 was identified to positively regulate miR\u2010302b\u20105p which could target iNOS. MiR\u2010302b\u20105p could abolish the inhibitory function IGF\u20101 exerted on cell apoptosis and iNOS could counteract miR\u2010302b\u20105p upregulation\u2010triggered inhibition on cell apoptosis as well. Besides, we observed the deficiency of miR\u2010302b\u20105p improved the lesioned neurobehavior of MPTP\u2010treated mice. To sum up, present study proved that miR\u2010302b\u20105p enhanced the neuroprotective effect of IGF\u20101 in MPTP\u2010induced PD by regulating iNOS, recommending a novel therapeutic target for PD treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance of the study<\/jats:title><jats:p>In this study, we mainly explored that IGF\u20101 was decreased while iNOS was boosted in MPTP\u2010induced PD mice model; IGF\u20101 suppressed while iNOS promoted MPP<jats:sup>+<\/jats:sup>\u2010induced toxicity and apoptosis in SH\u2010SY5Y cells; miR\u2010302b\u20105p ehanhced the neuroprotective effect of IGF\u20101 via targeting Inos; deficiency of miR\u2010302b\u20105p improved the lesioned neurobehavior of MPTP\u2010treated mice.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbf.3534","type":"journal-article","created":{"date-parts":[[2020,5,31]],"date-time":"2020-05-31T19:48:34Z","timestamp":1590954514000},"page":"1025-1035","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["<scp>MiR<\/scp>\u2010302b\u20105p enhances the neuroprotective effect of <scp>IGF<\/scp>\u20101 in methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine\u2010induced Parkinson's disease by regulating inducible nitric\u2010oxide synthase"],"prefix":"10.1002","volume":"38","author":[{"given":"Xiaorui","family":"Cui","sequence":"first","affiliation":[{"name":"Department of Neurology Affiliated Hospital of Xiangnan University  Chenzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6929-1454","authenticated-orcid":false,"given":"Mingpeng","family":"Li","sequence":"additional","affiliation":[{"name":"Department of 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