{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:40:21Z","timestamp":1787013621937,"version":"build-2736575974"},"reference-count":47,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:00:00Z","timestamp":1567987200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Hypoxia\u2010inducible factor\u20101 alpha (\n                    <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>\n                    \u20101\u03b1) and nuclear receptor related\u20101 (Nurr1) play pivotal roles in the development and survival of dopaminergic neurons, and deficiencies in these genes may be involved in Parkinson's disease (\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    ) pathogenesis. Recently, anthelminthic benzimidazoles were shown to promote\n                    <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>\n                    \u20101\u03b1 transcription in vitro and were proposed to activate Nurr1 via their benzimidazole group. Therefore, the aim of this study was to explore the neuroprotective effects of albendazole (\n                    <jats:styled-content style=\"fixed-case\">ABZ<\/jats:styled-content>\n                    ), an anthelminthic benzimidazole, in a rotenone model of Parkinson's disease (\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    ). Rotenone (1.5\u00a0mg\/kg) was subcutaneously injected into rats every other day for a period of 21\u00a0days, resulting in the development of the essential features of\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    . In addition to rotenone,\n                    <jats:styled-content style=\"fixed-case\">ABZ<\/jats:styled-content>\n                    (10\u00a0mg\/kg) was administered orally starting from the 11th day. Treatment of rats with\n                    <jats:styled-content style=\"fixed-case\">ABZ<\/jats:styled-content>\n                    markedly mitigated rotenone\u2010induced histological alterations in substantia nigra (\n                    <jats:styled-content style=\"fixed-case\">SN<\/jats:styled-content>\n                    ), restored striatal dopamine (\n                    <jats:styled-content style=\"fixed-case\">DA<\/jats:styled-content>\n                    ) level and motor functions and decreased the expression of \u03b1\u2010synuclein (a disease marker protein).\n                    <jats:styled-content style=\"fixed-case\">ABZ<\/jats:styled-content>\n                    also enhanced expression of Hypoxia\u2010inducible factor\u20101 alpha (\n                    <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>\n                    \u20101\u03b1) in the\n                    <jats:styled-content style=\"fixed-case\">SN<\/jats:styled-content>\n                    along with its downstream target, vascular endothelial growth factor, promoting neuronal survival. Similarly,\n                    <jats:styled-content style=\"fixed-case\">ABZ<\/jats:styled-content>\n                    augmented nuclear receptor related\u20101 (Nurr1) expression in the\n                    <jats:styled-content style=\"fixed-case\">SN<\/jats:styled-content>\n                    and increased transcriptional activation of Nurr1\u2010controlled genes, which are essential for regulation of\n                    <jats:styled-content style=\"fixed-case\">DA<\/jats:styled-content>\n                    synthesis; additionally, expression of neurotoxic proinflammatory cytokines that induce neuronal death was suppressed. In conclusion, the present study suggests that\n                    <jats:styled-content style=\"fixed-case\">ABZ<\/jats:styled-content>\n                    exerts a neuroprotective effect in a rotenone\u2010induced\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    model associated with\n                    <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>\n                    \u20101\u03b1 and Nurr1 activation and thus may be a viable candidate for treating\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    .\n                  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