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The work uses 6-hydroxydopamine–treated SH-SY5Y neuroblastoma cells to test antioxidant, anti-inflammatory, and neuroprotective effects. Molecular docking and dynamic simulations assess binding to dopamine-related receptors (AT1, AT2, D1A, D1B, D2). ELISA, gene expression by real-time PCR, and immunohistochemistry quantify biomarkers and α-synuclein-related changes, showing significant reductions in oxidative damage, α-synuclein aggregation, and neuroinflammation.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/cilazapril-and-benazepril-mitigate-neurodegeneration-and-synuclein-accumulation-in-a-cellular-model-of-parkinsons-disease/450438/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/cilazapril-and-benazepril-mitigate-neurodegeneration-and-synuclein-accumulation-in-a-cellular-model-of-parkinsons-disease/450438.png","ImageObject",300,407,{"name":92,"@type":93},"Kyle","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-05","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":19},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What Parkinson’s disease model and cell system were used to test cilazapril and benazepril?","Question",{"text":112,"@type":113},"The study used SH-SY5Y neuroblastoma cells in an in vitro Parkinson’s disease model induced by 6-hydroxydopamine (6-OHDA).","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How were the drugs’ molecular interactions with receptors evaluated?",{"text":117,"@type":113},"Molecular docking assessed binding affinity to dopamine-related receptors (AT1, AT2, D1A, D1B and D2), supported by dynamic simulations.",{"name":119,"@type":110,"acceptedAnswer":120},"Which outcomes indicated neuroprotection from oxidative damage and neuroinflammation?",{"text":121,"@type":113},"Treated cells showed reduced oxidative damage, decreased α-synuclein aggregation, and lower neuroinflammation, with biomarker evaluation via ELISA and related molecular assays.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},450438,1790815913,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":19,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":46,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":31},3985741905716,"https://ap-avatar.wpscdn.com/davatar_994ba38a5ba835b3df7d355c54d3ed8d","[www. nature.com/scientificreports](www. nature.com/scientificreports)  \nOPEN  \nCilazapril and benazepril mitigate neurodegeneration and α-synuclein accumulation in a cellular model of parkinson’s disease  \nOznurAltunlu1􀀍, Ahmet Hacimuftuoglu1􀀍, Irmak Ferah Okkay1􀀍, FatmaYesilyurt1, Mehmet Ali Yoruk2 & Mustafa Ozkaraca3  \nParkinson’s disease (PD) is characterised by progressive neuronal degeneration and oxidative stress, both of which significantly contribute to its pathology and clinical symptoms. This study investigated the antioxidant, anti-inflammatory and neuroprotective effects of cilazapril and benazepril in an in vitro PD model induced by 6-hydroxydopamine (6-OHDA) in SH-SY5Y neuroblastoma cells. We performed molecular docking of these compounds to dopamine-related receptors (AT1, AT2, D1A, D1B and D2), as well as dynamic simulations. Morphological analysis revealed structural preservation in treated cells, and key biomarkers (MTT, TAS-TOS, IL-10, IL-1β, TNF-α, LDH, MDA, SOD and TGF-β) were evaluated using ELISA. The gene expression ofthe D1 and D2 receptors was measured using realtime PCR, and the expression of α-synuclein and neuronal nitric oxide synthase was analysed using immunohistochemistry. Both drugs significantly reduced oxidative damage, α-synuclein aggregation and neuroinflammation (*p \u003C 0.05). They modulated genetic pathways involved in dopaminergic signalling and showed high binding affinity fortheAT1, AT2, D1A, D1B and D2 receptors. These findings suggest that cilazapril and benazepril exert multi-targeted protective effects that extend beyond simple antioxidant activity, and that they may be effective in treating or mitigating PD-related neurodegeneration.  \nKeywords Parkinson’s disease, Cilazapril, Benazepril, Oxidative stress, Neurodegeneration, Neuroinflammation  \nParkinson’s disease (PD) ranks as the second most widespread neurodegenerative disorder globally, after Alzheimer’s disease. Approximately 5–10% of PD cases are estimated to stem from genetic factors, which are typically correlated with advancing age. Although the prevalence of this condition is approximately 0.3% within the general population, this incidence increases to between 1% and 3% among individuals aged 65 years and older1. The motor manifestations of PD include tremors, bradykinesia, muscular rigidity, postural instability, and speech difficulties. The nonmotor manifestations include depression, dementia, and disturbances in sleep patterns2.  \nFrom a pathological perspective, cytoplasmic inclusions referred to as Lewy bodies and the degeneration of dopaminergic neurons within the substantia nigra pars compacta (SNc) are hallmark features of the disorder. Nonetheless, the misfolding and subsequent aggregation of the protein α-synuclein are instrumental inneurodegeneration in PD. Furthermore, pathophysiological mechanisms, including mitochondrial dysfunction, perturbations in protein homeostasis—most notably within the ubiquitin‒proteasome and autophagylysosomal systems—neuroinflammation, and oxidative stress contribute to cellular impairment and promote neurodegeneration3.  \nCurrenttherapeuticapproachesforPDfocusprimarilyonenhancingstriataldopaminergicneurotransmission4. The pharmacological agents employed in such treatment include levodopa (L-3,4-dihydroxyphenylalanine, L-DOPA), dopamine (DA) agonists, monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT)  \n1Department of Medical Pharmacology, Faculty of Medicine, Ataturk University, Erzurum 25100, Turkey.  \n2Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Ataturk University, Erzurum, Turkey. 3Department of Pathology, Faculty of Veterinary Medicine, Cumhuriyet University, Sivas, Turkey. 􀀍 email: [oznur.altunlu@atauni.edu.tr](oznur.altunlu@atauni.edu.tr); [hacimuftuoglu@gmail.com](hacimuftuoglu@gmail.com); [irmakferah@atauni.edu.tr](irmakferah@atauni.edu.tr)  \n[www. nature.com/scientificreports/](www. nature.com/scientificreports/)  \ninhibitors","cbCaiam0pTZ8gcCv","https://ap.wps.com/l/cbCaiam0pTZ8gcCv","pdf",3645273,"English","# Background\n## Parkinson’s disease characteristics and treatment limits\n## Pathological mechanisms and current therapeutic approaches\n# Experimental model and methods\n## SH-SY5Y cellular model and 6-OHDA induction\n## Molecular docking and dynamic simulations\n## Biochemical, molecular, and immunohistochemical evaluations\n# Results and implications\n## Effects on oxidative damage, α-synuclein aggregation, and neuroinflammation\n## Receptor targeting and pathway modulation","[{\"question\":\"What Parkinson’s disease model and cell system were used to test cilazapril and benazepril?\",\"answer\":\"The study used SH-SY5Y neuroblastoma cells in an in vitro Parkinson’s disease model induced by 6-hydroxydopamine (6-OHDA).\"},{\"question\":\"How were the drugs’ molecular interactions with receptors evaluated?\",\"answer\":\"Molecular docking assessed binding affinity to dopamine-related receptors (AT1, AT2, D1A, D1B and D2), supported by dynamic simulations.\"},{\"question\":\"Which outcomes indicated neuroprotection from oxidative damage and neuroinflammation?\",\"answer\":\"Treated cells showed reduced oxidative damage, decreased α-synuclein aggregation, and lower neuroinflammation, with biomarker evaluation via ELISA and related molecular assays.\"}]","Cilazapril and Benazepril Mitigate Neurodegeneration and α-Synuclein Accumulation in a Cellular Model of Parkinson’s Disease | PDF",1790733216]