Neuro-upalni odgovor i oksidacijski stres u štakorskom modelu Alzheimerove bolesti

master's thesis

• Title (english): Neuroinflammatory response and oxidative stress in a rat model of Alzheimer´s disease
• Author: Anamarija Mojzeš
• Mentor: Nada Oršolić (mentor)
• Committee member: Nada Oršolić (predsjednik povjerenstva)
• Committee member: Sunčica Bosak (član povjerenstva)
• Committee member: Davor Zanella (član povjerenstva)
• Committee member: Sofia Ana Blažević (član povjerenstva)
• Granter: University of Zagreb; Faculty of Science; (Department of Biology); Zagreb
• Defense date and country: 2018-02-15, Croatia
• Scientific / art field, discipline and subdiscipline: NATURAL SCIENCES; Biology

Abstract

Alzheimerova bolest je najčešći tip demencije od koje obolijeva sve više ljudi. Karakterizira ju vrlo složena etiologija, uključujući mutacije u nekim genima, oksidativni stres, poremećaj homeostaze kalcija, upala i poremećaj u hormonima i staničnom ciklusu. Do promjena u većini ovih parametara mogu dovesti tvari koje hranom, vodom ili lijekovima unosimo u organizam. U radu je istražen učinak aluminij klorida (AlCl3) i D- galaktoze (D- gal) na nastanak oksidativnog stresa u mozgu, te posljedično nastalu razinu upale i oštećenja. Poseban naglasak je bio na praćenju pokazatelja Alzheimerove bolesti. U pokusu smo koristili štakore soja Y59 kojima smo kroz 28 dana intraperitonealno injicirali AlCl3i D-gal. Dobiveni rezultati pokazuju da AlCl3i D-gal uzrokuju oksidativni stres u mozgu tako što povećavaju koncentraciju dušikova oksida, karboniliranih proteina i malondialdehida, te aktivnost superoksid dismutaze i katalaze. Povećane koncentracije proupalnih citokina i arginaze 1 u štakora izloženih AlCl3 i D- gal, ukazuju na prisutnost neuroupale koju karakterizira pojačana aktivnost mikroglija-stanica i to posebno M1, M2b i M2c oblika. Imunohistokemijska analiza mozga pokazala je povećanu prisutnost amiloidnih plakova u regijama mozga koje su bile jače izložene oksidativnom stresu i neuroupali.

Abstract (english)

More and more people are suffering from Alzheimer's Disease, the most common type of dementia. Alzheimer's disease development probably is triggered by a combination of many factors like mutations in some genes, oxidative stress, dysfunctional calcium homeostasis and with hormonal, inflammatory and cell cycle dysregulation. Changes in the most of these factors can be caused by substances that we get into our body through food, water and medicine. The main aim of this study was to investigate the effect of aluminum chloride (AlCl3) and D-galactose (D-gal) on the formation of oxidative stress in the brain and consequently the level of inflammation and brain damage. Particular emphasis was placed on tracking indicators of Alzheimer's disease. In the experiment we had been intraperitoneally injecting AlCl3 and D-gal into rats of the Y59 strain for 28 days. The results show that AlCl3 and D-gal causes an increased level of oxidative stress in brain. That is especially visible in the increased concentration of nitric oxide, carbonyl proteins and malondialdehyde. Also in the increased activity of catalase and superoxide dismutase. Increased concentration of proinflammatory cytokines and arginase 1 in rats exposed to AlCl3 and D-gal indicate on neuroinflammation. Neuroinflammation is characterised by bigger microglia-cell (M1, M2b and M2c) activity. Immunohistochemical brain analysis show bigger presence of amyloid plaques in the brain regions which had been more exposed to oxidative stress and neuroinflammation.

• Keywords: aluminij klorid; D- galaktoza; neuroupala; oksidativni stres; Alzheimerova bolest
• Keywords (english): aluminum chloride; D-galactose; neuroinflammation; oxidative stress; Alzheimer's disease
• Language: croatian
• URN:NBN: urn:nbn:hr:217:851648
• Study programme: Title: Experimental Biology; Study programme type: university; Study level: graduate; Academic / professional title: magistar/magistra eksperimentalne biologije (magistar/magistra eksperimentalne biologije)
• Type of resource: Text
• File origin: Born digital
• Access conditions: Open access; Embargo expiration date: 2020-02-15
• Created on: 2018-03-14 12:29:02