Neda Nikokalam Nazif; Maryam Khosravi; Ramesh Ahmadi; Maryam Bananej; Ahmad Majd
Volume 21, Issue 12 , 2019, Pages 1-7
Abstract
Background: Parkinson’s disease is a progressive nervous system disorder caused by a degenerative loss of dopaminergic neurons of midbrain, from the substantia nigra to the corpus striatum pathway. Quercetin has a neuroprotective effect to prevent the greater loss of substantia nigra dopaminergic ...
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Background: Parkinson’s disease is a progressive nervous system disorder caused by a degenerative loss of dopaminergic neurons of midbrain, from the substantia nigra to the corpus striatum pathway. Quercetin has a neuroprotective effect to prevent the greater loss of substantia nigra dopaminergic neurons in Parkinson’s disease model.Objectives: This study aimed to investigate the effect of the flavonoid quercetin on the behavioral test in 1-methyl-4-phenyl,2,3,6- tetrahydropyridine(MPTP)-induced male NMRI mice.Methods: Animals were divided into eight groups (n = 12). Behavioral tests of bar test and treatment with quercetin began one day after inducing the disease and lasted for 35 days. Then, brains were excluded from craniums for histology, immunohistochemistry tyrosine hydroxylase, measurement of TNF-α levels, and gene expression of caspase 3.Results: Data showed that orally taking quercetin for 35 days improved the behavioral test of bar tests in Parkinson’s disease. Cell density in TH staining was counted and showed considerable decreases in the substantia nigra in Parkinson’s disease group (83.67 ± 12.811) while it was higher in quercetin-treated groups PD + Q1 (103.67 ± 8.090) and PD + Q2 (145.33 ± 13.908) than in Parkinson’s disease group (P < 0.05). Quercetin decreased inflammation due to MPTP in the substantia nigra in PD + Q1 (1395.73 ± 1.058) and PD + Q2 (1250.66 ± 1.95), and corpus striatum in PD + Q1 (1207.033 ± 2.228) and PD + Q2 (1187.44 ± 1.64) and TNF-α protein levels in the quercetin-treated group (P < 0.05). Parkinson’s disease decreased gene expression of caspase 3 (0.35 ± 0.019) and increased it in quercetin-treated groups PD + Q1 (1.26 ± 0.062) and PD+Q2 (2.27 ± 0.144) (P < 0.0001).Conclusions: Quercetin is a natural flavonoid with neuroprotection effect and antioxidant, anti-inflammatory, and anti-apoptosis properties preventing the loss of dopaminergic neurons in mice with Parkinson’s disease.
Atossa Jozaei; Monireh Movahedi; Maryam Khosravi; Fereshteh Golab
Volume 21, Issue 12 , 2019, Pages 1-8
Abstract
Background: Apoptosis is a programmed cell death that occurs due to various factors such as reperfusion ischemia. As a purinergic receptor, A1AR acts as an oxidative stress sensor and an antioxidant during reperfusion ischemia.Objectives: The purpose of the present study was to investigate the effect ...
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Background: Apoptosis is a programmed cell death that occurs due to various factors such as reperfusion ischemia. As a purinergic receptor, A1AR acts as an oxidative stress sensor and an antioxidant during reperfusion ischemia.Objectives: The purpose of the present study was to investigate the effect of adenosine injection following cerebral reperfusion ischemia on A1AR gene expression and apoptosis in the brain hippocampal tissue of male Wistar rats.Methods: This experimental study was conducted at Shahid Mirghani Research Institute in Gorgan, Iran, from January 21, 2019, to March 18, 2019. The sample size was determined according to previous studies and a pilot study. Thus, 30 male Wistar rats were divided into three groups by simple random sampling (using a random-number table): Control group (n = 10), Reperfusion ischemia group (n = 10), and Reperfusion ischemia + adenosine group (n = 10). Ischemia was induced in animals by closing the carotid artery for 45 min. Adenosine was injected 24 h after ischemia. We measured A1AR gene expression, SOD protein expression, and apoptosis by real-time PCR, immunohistochemistry, and the TUNEL method, respectively.Results: The results showed that cerebral reperfusion ischemia significantly increased A1AR gene expression (596%) and apoptosis (378%) and decreased SOD protein expression (72%) compared to the control group (P < 0.001). On the other hand, adenosine sig- nificantly reduced A1AR gene expression (46%) and apoptosis (69%) and increased SOD protein expression (94%) compared to the ischemic group (P < 0.001).Conclusions: Ischemic brain reperfusion causes oxidative stress. Also, adenosine injection seems to be effective in reducing oxida- tive stress and apoptosis induced by cerebral reperfusion ischemia.
