ABSTRACT
Objective To explore the neuroprotective effects of edaravone in 1-methyl-4-phenyl-1, 2, 3, 6- tetrahydropyridine (MPTP)-C57BL/6J-Parkinson?s disease (PD) model mice and the related mechanisms. Methods Totally 90 male C57BL/6J mice were evenly randomized into edaravone (ED) group, PD model group and normal saline (NS) group. Subcutaneous injection of MPTP was used to make PD model, and ED group was then administered with ED (3 mg/kg). Rotarod number was detected by rotarod test. Tyrosine hydroxylase-immunoreactive (TH-ir) neurons expression in the substantia nigra (SN) of mice was observed by immunohistochemistry staining. Brain-derived neurotrophic factor (BDNF) mRNA and protein expression in the SN of mice were tested by RT-PCR and Western blotting analysis, respectively. Results Compared with NS group, rotarod numbers in ED and PD groups were significantly less (P(0. 05, P(0. 01), the number of TH-ir neurons in SN was significantly reduced (P(0. 05, P(0. 01), and BDNF mRNA (all P(0. 01) and protein (all P(0. 05) expression was significantly decreased. Compared with PD mice, rotarod number in ED mice was significantly more (P(0. 05), the number of TH-ir neurons in the SN was significantly increased (P(0. 05), and BDNF mRNA (P(0. 01) and protein (P(0. 05) expression was significantly enhanced. Conclusion ED can increase the expression of BDNF mRNA and protein in the SN of C57BL/6J-PD model mice, alleviate MPTP damage, and has a protection effect on dopaminergic neurons.
ABSTRACT
Objective To observe the effects of voluntary exercise on the learning ability, memory and hippocampus growth-associated protein 43 (GAP43) expression in senescence-accelerated prone mouse (SAMP8), so as to explore the possible mechanism of exercises on improving the cognitive ability and delaying aging. Methods A total of 60 three-month old female SAMP8 mice were evenly assigned to running cage environment (RCE) group and standard environment (SE) group at random. After three months, Morris water maze test was used to test the platform-seeking latency and search strategy. Then 10 mice were sacrificed in each group for RT-PCR analysis of hippocampus GAP43 mRNA expression, 10 for Western blotting analysis of hippocampus GAP43 protein expression, and 10 for immunohistochemistry staining of hippocampus GAP43 expression. Results Morris water maze test showed that RCE mice had a significant shorter platform-seeking latency than SE mice(P<0. 01, P<0. 05), and RCE mice had a significant longer time in the first quadrant (P<0. 01) and a shorter time in the fourth quadrant (P<0. 05) compared with SE mice. RCE mice had a significantly higher GAP43 expression in the hippocampus compared with SE mice (P<0. 01). Conclusion Voluntary exercise can improve the learning ability and memory of SAMPS, which might be associated with the increase of GAP43 in the hippocampus.
ABSTRACT
Objective: To observe the effects of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) on the spatial learning ability/memory and dopaminergic neurons in the Nigra of senescence accelerated-prone 8 (SAMP8) mice. Methods: Three-month old male SAMP8 mice were injected with MPTP (36 mg/ kg,s. c.) for 5 days,and animals in the control group were injected with NS (36 ml/kg, s. c.) in the same manner. Morris water maze was used to examine the searching strategy, seeking-platform latency,and the swimming time in the aimed quadrant. Immunohistochemistry was used to observe the changes of TH-ir positive neurons in substantia nigra. Results: The number of TH-ir neurons in substantia nigra pars compacta was significantly reduced in MPTP group compared with the control group(P<0.01). Morris water maze showed that the searching strategy of animals in MPTP group was worse than in the control group, with the seeking-platform latency of MPTP mice significantly prolonged (P<0.01), the time spent in the aimed quadrant significantly decreased (P<0.01) and time in the opposite quadrant significantly prolonged (P<0.05). Conclusion: MPTP can cause damage to the dopaminergic neurons in the substantia nigra of SAMP8 mice,which is subsequently followed by deficit in the spatial learning and memory in the animals.
ABSTRACT
Objective To observe the effects of enriched environmen(EE) on brain-derived neurotrophic factor (BDNF) in substantia nigra (SN) of senescence-accelerated prone mice, so as to explore the possible mechanism of EE in alleviating MPTP-induced damage and in protecting dopaminergic neurons in the SN. Methods Totally 80 3-month old female SAMP8 mice were averagely assigned to EE and standard environment (SE) groups at random. After three months, the mice in each group were further divided into 2 subgroups at random, MPTP group and NS group (n = 20). The MPTP groups received subcutaneous injection of MPTP, and the NS mice were treated with an equal volume of NS. At the seventh day, the mice were sacrificed for RT-PCR and immunohistochemistry staining. RT-PCR was used to examine BDNF mRNA expression and immunohistochemistry staining was used to examine BDNF-ir expression. Results Compared with SE+NS mice, EE+NS mice had significantly increased BDNF mRNA expression(P<0.01), and the number of BDNF-ir cell and COD values in SN were also significantly increased (P<0.01). Compared with SE+NS mice, SE+MPTP mice showed significantly decreased BDNF mRNA expression (P<0.001) , and the number of BDNF-ir cells and the COD values in SN of mice were significantly decreased (P<0.01). Compared with SE+MPTP mice, EE+MPTP mice showed increased BDNF mRNA expression (P<0.01), and the number of BDNF-ir cells and the COD values in SN were significantly increased (P<0.01). Conclusion EE can increase BDNF mRNA expression and BDNF-ir cell number in SN of SAMP8 mice, alleviating MPTP-induced SN damage.