Intermittent fasting protects the nigral dopaminergic neurons from MPTP-mediated dopaminergic neuronal injury in mice
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MPTP
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Intermittent Fasting
The objective of this study was to investigate and analyze the behavioral and neurochemical effects of monosodium glutamate (MSG) injections at various and subsequent dosages on male Wistar rats during the neonatal period.In order to determine the behavioral and neurochemical effects of MSG, the experiment was implemented on neonatal male Wistar rats and the test was repeated for various MSG dosages. After completing the experiment, additionally, levels of dopamine, GABA, catecholamine (dopamine, noradrenaline, and adrenaline) and glutamate in the brain cells of the decapitated rats were also measured using the ELISA method.Considering the results of the behavioral test, when we compared the test values of the control group with the values of the MSG-injected groups we noted that there were significant differences in the statistical figures obtained. Additionally, we found that the statistical figures of some neurochemical parameters were also significantly different when we compared the values of the MSG group with the control values.MSG injection has a clear effect on the neurochemical parameters, learning memory, and locomotor activities of rats.
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Monosodium glutamate
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Microdialysis
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We investigated the effect of GM1 gangliosides on a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson disease. Five groups of mice (saline, GM1 (30 mg/kg), MPTP, MPTP + GM1 (15 mg/kg), MPTP + GM1 (30 mg/kg] were compared. GM1 was given daily via intraperitoneal injection before and during 13 daily doses of MPTP (30 mg/kg). Mice were tested for locomotion (1) within 2 h of an MPTP dose (to measure reduced motor activity), and (2) within 24 h of an MPTP dose (after animals had recovered and exhibited hyperactivity). We found that mice given GM1 gangliosides exhibited significantly less MPTP-induced behavior. This effect was most evident with the 15 mg/kg GM1 dose. GM1 also appeared to attenuate MPTP-induced neurochemical changes. GM1 effects indicating enhancement of DA turnover and preservation of DA, DOPAC and HVA concentrations in the striatum were found after the 8th MPTP dose. These latter neurochemical changes, however, were transient and not present after the 13th MPTP dose. Our data would suggest that gangliosides may reduce acute MPTP-induced neurotoxicity in mice either through an increase in DA neuron survival and/or the augmentation of striatal DA activity.
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The present study was designed to evaluate dopaminergic neuronal loss in the substantia nigra pars compact (SNpc) with immunohistochemical staining. C57BL/6 mice were intraperitoneally injected four times with 15 mg/kg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), at 2 h intervals on 10 and 21 days, and 6, 12, 24 and 48 weeks of age. Animals were sacrificed 48 hours after the last injection. No change in the number of tyrosine hydroxylase (TH)-positive neurons was observed in 10- and 21-day-old mice after MPTP treatment compared with their corresponding controls. In contrast, MPTP produced a loss of 20.3% of TH-positive neurons in 6 week-old mice, and further decreases with advancing age, i.e., 35.8%, 39.9% and 56.2% TH-positive neuronal loss at 12, 24 and 48 weeks of age, respectively. These results provide evidence of age-related susceptibility of C57BL/6 mice to MPTP using TH immunohistochemistry. However, we failed to observe apoptosis of neurons in SNpc of mice of all ages after a subacute protocol of MPTP treatment (30 mg/kg/day × 5days).
MPTP
Neurotoxin
Neurotoxicity
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MPTP
Neurotoxin
Neurotoxicity
Nigrostriatal pathway
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Neurochemical
Neurochemistry
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목적 : 최근 한의학에서 널리 사용되며, 신경계 질환에도 응용되고 있는 봉약침의 농도의존적 효과를 알아보기 위하여, 대표적인 신경 퇴행성 질환인 파킨슨병의 동물모델을 통해 세포보호효과와 세포사멸 및 신경염증 기전을 관찰하였다. 방법 : C57BL/6 mice에 신경독소인 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine(MPTP)를 4번 복강내 주입하여 중뇌의 흑질 도파민 신경세포를 파괴하여 Parkinson 질병동물 모델을 만든 후, 2개의 군에는 마지막 MPTP 투여 2시간 후에 1차, 그 후로 48시간이 지날 때마다 양측 신수에 각각 0.06mg/kg 농도와 0.6mg/kg 농도의 봉약침을 시행하여 총 4회 시술한 후, 도파민 세포를 측정하는 TH 면역조직 화학법을 통해 세포의 보존 정도를 관찰하고, 세포사멸과 관련된 양상을 확인하기 위하여 Caspase 3, 신경염증과 관련된 양상을 확인하기 위하여 iNOS의 발현여부를 면역 조직화학법을 이용하여 관찰하였다. 결과 : 관찰결과 MPTP 투여 후 MPTP 투여군의 흑질의 도파민 세포 수는 감소하였으나 0.6mg/kg 봉약침을 투여한 경우에는 유의성 있게 세포 수가 유지되었다. Caspase-3와 iNOS 발현억제 실험에서 0.6mg/kg 봉약침군은 MPTP 투여군과 0.06mg/kg의 봉약침군과 비교하여 Caspase-3, iNOS 발현을 유의하게 억제하였다. 결론 : 봉약침은 MPTP 투여로 인한 신경세포 손상에 대하여 농도에 따라 세포사멸 기전과 신경염증 기전을 억제함으로 신경세포를 보호하는 것으로 추정되며, 추후 적절한 경혈점 및 최적의 봉약침 농도를 찾는데 지속적인 연구가 필요할 것이다.
MPTP
Bee Venom
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목적: 파킨슨 병은 기저핵 흑질의 치밀부에서 도파민성 신경세포의 퇴행으로 인하여 발생하는 질병으로 신경 염증이 주요 병인으로 밝혀져 있다. 이 연구는 MPTP 유발 파킨슨 병 동물 모델에서 신수혈(BL23)에 대한 봉독 약침의 항염증 효과 및 그 기전을 확인하기 위해 시행되었다. 방법: C57BL/6쥐를 무처치군, MPTP+saline군, MPTP+BVA(0.06mg/kg)군, MPTP+BVA(0.6mg/kg)군의 4군으로 나눈 뒤 무처치군을 제외한 모든 그룹에 총 8시간 동안 2시간 간격으로 MPTP-HCl(20mg/kg per dose×4)을 복강내로 주입하였다. MPTP+BVA 군에서 봉독약침은 마지막 MPTP 주입 2시간 후부터 48시간 간격으로 신수혈(BL23)에 양측으로 각 20㎕씩 주입하였고 MPTP+saline군에서는 봉독약침 대신 Saline을 주입하였다. 마지막 MPTP 주입 후 7일째에 쥐의 뇌를 적출한 후 면역조직화학법을 시행하였다. 결과: MPTP 유발 파킨슨 병 동물 모델에서 신수혈에 대한 봉독약침은 농도 의존적으로 TH-Immunoreactivity neuron의 감소와 microglial activation을 억제하였다. HSP70-IR neuron은 모든 군에서 나타나지 않았다. 결론: 봉독약침이 용량의존적으로 microglial activation을 억제하는 효과를 통해 도파민성 신경세포의 파괴를 억제함으로써 항염 효과를 나타냄을 알 수 있었다. 이 결과는 봉독약침이 microglial activation 억제를 통해 임상적으로 파킨슨 병과 같은 신경 퇴행성 질병에 있어 유용한 치료수단이 될 수 있음을 시사한다.
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Parkinson's disease (PD) is the second most common neurodegenerative disease that severely affects the quality of life of patients and their family members. Exposure to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to reflect behavioral, molecular, and proteomic features of PD. This study aimed to assess the protocol for inducing PD following MPTP injection in adult zebrafish.Fish were injected with 100 μg/g of MPTP intraperitoneally once or twice and then assessed on days 1 to 30 post-injection.Between one-time and two-time injections, there was no significant difference in most locomotor parameters, expressions of tyrosine hydroxylase-2 (th2) and dopamine transporter (dat) genes, and dopaminergic neurons (tyrosine hydroxylase positive, TH+ cells) counts. However, caspase-3 levels significantly differed between one- and two-time injections on the day 1 assessment.Over a 30-day period, the parameters showed significant differences in swimming speed, total distance traveled, tyrosine hydroxylase-1 (th1) and dat gene expressions, caspase-3 and glutathione protein levels, and TH+ cell counts. Days 3 and 5 showed the most changes compared to the control. In conclusion, a one-time injection of MPTP with delayed assessment on days 3 to 5 is a good PD model for animal studies.
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Intraperitoneal injection
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The recent discovery that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes a syndrome of Parkinsonism in man and monkey has stimulated the search for a small animal model of Parkinsonism. In this study, MPTP was administered to a series of small animals and observations made on clinical and neurochemical changes. The clinical effects of MPTP in rabbits, guinea pigs, and rats were short lived, and no chronic Parkinsonian syndrome developed. The C57 black mouse, however, although also not showing clinical changes, proved to be an ideal neurochemical model in which to study the effects of MPTP since striatal dopamine levels were reliably reduced to 13% of control values after 4 intraperitoneal injections of 30 mg/kg MPTP. Pathological study of the striatum and substantia nigra in the mouse model failed to show any alteration in neuronal morphology or numbers. Although the effect of MPTP on striatal dopamine lasted for up to 2 weeks after the last MPTP injection, the possibility exists that no neurotoxic effects occur and the observed dopamine depletion is pharmacological only.
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