Neuroprotective effects of Danshensu in Parkinson’s disease mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
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Abstract:
Parkinson’s disease (PD) causes major changes in dopaminergic neurons of the brain, resulting in motor symptoms in older adults. A previous study showed that Danshensu alleviates the cognitive decline by attenuating neuroinflammation. In the present study, we investigated the neuroprotective effect of Danshensu in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. C57BL/6 mice were randomly divided into the following four groups: control, MPTP, Danshensu at 15 mg/kg, and Danshensu at 60 mg/kg. The mice were administered Danshensu intragastrically for 14 days. In the behavioral tests, Danshensu treatment alleviated motor dysfunction induced by MPTP. The number of tyrosine hydroxylase-positive neurons in the substantia nigra was significantly reduced in the MPTP group, relative to the control group; Danshensu partially blocked this reduction in tyrosine hydroxylase-positive neurons. In addition, Danshensu attenuated the reductions in striatal dopamine and 5-HT levels induced by MPTP. Danshensu also diminished the increase in Iba1-positive cells in the substantia nigra and reduced the levels of interleukin-1β and tumor necrosis factor-α in the striatum. These findings suggest that Danshensu exerts neuroprotective effects and improves motor function in PD mice, at least in part, by reducing neuroinflammation.Keywords:
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Parkinson’s disease one of the most complex neurological disorder. The disease risk and progression are due to common genetic variants. Approximately 6.2 million cases are reported each year according to the statistics published in 2015 whereas it is expected that this number will be twice by 2040. There are two types of Parkinson’s disease, familial Parkinson’s disease, and sporadic Parkinson’s disease. The disease is characterized by the presence of Lewy bodies. Adult age increases the risk of Parkinson’s disease. In this review, we provide an overview of the disease pathology of Lewy bodies in the occurrence of Parkinson’s disease, in vitro studies to determine the role of iPSCs in treatment of Parkinson’s disease, in vivo studies to determine the role of animal model in studying disease modeling, and future prospective how single-cell RNA sequencing technology is a major advancement in studying and find the treatment for Parkinson’s disease.
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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.
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The current review describes the modem Parkinson's disease models in animals, their advantages, limitations and disadvantages. It was noted that the most widespread up-to-date models based on etiology of the Parkinson's disease. Although toxins mostly produce the Parkinson's disease, a study of involved genes allows investigating not only inherited but also sporadic (not inherited) forms of disease since the same genes are involved in both cases. Mutations of genes lead to formation of mutant toxic proteins, which produce a death of the specialized neurons of the nigrostriatal dopaminergic system and the development of Parkinson's disease. A significant place in the review takes adescription of characteristics of the toxic models produced by 6-OHDA, MPTP and rotenone, their similarities and differences in pathogenetic mechanisms of the Parkinson's disease development. On the basis of the considered experimental models of Parkinson's disease a conclusion has been done that none of these models may in full and adequate scale imitate the entire clinical, pathophysiological, morphological, biochemical and other aspects of the Parkinson's disease development.
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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 is caused by the reduction of dopamine in the brain and related to many genes. In addition, the getting together of the α-Synuclein is the important factor of Parkinson's disease. This research mainly discusses the effect of heavy metals and genetics on the prevalence of Parkinson's disease. The author found 10 articles that investigate the relationship between the heavy metals, genetics and the prevalence of Parkinson's disease. In all these materials, 9 of 10 articles focus on the relationship between the heavy metals and the prevalence of Parkinson's disease, namely, how different heavy metals can cause Parkinson's disease. The last reference article is about the genetics and the prevalence of Parkinson's disease. This article is mainly about which gene is changed and will let people get Parkinson's disease. Iron, copper and lead can contribute to the prevalence of Parkinson's disease, while the manganese does not show much related to the prevalence of Parkinson's disease. Besides, many genes together will contribute to the prevalence of Parkinson's disease. Different genes getting together will cause different Parkinson's disease.
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Administration of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to adult (2-month to 4-month-old) male C57BL/6 mice (MPTP-sensitive) is a valuable Parkinson's disease model. At comparable age, other strains, such as BALB/c, are minimally affected by MPTP (MPTP-resistant). However, the maintenance of resistance to MPTP throughout aging in MPTP-resistant strains has not been studied. Here, we show that, as previously reported, 1-month and 18-month-old C57BL/6 mice are least and most sensitive to MPTP, respectively. MPTP, as expected, did not affect the younger (1-month and 3-month-old) BALB/c mice, but it markedly decreased striatal dopamine in the older (10-month and 18-month-old) BALB/c mice. These data suggest that the sensitivity to MPTP is age dependent and that mice from an MPTP-resistant strain lose their resistance as they age.
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