Erratum: Therapeutic effect of a novel anti-parkinsonian agent zonisamide against MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine) neurotoxicity in mice

Yokoyama, Hironori; Yano, Ryohei; Kuroiwa, Hayato; Tsukada, Tatsuya; Uchida, Hiroto; Kato, Hirokazu; Kasahara, Jiro; Araki, Tsutomu

doi:10.1007/s11011-010-9228-4

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MPTP is an exogenous neurotoxin most commonly used to model PD in rodents and primates. In the presence of monoamine oxidase B in the brain, MPTP is converted into 1-methyl-4-phenyl- pyridinium (MPP + ), which can cause selective damage to DAn, inducing neuronal apoptosis and the occurrence and development of PD [22,23]. TH is a rate-limiting enzyme in catecholamine biosynthesis.…”

Section: Discussionmentioning

confidence: 99%

Paeoniflorin protects 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease mice by inhibiting oxidative stress and neuronal apoptosis through activating the Nrf2/HO-1 signaling pathway

Zhang

Bai

et al. 2023

NeuroReport

View full text Add to dashboard Cite

ObjectivesThis study aimed to explore the neuroprotective effects of paeoniflorin on oxidative stress and apoptosis in 1-methyl-4-phenyl-1,2,3,6tetrahydropyridine (MPTP)-induced Parkinson's disease (PD) mice. MethodsThe effects of paeoniflorin on motor function in mice were evaluated by behavioral test. Then substantia nigra of mice were collected and neuronal damage was assessed using Nissl staining. Positive expression of tyrosine hydroxylase (TH) was detected by immunohistochemistry. Levels of malondialdehyde, superoxide dismutase (SOD) and glutathione were measured by biochemical method. terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay was used to detect apoptosis of dopaminergic neurons. Western blotting and real-time fluorescence quantitative PCR were used to detect the protein and mRNA expressions of Nrf2, heme oxygenase-1 (HO-1), B-cell lymphoma-2(Bcl-2), Bax and cleaved caspase-3. ResultsPaeoniflorin treatment significantly ameliorated the motor performance impairment in MPTP-induced PD mice. Moreover, it notably increased the positive expression rate of TH and reduced the damage and apoptosis of dopaminergic neurons in the substantia nigra. Furthermore, paeoniflorin increased the levels of SOD and glutathione and decreased the malondialdehyde content. It also promoted Nrf2 nuclear translocation, increased the protein and mRNA expressions of HO-1 and Bcl-2 and reduced the protein and mRNA expressions of BCL2-Associated X2 (Bax) and cleaved caspase-3. Treatment with the Nrf2 inhibitor, ML385, notably reduced the effects of paeoniflorin in MPTP-induced PD mice. ConclusionsNeuroprotective effects of paeoniflorin in MPTP-induced PD mice may be mediated via inhibition of oxidative stress and apoptosis of dopaminergic neurons in substantia nigra through activation of the Nrf2/HO-1 signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Paeoniflorin protects 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease mice by inhibiting oxidative stress and neuronal apoptosis through activating the Nrf2/HO-1 signaling pathway

Zhang

Bai

et al. 2023

NeuroReport

View full text Add to dashboard Cite

show abstract

Erratum: Therapeutic effect of a novel anti-parkinsonian agent zonisamide against MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine) neurotoxicity in mice

Abstract: Springer apologizes for any confusion caused by the duplicate publication. T. Araki: DeceasedThe online version of the original article can be found at http://dx.doi.

Cited by 1 publication

References 0 publications

Paeoniflorin protects 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease mice by inhibiting oxidative stress and neuronal apoptosis through activating the Nrf2/HO-1 signaling pathway

Paeoniflorin protects 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease mice by inhibiting oxidative stress and neuronal apoptosis through activating the Nrf2/HO-1 signaling pathway

Contact Info

Product

Resources

About