Quinpirole ameliorates nigral dopaminergic neuron damage in Parkinson's disease mouse model through activating GHS-R1a/DR heterodimers.

Growth hormone secretagogue receptor 1a (GHS-R1a) is an important G protein-coupled receptor (GPCR) that regulates a variety of functions by binding to ghrelin. It has been shown that the dimerization of GHS-R1a with other receptors also affects ingestion, energy metabolism, learning and memory. Dopamine type 2 receptor (DR) is a GPCR mainly distributed in the ventral tegmental area (VTA), substantia nigra (SN), striatum and other brain regions.

Role of upregulation of the K channel subunit SUR1 in dopaminergic neuron degeneration in Parkinson's disease.

Accumulating evidence suggests that ATP-sensitive potassium (K ) channels play an important role in the selective degeneration of dopaminergic neurons in the substantia nigra (SN). Furthermore, the expression of the K channel subunit sulfonylurea receptor 1 (SUR1) is upregulated in the remaining nigral dopaminergic neurons in Parkinson's disease (PD). However, the mechanism underlying this selective upregulation of the SUR1 subunit and its subsequent roles in PD progression are largely unknown.

The expression change of OTUD3-PTEN signaling axis in glioma cells.

Background: OTU domain-containing protein 3 (OTUD3), as a deubiquitinase (DUB) belonging to the ovarian tumor protease (OTU) family, has been reported to suppress tumor via OTUD3-PTEN signaling axis. Glioma is the most common primary intracranial tumor with high invasiveness and poor prognosis. Although less than half of the patients have phosphatase and tension homologue deleted in chromosome 10 (PTEN) mutations or homozygous deletions, two-thirds of glioma possess diminished PTEN expression.

The petrosal vein mutilation affects the SOD activity, MDA levels and AQP4 level in cerebellum and brain stem in rabbit.

Cerebral edema after brain surgery remains a life-threatening complication in the clinic. For a better operating field view, superior petrosal vein (SPV) can be easily damaged during neurosurgery. SPV sacrifice may sometimes be inevitable in clinic.

The expression of K channel subunits in alpha-synuclein-transfected MES23.5 cells.

Background: SUR1, one of the subunits of ATP-sensitive potassium (K) channels, was found to be highly expressed in mRNA levels in the substantia nigra (SN) of Parkinson's disease (PD) brains. Though the mechanism of the selective dopamine (DA) neurons death is still unknown, some studies have demonstrated that selective activation of the K channels in the SN might be associated with the degeneration of DA neurons. The objective of our study is to examine the expressions of K channel subunits in dopaminergic cells with alpha-synuclein (α-Syn) transfection.

Influence of sodium nitroprusside on expressions of FBXL5 and IRP2 in SH-SY5Y cells.

Iron accumulation in the brain is associated with the pathogenesis of Parkinson's disease (PD). Misexpression of some iron transport and storage proteins is related to iron dyshomeostasis. Iron regulatory proteins (IRPs) including IRP1 and IRP2 are cytosolic proteins that play important roles in maintaining cellular iron homeostasis.

Nesfatin-1 protects dopaminergic neurons against MPP/MPTP-induced neurotoxicity through the C-Raf-ERK1/2-dependent anti-apoptotic pathway.

Several brain-gut peptides have been reported to have a close relationship with the central dopaminergic system; one such brain-gut peptide is nesfatin-1. Nesfatin-1 is a satiety peptide that is predominantly secreted by X/A-like endocrine cells in the gastric glands, where ghrelin is also secreted. We previously reported that ghrelin exerted neuroprotective effects on nigral dopaminergic neurons, which implied a role for ghrelin in Parkinson's disease (PD).

[An overview on autophagy in neural stem cells].

Neural stem cells (NSCs) offer great promise for the treatment of multiple neurodegenerative diseases. However, the survival and differentiation rates of grafted cells in the host brain need to be enhanced. In this regard, understanding of the underlying mechanism of NSCs survival and death is of great importance for the implications of stem cell-based therapeutic application in the treatments of neurological disorders.

[Advances in the association of ATP-sensitive potassium channels and Parkinson's disease].

ATP-sensitive potassium channels (K), as an inward rectifying potassium channel, are widely distributed in many types of tissues. K are activated by the depletion of ATP level and the increase in oxidative stress in cells. The activity of K couples cell metabolism with electrical activity and results in membrane hyperpolarization.

Curcumin protects nigral dopaminergic neurons by iron-chelation in the 6-hydroxydopamine rat model of Parkinson's disease.

Objective: Curcumin is a plant polyphenolic compound and a major component of spice turmeric (Curcuma longa). It has been reported to possess free radical-scavenging, iron-chelating, and anti-inflammatory properties in different tissues. Our previous study showed that curcumin protects MES23.

Curcumin attenuates 6-hydroxydopamine-induced cytotoxicity by anti-oxidation and nuclear factor-kappa B modulation in MES23.5 cells.

Oxidative stress has been implicated in the degeneration of dopaminergic neurons in the substantia nigra of Parkinson's disease patients, and several anti-oxidants have been shown to be effective on the treatment of Parkinson's disease. Curcumin has been previously reported to possess radical scavenger, iron chelating, anti-inflammatory properties in different tissues. The aim of present study is to explore the cytoprotection of curcumin against 6-hydroxydopamine (6-OHDA)-induced neuronal death, as well as the underlying mechanisms in MES23.

Rg1 reduces nigral iron levels of MPTP-treated C57BL6 mice by regulating certain iron transport proteins.

Elevated iron levels in the substantia nigra (SN) participate in neuronal death in Parkinson's disease, in which the misregulation of iron transporters such as divalent metal transporter (DMT1) and ferroportin1 (FP1) are involved. Our previous work observed that nigral iron levels were increased in MPTP-treated mice and Ginsenoside Rg1 which is one of the main components of ginseng, had neuroprotective effects against MPTP toxicity. Whether Rg1 could reduce nigral iron levels to protect the dopaminergic neurons? And whether its neuroprotective effect is achieved by regulating certain iron transporters? The present studies showed that Rg1 pre-treatment increased the dopamine and its metabolites contents in the striatum, as well as increased tyrosine hydroxylase expression in the SN.