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DJ-1, originally identified as an oncogene product, is involved in multiple processes, including cellular transformation, the oxidative stress response, and transcriptional regulation. We had previously found that DJ-1 was closely associated with the proliferation and differentiation of cultured neuronal stem cells. In this study, we further investigated the functions of DJ-1 to determine how adult neurogenesis was affected in the subgranular zones (SGZ), subventricular zone (SVZ), and olfactory bulb (OB), which are brain areas closely related to early nonmotor symptoms of Parkinson’s disease, using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of Parkinson’s disease. The results showed that the numbers of 5-bromo-2-deoxyuridine-positive (BrdU+) cells in the SGZ and SVZ of mice in the MPTP group were not significantly different from those in the saline controls, whereas the number of BrdU+cells in the olfactory granule cell layer and glomerulus layer of the OB in the MPTP group changed markedly. We also found that DJ-1 was translocated into the nuclei of BrdU+cells in the SGZ and SVZ, but not in the OB. This may indicate that the nuclear translocation of DJ-1 in the SGZ and SVZ protects adult neuronal stem cells from damage caused by MPTP so that the normal number is maintained, but is not involved in the protective mechanism in the OB.

Cyclosporine A (CsA) is a effective and widely used immunosuppressive agent. Nevertheless, its intense nephrotoxicity restricts clinical application. In this study, wistar rats were randomly divided into a control group, a low-dose group and a high-dose group. The rats in the low-dose group and those in the high-dose group were given CsA at a daily dose of 5 mg per kg and 100 mg per kg by gavage for 7 d respectively, while the control group was given distilled water of equal volume. The extent of renal impairment was evaluated by renal function assay, and urease and pathological observation. The results showed that the rats in the low-dose group did not suffer remarkable renal impairment, while the rats in the high-dose group did. Two-dimensional gel electrophoresis (2DE) was utilized to resolve the plasma protein profile. Six spots showing stable and significantly different expression were identified by MALDI-TOF-MS and ESI-TOF-MS/MS respectively, the two induced proteins were identified respectively as α-1-acid glycoprotein (AAG) and clusterin (CLUS), and the one inhibited was haptoglobin (Hp).

A 35 kDa protein was purified from rat spinal ganglia and sensory fibers. Combined direct trypsin digest and liquid chromatography ion trap mass spectrometry analysis, the 35 kDa protein was identified as annexin V. We then studied the distribution of serum antibodies to annexin V in patients with peripheral neuropathy. We found serum positive antibodies to annexin V only in some patients with immune-mediated neuropathy. This indicated that humoral immune responses to annexin V might play a role in the pathogenesis of autoimmune sensory neuropathy or sensory neuronopathy.

In this study we assessed the effect of acteoside that significantly improved cell viability and inhibited lactate dehydrogenase (LDH) release. Furthermore acteoside prevented a neurotoxin 1-methyl-4-phenylpyridinium ion (MPP +)-induced apoptosis in CGNs. Accordingly, our flow cytometric analysis of CGNs after acteoside treatment revealed a decrease in the number of the MPP +-induced apoptotic cells (P < 0.001). Western blot analysis demonstrated that acteoside inhibits the active caspase-3 fragment (17 kDa) (P < 0.001) and the proteolytic poly (ADP-ribose) polymerase (PARP) fragment (85 kDa) expression (P < 0.001) following MPP + treatment in CGNs. We conclude that acteoside prevents the MPP +-induced apoptosis and inhibits the apoptosis-related pathway.