Scorpion venom heat-resistant protein decreases immunoreactivity of OX-42-positive microglia cells in MPTP-treated mice

BACKGROUND： Microglia function as the immune surveyors of the brain under normal physiologica conditions. However, microglia become activated in response to brain injuries and immunological OBJECTIVE： To explore the influence of scorpion venom （SV） heat-resistant protein on frontal cortex and hippocampal microglia cells in a mice model of Parkinson＇s disease. DESIGN, TIME AND SETTING： Randomized, controlled, cellular immunity study. The experiment was performed at the Physiology Department Laboratory in Dalian Medical University between June 2005 and July 2008. MATERIALS： Ninety-six healthy, C57B1/6 mice; 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine （MPTP） from Sigma, USA; SV heat-resistant protein （Experimental Base Institute in Dalian Medical University）. The mice were randomly divided into four groups （n = 24）： normal control, negative control, model, and SV heat-resistant protein. METHODS： Mice in the model and SV heat-resistant protein groups were subcutaneously injected with MPTP （20 mg/kg） to model Parkinson＇s disease, while the normal control and negative control groups were injected with physiological saline in the neck for 8 successive days. In addition, mice in the model and normal control groups were intraperitoneally injected with physiological saline 2 hours following administration, while SV heat-resistant protein and negative control groups were injected SV heat-resistant protein （0.01 mg/kg）. MAIN OUTCOME MEASURES： lmmunoreactivity of microglia cells in MPTP-treated mice. RESULTS： Compared with normal control mice, MPTP-treated mice displayed increased OX-42 expression in the brain. However, in the SV heat-resistant protein-treated mice, OX-42 expression was decreased, compared to the model group. In the model mouse group, the number of OX-42-positive microglia was increased in the frontal cortex, caudatum, and hippocampal hilus, compared to the normal control mice （P 〈 0.01）. However, in the SV heat-resistant protein-treated mice, the number of OX-42-positive microglia significantly decreased in the frontal cortex, caudatum, and hippocampal hilus, compared to the model group （P 〈 0.01）. CONCLUSION： SV heat-resistant protein inhibited MPTP-induced microglial activation in the mouse frontal cortex and hippocampus, resulting in reduced microglial activation in the brain.

Effect of Cr_(2)O_(3) nanosheet insertion on the deuterium permeation behavior of a Cr-Zr-O coating

In this study,a Cr_(2)O_(3) nanosheet(Cr_(2)O_(3) NS)inserted Cr-Zr-O coating was developed as a hydrogen isotope permeation barrier.The Cr_(2)O_(3) NSs,fabricated by rapid heat treatment,were amorphous with a thickness of only several nanometers.These Cr_(2)O_(3) NSs were then incorporated into a Cr-Zr-O multi-metal oxide composite coating via a dip-coating method to form a coating.The effect of the Cr_(2)O_(3) NS concentration on the morphology,microstructure and deuterium permeation resistance of the coating was studied.With the addition of 1.0 g 1^(-1)Cr_(2)O_(3) NSs,compared with the Cr-Zr-O coating without NSs,the permeation reduction factor of the resultant coating was enhanced from 249℃to 575℃ at 500℃.The coating,with a thickness of nearly 193 nm,achieved a comparable deuterium resistance that was above two orders of magnitude higher than the steel substrate.The results show that ceramic NSs can serve as effective fillers for enhancing the coating performance when functioning as a hydrogen isotope barrier.

Protective effects of nicotine on gamma-aminobutyricacid neurons and dopaminergic neurons in micewith Parkinson disease

This study aimed to investigate the protective effect of nicotine on dopaminergic neurons and its mechanisms in mice with Parkinson disease(PD)induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP).C57BL/6J mice were injected with MPTP for 8 days to establish a PD model.Nicotine was given for 10 days in the nicotine therapeutic group.Animals were examined behaviorally with the pole test and traction test.Tyrosine hydroxylase(TH)andγ-aminobutyric acid(GABA)were determined by using the immunocytochem-istry(ICC)method.The ultrastructural changes of the caudate nucleus(CN)were observed under electron microscopy.The results showed that pretreatment with nicotine could improve the dyskinesia of PD mice markedly.Simultaneously,TH-positive(P<0.01)neurons and GABA-positive(P<0.05)neurons in the nicotine therapeutic group were significantly more than those in the model group.The ultrastructural injury of the nicotine therapeutic group was also ameliorated.Nicotine has protective effects on theγ-aminobutyric acid neurons and dopaminergic neurons in the MPTP-treated mice.