Publications (3)1.38 Total impact
Article: [Expression and function of Cx32 and Cx43 junctions in medically intractable temporal lobe epilepsy in human].[show abstract] [hide abstract]
ABSTRACT: To study the expression of Cx32 and Cx43 in medically intractable temporal lobe epilepsy in human and investigate the pathogenic relationship between gap junctions and seizures. The expression of Cx32 and Cx43 was detected by Western blot and immunohistochemistry in 14 consecutive samples of hippocampus from epileptic patients undergoing an amygdalohippocampectomy for the treatment of intractable seizures. During postmortem dissection, 8 samples of hippocampus in nonepileptic patients dying of other diseases were taken as control group. The expression of Cx32 and Cx43 was at a low level in the control group [Cx32: count of positive cell (9.4 +/- 1.1), ratios of gray scale (0.2 +/- 0.1); Cx43: count of positive cell (9.2 +/- 4.7), ratios of gray scale (0.5 +/- 0.2)], but Cx43 and Cx32 appeared to be expressed at a higher level in epileptic patients compared with that of the control group by immunohistochemistry [Cx32: count of positive cell (14.6 +/- 3.4), Cx43: count of positive cell (16.5 +/- 3.1)] (P < 0.01), and their expression significantly increased by Western blot [Cx32: ratios of gray scale (1.5 +/- 0.2), Cx43: ratios of gray scale (1.4 +/- 0.3)] (P < 0.01). Over-expression of Cx32 and Cx43 was found in 14 consecutive samples of hippocampus from epileptic patients. Gap junctions play an important role in the occurrence and progression of intractable seizures.Zhonghua yi xue za zhi 11/2009; 89(43):3058-60.
Article: [Effect of local mild hypothermia on expression of aquaporin-4 following intracerebral hemorrhage in rats].[show abstract] [hide abstract]
ABSTRACT: To examined the effect of local mild hypothermia on the expression of aquaporin-4 (AQP-4) following intracerebral hemorrhage (ICH) in rats and clarified the mechanism of hypothermia on brain edema formation following ICH. Two hundreds and forty male Wistar rats were randomly divided into two groups: the intracerebral hemorrhage (ICH) group, in which autologous arterial blood were stereotaxically injected into right caudate nucleus; the local mild hypothermia (ICH + H) group, in which the rats were given 4 h local mild hypothermia after the injection of blood. Each group was divided into 6 subgroups: control, 6 h, 24 h, 72 h, 5 d and 7 d after operation; Brain water content was determined by dry-wet weight method and the permeability of BBB was measured by Evans-Blue extravasation. RT-PCR and Western blot were respectively used to evaluate AQP-4 mRNA and protein expression. In ICH group, compared with control, ICH significantly increased BWC, the permeability of BBB and the expression of AQP-4 mRNA, all began at 6 h and peaked at 72 h (P < 0.01), the increased protein expression of AQP-4 began at 24 h and also peaked at 72 h (P < 0.01). AQP-4 expression positively correlated, both at the mRNA and the protein level, with the permeability of BBB (r = 0.78 and r = 0.76 respectively). In ICH + H group, compared with ICH group, the elevation of BWC, BBB permeability and AQP-4 protein expression were strongly attenuated at all time point by hypothermia treatment (P < 0.01), while AQP-4 mRNA levels demonstrated a modest attenuation from 48 h. At 72 h, AQP-4 mRNA optical density (A) decreased from 1.25 +/- 0.03 (ICH group) to 1.04 +/- 0.02 (P < 0.01), AQP-4 protein expression (A) decreased from 0.77 +/- 0.08 (ICH group) to 0.25 +/- 0.04 (P < 0.01). This study indicates that BBB breakdown can increase the expression of AQP-4; local mild hypothermia can significantly reduce brain edema formation after ICH by suppressing the elevation of AQP-4 protein expression; Inhibition of BBB breakdown and the elevation of AQP-4 protein expression with local mild hypothermia appear to contribute to brain protection in this model.Zhonghua yi xue za zhi 04/2006; 86(13):906-10.
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ABSTRACT: The prion protein peptide PrP106-126 induces cell apoptosis through mechanisms involving production of intracellular reactive oxygen species. The present study investigated the effects of edaravone, a potent free radical scavenger in clinical use, on cell cytotoxicity induced by PrP106-126. Results showed that PrP106-126 decreased PC12 cell viability in a dose- and time-dependent manner. Edaravone significantly antagonized the cytotoxic effects of PrP106-126. Mechanistically, PrP106-126 decreased PC 12 intracellular glutathione (GSH) concentrations, decreased superoxide dismutase (SOD) enzyme activity, increased concentrations of the oxidation end product malondialdehyde (MDA), depolarized the mitochondrial membrane, and increased caspase-3 activity. Edaravone alone did not affect GSH, SOD, or MDA but did effectively reverse all of the intracellular prooxidant effects induced by PrP106-126 and inhibit induced apoptosis in PC12 cells. In conclusion, edaravone may be a viable candidate for the treatment of oxidative stress-induced neurodegenerative disease.Journal of Biochemical and Molecular Toxicology 24(4):235-41. · 1.38 Impact Factor