ABSTRACT
Objective To explo the antioxidant effect and molecular mechanism of gastrodin (Gas) in epilepsy (EP) rats induced by LiCl-pilocarpine (PILO) . Methods Eighty male SD rats were randomly divided into 5 groups: sham group, EP group, therapy groups (pretreated with 60 mg/kg, 90 mg/kg, 120 mg/kg of gastrodin respectively) . The EP model was esteblished by peritoneal injection of LiCl-PILO. Therapy groups were pretreated with various concerntration of Gas. The control group was given the same dosage of normal saline. The alteration of behavior was observed, the concentration of catalase (CAT), glutathion (GSH), superoxide dismutase (SOD), glutathion reductase (GR), total antioxidtion (T-AOC) and malondialdehyde (MDA) in rats brain cortex were detected by chemical colorimetric method, phosphorylation of p38 was determined by western blot. Results There was no EP seizure in sham group,and the EP seizure degree in therapy groups (gas pretreated groups) was significantly decreased,and had statistically significant difference with EP group (P<0.05) . The EP model rats exhibited a significant decrease in the concentration of endogenous antioxidants (CAT, GSH, SOD, GR and T-AOC), while an increase of the concentration of MDA and phosphorylation p38 protein as compared to sham group (P<0.05) . After treatment of the Gas,treatment group rats attenuated the seizure degree,exhibited a significant increase of the concentration of endogenous antioxidants (P<0.05),while a decrease in concentration of MDA and phosphorylation of p38 as compared to model group (P<0.05) . Conclusion Gas may have a neuroprotective role in central nervous system of epileptic rats modle by down-regulateing the seizure degree and the activity of p38 kinase and up-regulateing the content of endogenous antioxidants.
ABSTRACT
Objective To explore the activition and polarization of microglia in the epileptic rats induced by lithium chloride-pilocarpine. Methods One hundred male SD rats were randomly divided into five groups: control group and different time points model groups including 1d,3d,7d and 14d. Epilepsy models were established by lithium chloride-pilocarpine intraperitoneal injection. The control group was given the same dosage of normal saline. The morphology change was detected by immunofluorescence,and the expressions of iNOS and Arg-1 were determined by IHC at respective time points. Results Compared the model groups with control group,microglia was activated,synapsis was shorten,volume got bigger,most of them seemed as amoebocyte,the expression of iNOS increased and Arg-1 decreased,especially at 3d.ConclusionThe results from this study indicated that microglia was activated and polarized in epileptic rats induced by pilocarpine.
ABSTRACT
Objective: To investigate the effect of ginsenoside-rg1 (G-Rg1) on rat’s cardiomyocytes H9c2 with its mechanism of signal pathwayin vitro. Methods: H9c2 cells were cultured and treated in different conditions by following groups:①Blank control group,②Hypoxia alone group, the cells were treated for (2, 6, 12, 24, 48) hr respectively,③G-Rg1 group, the cells were treated by G-Rg1 at (5, 10, 50) μmol/L respectively,④YC-1 group, which is the speciifc inhibitor of hypoxia inducible factor-1α (HIF-1α),⑤YC-1 + G-Rg1 group,⑥Wortmannin group, which is the speciifc inhibitor for protein kinase B (Akt) phosphorylation and⑦Wortmannin + G-Rg1 group. Each experiment was conducted with 5 replicates. The effects of G-Rg1, hypoxia and YC-1 on cell activity and injury were studied; intracellular mRNA expressions of HIF-1α, glucose transporter-1 (GLUT-1) and heme oxygenase-1 (HO-1) were examined by RT-PCR; protein expressions of HIF-1α, GLUT-1, HO-1, activating transcription factor-6 (ATF-6), CCAAT/enhancer binding protein homologous protein (CHOP) and Akt with its signal pathway factors were measured by Western blot analysis. Results: The time of hypoxia was negatively related to cell activity (r=-0.8580,P Conclusion: G-Rg1 may protect rat’s H9c2 cellsin vitro by activating expressions of HIF-1α with its downstream factors and inhibiting endoplasmic reticulum stress, which might be related to the effect of G-Rg1 on Akt activation.