ABSTRACT
Objective To study the immunomodulatory effect of polysaccharides (CRPS25-Ⅱ) derived from Chroogomphus rutilus on mouse mononuclear macrophages, RAW264.7 cells. Methods RAW264.7 cells were resuspended and cultured, cell suspension was prepared. The blank control group and CRPS25-Ⅱ groups with different mass concentrations (1, 20, 40, 80 and 160 μg/ml) were set up. MTT assay was used to determine the cytotoxicity of CRPS25-Ⅱ on RAW264.7 cells. RT-PCR was used to detect the effects of CRPS25-Ⅱ on the secretion of immune regulatory factors IL-6 and TNF-α from RAW264.7 cells. Western blot was used to detect the effects of CRPS25-Ⅱ on the expression of p-P65 protein in NF-κB pathway of RAW264.7 cells. Results The results showed that CRPS25-Ⅱ (1−160 μg/ml) had no obvious cytotoxicity. CRPS25-Ⅱ (1−160 μg/ml) increased the secretion of cytokines, and thus promoted the mRNA expression of IL-6 and TNF-α. CRPS25-Ⅱ increased the phosphorylation of p-P65 protein and activated the NF-κB signaling pathway, and thus promoted the immune regulation of cells. CRPS25-Ⅱ (1−160 μg/ml) could increase the p-P65 protein, and the promoting effects of CRPS25-Ⅱshowed an upward trend in the concentration range of 1−40 μg/ml and gradually weakened in the concentration range of 40−160 μg/ml. Conclusion Polysaccharides derived from chroogomphus rutilus had no cytotoxicity to mouse macrophages, and could promote the secretion of inflammatory factors IL-6 and TNF-α and activate the NF-κB signaling pathway, thus playing an immunomodulatory role.
ABSTRACT
<p><b>BACKGROUND</b>We previously demonstrated that the aqueous extract of the Schizandra chinensis fruit (AESC) ameliorated Cd-induced depletion of monoamine neurotransmitters in the brain through antioxidant activity. In the present study, we investigated the effect of AESC on anxiety-like behavior and the levels of norepinephrine and 3-methoxy-4-hydroxy-phenylglycol (a metabolite of norepinephrine) in different brain regions during ethanol withdrawal in rats.</p><p><b>METHODS</b>Male Sprague-Dawley rats were treated with 3 g/kg of ethanol (20%, w/v) or saline by daily intraperitoneal injection for 28 days followed by three days of withdrawal. During withdrawal, rats were given AESC (100 mg × kg(-1)× d(-1) or 300 mg × kg(-1)× d(-1), P.O.) once a day for three days. Thirty minutes after the final dose of AESC, the anxiogenic response was evaluated using an elevated plus maze, and the plasma corticosterone levels were examined by radioimmunoassay. Meanwhile, the concentrations of norepinephrine and 3-methoxy-4-hydroxy-phenylglycol in the hypothalamic paraventricular nucleus and hippocampus were also measured by high performance liquid chromatography.</p><p><b>RESULTS</b>Rats undergoing ethanol withdrawal exhibited substantial anxiety-like behavior, which was characterized by both the decrease in time spent in the open arms of the elevated plus maze and the increased level of corticosterone secretion, which were greatly attenuated by doses of AESC in a dose-dependent manner. The high performance liquid chromatography analysis revealed that ethanol withdrawal significantly increased norepinephrine and 3-methoxy-4-hydroxy-phenylglycol levels in the hypothalamic paraventricular nucleus, while not significantly altering them in the hippocampus. Similar to the results from the elevated plus maze test, the AESC significantly inhibited the elevation of norepinephrine and its metabolite in the hypothalamic paraventricular nucleus in a dose-dependent manner.</p><p><b>CONCLUSIONS</b>These results suggest that AESC attenuates anxiety-like behavior induced by ethanol withdrawal through modulation of the hypothalamic norepinephrine system in the brain.</p>
Subject(s)
Animals , Male , Rats , Anxiety , Drug Therapy , Behavior, Animal , Ethanol , Fruit , Chemistry , Plant Extracts , Therapeutic Uses , Rats, Sprague-Dawley , Schisandra , Chemistry , Substance Withdrawal Syndrome , Drug TherapyABSTRACT
The constant iv. of aconitine can induce the varied arrhythmias in mice. Taurine 100mg/kg iv. or Quinidine 5 mg/kg iv. can delays the onset time of arrhythmias, and increases the dose of aconitine, respectively .But no effects were seen in mice pretreated with taurine 50mg/kg or quinidine 2.5mg/kg. However their combination can significantly decrease the incident of ventricular fibrillation and delay the onset time of death. Our results suggested that taurine, quinidine and their combination are effective on arrhythmias induced by aconitine in mice.