Effects of ginsenoside Rh1 on expression of inflammatory factors in mouse asthma model / 中国病理生理杂志

AIM:To observe the effects of ginsenoside Rh 1 on the levels of inflammatory factors in serum and bronchoalveolar lavage fluid(BALF),and the pathological changes of the lung tissues in an experimentally induced mouse asthma model.METHODS:Male BALB/c mice(n=40)were divided into 4 groups:normal control group,asthma mo-del group,and low-dose(40 mg· kg-1 · d-1 )and high-dose(80 mg· kg-1 · d-1 )ginsenoside Rh1 groups.The bron-chial asthma mouse model was established by the method of ovalbumin induction and excitation ,and during the excitation period,the mice were daily treated with ginsenoside Rh 1 for 2 weeks.At 24 h after the final dose of ginsenoside Rh 1,the mice were sacrificed.The number of eosinophils(EOS)and the concentrations of interleukin(IL)-4,IL-5 and interferon(IFN)-γin BALF were determined.The levels of IgG and IgE in serum were measured ,and the expression of transforming growth factor(TGF)-β1 and the pathological changes in lung tissues were evaluated.RESULTS:Ginsenoside Rh1 inhibi-ted the increases in the number of EOS and the concentrations of IL-4,IL-5,IFN-γand IgE,reversed the increased ex-pression of TGF-β1,and improved the pathological changes of the lung tissues in asthmatic mice.CONCLUSION:Gin-senoside Rh1 improves the immuno-inflammatory profile and pathological changes in the experimentally induced mouse asth -ma model,implying its potential therapeutic effect on asthma.

Saeng-Kankunbi-Tang () protects liver against oxidative damage through activation of ERK/Nrf2 pathway / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the cytoprotective effects of Saeng-kankunbi-tang (, SKT), a herbal prescription consisting of Artemisia capillaris and Alisma canaliculatum, and its underlying mechanism involved.</p><p><b>METHODS</b>In mice, blood biochemistry and histopathology were assessed in carbon tetrachloride (CCl4)-induced oxidative hepatic injury in vivo. The animal groups included vehicle-treated control, CCl4, SKT 500 mg/(kg day) CCl4+SKT 200 or 500 mg/(kg day). In HepG2 cell, tert-butyl hydroperoxide (tBHP) induced severe oxidative stress and mitochondrial dysfunction in vitro. The cyto-protective effects of SKT were determined by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay, flfluorescence activated cell sorting analysis and western blotting.</p><p><b>RESULTS</b>The administration of SKT prevented liver damage induced by CCl4 in mice, by inhibition of hepatocyte degeneration and inflflammatory cell infifiltration as well as plasma parameters such as alanine aminotransferase (P<0.01). Moreover, treatment with tBHP induced hepatocyte death and cellular reactive oxygen species production in hepatocyte cell line. However, SKT pretreatment (30-300 μg/mL) reduced this cell death and oxidative stress (P<0.01). More importantly, SKT inhibited the ability of tBHP to induce changes in mitochondrial membrane transition in cell stained with rhodamine 123 P<0.01). Furthermore, treatment with SKT induced extracellular signal-regulated kinases-mediated nuclear factor erythroid-2-related factor 2 (Nrf2) activation as well as the expressions of heme oxygenase 1 and glutamate- cystein ligase catalytic, Nrf2 target genes.</p><p><b>CONCLUSIONS</b>SKT has the ability to protect hepatocyte against oxidative stress and mitochondrial damage mediated by Nrf2 activation.</p>

Regulation of 3HNorepinephrine Release by Opioids in Human Cerebral Cortex

To investigate the receptors mediating the regulation of norepinephrine (NE) release in human cerebral cortex slices, we examined the effects of opioid agonists for mu-, delta-, and kappa -receptors on the high potassium (15 mM) -evoked release of [3H]NE. [3H]NE release induced by high potassium was calcium-dependent and tetrodotoxin-sensitive. [D-Pen2, D-Pen5]enkephalin (DPDPE) and deltorphin II (Delt II) inhibited the stimulated release of norepinephrine in a dose-dependent manner. However, Tyr-D-Ala-Gly- (Me) Phe-Gly-ol and U69, 593 did not influence the NE release. Inhibitory effect of DPDPE and Delt-II was antagonized by naloxone, naltrindole, 7-benzylidenaltrexone and naltriben. These results suggest that both delta 1 and delta 2 receptors are involved in regulation of NE release in human cerebral cortex.