The protective effect of water-soluble proteins from selenium-enriched Bifidobacterium longum on lipopolysaccharide-induced injury in rat IEC6 cells / 中国药理学通报

To investigate the protective effect of selenium-enriched Bifidobacterium longum preparation on rat IEC6 cells via the application of lipopolysaccharide (LPS)-induced IEC6 cell injury model. Methods The experiment was divided into five groups; negative control group treated with phosphoric acid equilibrium salt solution, model group treated with LPS, and low, medium, high concentration group in which IEC6 cells were treated with LPS plus 10, 30, 100 mg • L"1 water-soluble proteins from selenium-enriched Bifidobacterium longum respectively. After treatment with LPS for 24 hours, IEC6 cell viability, apoptosis, mitochondria membrane potential, and the expression of zonula occludens 1 (ZO-1) and Occludin were detected. Results LPS induced rat intestinal epithelial cell damage, such as the decrease of cell viability, the increase of cell apoptosis, the collapse of mitochondria membrane potential, and the decrease of cell tight junction protein expression. Water-soluble proteins from selenium-enriched Bifidobacterium longum inhibited LPS-induced IEC6 cell damage, decreased cell apoptosis and increased cell tight junction between cells. Conclusion Water-soluble proteins from selenium-enriched Bifidobacterium longum have protective effect on LPS-induced rat intestinal epithelial cell injury.

5, 7, 2', 4', 5'-Pentamethoxyflavanone regulates M1/M2 macrophage phenotype and protects the septic mice / 中国天然药物

Flavonoids have been reported to exert protective effect against many inflammatory diseases, while the underlying cellular mechanisms are still not completely known. In the present study, we explored the anti-inflammation activity of 5, 7, 2', 4', 5'-pentamethoxyflavanone (abbreviated as Pen.), a kind of polymethoxylated flavonoid, both in vitro and in vivo experiments. Pen. was showed no obvious toxicity in macrophages even at high dosage treatment. Our results indicated that Pen. significantly inhibited both mRNA and protein level of proinflammatory cytokines, IL-1β, IL-6, TNF-α and iNOS, which was characteristic expressed on M1 polarized macrophages. These effects of Pen. were further confirmed by diminished expression of CD11c, the M1 macrophage surface marker. Further researches showed that the mechanism was due to that Pen. downregulated the activity of p65, key transcription factor for M1 polarization. On the other hand, Pen. also enhanced M2 polarization with upregulation of anti-inflammatory factors and increase of M2 macrophage surface markers, which lead to the balance of M1 and M2 macrophages. Moreover, in vivo research verified that Pen. treatment alleviated LPS-induced sepsis in mice by increasing survival rate, decreasing inflammatory cytokines and improving lung tissue damage. In summary, our results suggested that Pen. modulated macrophage phenotype via suppressing p65 signal pathway to exert the anti-inflammation activity.

Changes of brain mast cells after transient global ischemia in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate changes of brain mast cells after transient global ischemia in rats.</p><p><b>METHODS</b>Transient global ischemia damage was induced by four-vessel occlusion. After 1 h to 14 days of ischemia, rats were perfused intracardially by 4% paraformaldehyde. The brains were dissected to serial sections using freeze microtome, and then stained with toluidine blue. Brain mast cell was observed under microscope.</p><p><b>RESULT</b>Most brain mast cells were located in thalamus. The number of mast cells in thalamus markedly decreased during reperfusion after transient global ischemia. However, the degranulation rate of thalamus mast cells showed reverse change after ischemia.</p><p><b>CONCLUSION</b>Brain mast cells markedly degranulate after transient global ischemia, which may be involved in the pathological process after ischemia.</p>

Effect of alahistidine on brain histamine content and seizure development / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of alahistidine on brain histamine content and seizure development.</p><p><b>METHODS</b>The kindling seizure was induced by ip injection with subconvulsant dose of pentylenetetrazole every 48 h. Monoamines and their metabolites were measured using a HPLC system and fluorometric assay.</p><p><b>RESULT</b>Chronic low histamine feeding markedly decreased histamine content in cortex and hypothalamus, and promoted seizure development induced by pentylenetetrazole. However, alahistidine feed reversed the decreased histamine content and slowed seizure development caused by low histamine feed. Both low histamine and alahistidine feed had no effect on norepinephrine, dopamine and its metabolites.</p><p><b>CONCLUSION</b>Alahistidine may affect histaminergic system and seizure development.</p>