Idiopathic pulmonary fibrosis(IPF), with unknown pathogeny, is an interstitial lung disease.The pathological features are diffuse epithelial-cell lesion, fibroblast proliferation, myofibroblast differentiation and excessive extracellular matrix deposition.CXCR4 is the predominant chemokine receptor on fibrocytes;CXCL12 is the only ligand of CXCR4.A large number of studies have shown that CXCL12/CXCR4 biological axis plays an important role in the pathogenesis of idiopathic pulmonary fibrosis.Under the regulation of hypoxia, HIF-1α and PI3K-Akt-mTOR path, CXCL12/CXCR4 biological axis promotes lung fibroblast proliferation, myofibroblast differentiation and extracellular matrix deposition, resulting in development and progression of IPF.

Aim To investigate the effect of puerarin(Pue)on the experimental insulin resistance(IR)and the mechanism of Pue-treated metabolic syndrome(MS).Methods IR rat model was induced by i.v.small dosage streptozotocin(STZ)and high fatty diet.The effect of Pue on insulin sensitivity was studied by reformed hyperinsulinism euglycemia clamp technique(HEPC)on IR rats.Results The basic blood glucose(BBG),basic blood plasma insulin(BINS)and stable basic blood plasma insulin(SINS)of IR rats induced by high-fat feed were higher than those of control group,and those of the group treated by Pue were observably lower than those of IR model group.In HECT text,the average rate of glucose injection of IR model group was lower than that of control group from 60 min to 120 min,but the rate of high dose and middle dose of Pue group was significantly higher than that of IR model group.Conclusion The results suggest that Pue can improve the insulin sensitivity,and reduce basic blood glucose and blood plasma insulin of the experimental insulin resistance rats.

Aim To investigate the mechanisms in protecting HUVEC against ischemia/reperfusion(I/R) injury directed by curcumin.Methods Hypoxia/reoxgenation(H/R) model was established on HUVEC.MTT colorimetric assay was used to observe the injury degree of hypoxia and reoxygenation at the different time.With preconditioning by different concentration of Cur,the survival rate of HUVEC subjected to H/R was assessed by MTT colorimetric assay.Pretreated with Cur(5 ?mol?L-1),the expression of LC3,cathepsin B,cathepsin L,Bax and Bcl-2 were observed by fluorescent staining and Western blot in HUVEC during H/R process.Results Cur(1.25~5 ?mol?L-1) played a protective role during H/R in HUVEC in a dose-dependent manner.During H/R,the expressions of LC3,cathepsin B and the ratio of Bax/Bcl-2 increased,and the nuclear translocation of cathepsin L was induced;when cur was pretreated,LC3 was furtherstrengthened,at the same time,the up-regulation of cathepsin B,the ratio of Bax/Bcl-2 and the nuclei-location of cathepsin L were inhibited partly by Cur.Conclusions Cur can raise the survival rate of HUVEC in the process of H/R.Cur increases the autophagy activity,depresses cathepsins and Bax/Bcl-2 to protect the endothelial cells.

Aim To study the inhibitory effects and its mechanisms of oridonin on human pancreas adenocarcinoma SW1990 cells.Methods Cell growth inhibition mediated by oridonin on SW1990cells was measured by MTT assay.The morphological changes were observed by Hoechst33258 fluorochrome staining and electron microscope.Cell cycle and apoptosis rate were analyzed by flow cytometry. The molecular mechanisms involved in the effects of oridonin on SW1990 cells were studied by RT-PCR.Results The growth of humen pancreas adenocarcinoma SW1990 cells was significantly inhibited by oridonin.Apoptosis morphological changes about chromatic agglutination and nuclear condensation were detected by Hoechst 33258 fluorochrome staining and electron microscope in oridonin treated SW1990 cells."Sub-G_1" phase peak and G_2/M growth arrest werer found with flow cytometry.The upregulating mRNA expression of p21 and downregulating mRNA expression of survivin were detected by RT-PCR.Conclusion The inhibitory effect of oridonin on human pancreas adenocarcinoma SW1990 cells through induced apoptosis and G_2/M growth arrest and the mechanisms may be through surviving-p21 co-regluation pathway.

Osteopontin (OPN) is a secreted O-glycosylated phosphoprotein that exists in a variety of tissues and body fluids, with a variety of biological activity. Integrin α_vβ_3 is the main receptor. OPN mainly involves in cell proliferation, differentiation, migration and adhesion. The study of OPN at home and abroad mainly focuses on the bone resorption, angiogenesis, atherosclerosis, digestive system, urinary system, wound healing, skin fibrosis, liver fibrosis, kidney fibrosis, etc.But reports about OPN in pulmonary fibrosis are much less, now the relationships between OPN and pulmonary fibrosis are reviewed.