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 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.

Objective Hirsutella sinensis (HS) is the anmorph of Ophiocordyceps sinensis (Cordyceps sinensis). O.sinensis and Panax notoginseng are two popular Chinese herbs, commonly used in traditional Chinese prescriptions for the treatment of various diseases. A combination of HS extract with P. notoginseng saponin (PNS) extract demonstrated more prominent lung-protective activity than the two herbs individually used in our preliminary studies. This study further investigated the action of their combination (HSPNS) on anti pulmonary fibrosis using a Bleomycin (BLM)induced mouse model. Methods BLM-treated Kunming mice was given HSPNS daily for 7, 14 or 28 d via ig administration. After treatment, following parameters were monitored using proper methods, respectively. Lung index, serum and lung malondialdehyde (MDA) and hydroxyproline (HYP) contents, lung superoxide dismutase (SOD) activity, transforming growth factor β1 (TGF-β1), and expression levels of collagen Ⅰ (Col- Ⅰ) and collagen Ⅲ (Col-Ⅲ). The lung biopsies were also dissected for semiquantitative histological analysis. Results The results indicated that HSPNS significantly reduced lung index, MDA and HYP contents, and expression levels of TGF-β1,Col- Ⅰ, and Col-Ⅲ. The combination also remarkably enhanced SOD activity compared with BLM-induced group.Moreover, the severe pulmonary fibrosis histopathological changes induced by BLM could be attenuated by HSPNS treatment. Conclusion These results suggest that HSPNS could significantly inhibit the progression of pulmonary fibrosis induced by BLM and its inhibitory effect might associate with its ability to scavenge free radicals, decrease TGF-β1 level, and inhibit collagen synthesis.

Objective:To study the effect of flavonoids extracts from semen Astragali complanati (FAC) on the growth of hepatocellular H22 cells and elucidate its action mechanism. Methods:The mouse model bearing H22 tumor cells was established. The effects of FAC on the growth of xenografted H22 tumor, the immune organ, survival time, phagocytic function of macrophages, and lymphocyte transformation in tumor-bearing mice were observed. Results:The growth of H22 transplanted tumor was significantly inhibited by FAC at high, middle and low doses,compared with normal control group (P<0.05). The tumor-inhibiting ratio in cyclophosphamide (CTX) group was similar with that in FAC high-dose group (P>0.05). FAC markedly elongated the survival time of tumor-bearing mice. The high, middle and low doses of FAC elongated the survival time of tumor-bearing mice by 64.9%, 56.7% and 28.1%, which were significantly different with control group (P<0.01). The high, middle and low doses of FAC greatly increased the thymus index and spleen index of tumor-bearing mice (P<0.05, vs control) and elevated the phagocytic function of macrophages and lymphocyte transformation capability (P<0.01, vs control). The effect of CTX on immune function of tumor-bearing mice was opposite with FAC. The difference between CTX group and control group was significant (P<0.01). Conclusion: FAC inhibits the growth of H22 hepatoma, elongates the survival time, and elevates the non-specific immune function of tumor-bearing mice, indicating that FAC maybe exert its anti-tumor effect via regulating immune function of tumor-bearing mice.

[Objective]The study focus on the analgesic effect of polysaccharopeptide(PSP)and discuss the mechanism of this analgesia. [Methods]A total of 80 rats were divided randomly into high dose of psp,medium dose of psp,low doses of psp,positive control group,negative control group.After intragastric(ig) administration of different(high,medium and low)doses of PSP for 6 days,The tail stimulation-vocalization test was used to observe the analgesic effect of PSP.The IL-2 and IL-2R expression in mediobasal hypothalamus(MBH) was studied immunohistochemically.[Results]After intragastric(ig) administration of PSP for 6 days,the pain threshold was increased significantly and a dose-effect relationship was observed.After PSP administration the IL-2 expression in MBH was increased,while the IL-2R expression in MBH was decreased.[Conclusion]PSP has a definite analgesic effect and its analgesic site is in the MBH.The analgesia might be produced by the binding with the IL-2R in MBH by IL-2 secreted by T cells after PSP was injected into the brain.

Aim To study the effects of ferulic acid (FA) on E-selectin expression in human umbilical vein endothelial cells (HUVECs) activated by lipopolysaccharide and leukocyte-endothelial cell adhesion. Methods The effects of FA on E-selectin and E-selectin mRNA expression were determined by flow cytometry and reverse transcription polymerase chain reaction. The effect of FA on HL60-HUVEC adhesion was evaluated with the method of staining the cells by Rose Bengal. Results The expression of tively). Conclusion FA can inhibit the expression of E-selectin and E-selectin mRNA and HL60-HUVEC adhesion. This may contribute to its protective effect against ischemia-reperfusion injury.

Aim To study the effects of aspirin on increasing the atherosclerotic plaque stability and its possible mechanisms.Methods The hyperlipidemic atherosclerotic model was generated in male New Zealand rabbits given high fat diet and endothelial abrasion of abdominal aorta.These rabbits were then treated with aspirin 5～20 mg?kg-1 for 4 weeks.At experimental end,the plaques were evoked into rupture by injection of Russell's viper venom and histamine.Areas of thrombosis on atherosclerotic aorta were determined by image analysis,morphologic character of plaque rupture was examined by light microscope,the protein expression of macrophages was detected by immunohistochemistry,and the mRNA expression of COX-2 and MMP-2 was determined by hybridization in situ,respectively.Results Aspirin at doses of 5～10 mg?kg-1 was able to inhibit thrombosis on atherosclerotic plaque(P

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 effects of Quercetin on the angioge ne sis and cultured human vascular endothelial cells (HUVEC).Methods In vivo, the effects of Quercetin on angiogenesis induced by vascular en dothelial growth factor (VEGF) and basic fibroblast growth factor(bFGF), were observ ed by chorioallantioic membrane (CAM) test. The effects of quercetin on proliferation of human vascular endothelial cells (HUVEC) were assessed by MTT assay. The effects of Quercetin on cell cycle of HUCEC were observed by flow cytometer (FCM ).Results The angiogenesis induced by VEGF in CAM was strongly inhibited by Quercetin with 0.1, 0.05 and 0.025 mmol?L -1; The angiogen esis induced by bFGF in CAM. was strongly inhibited by Quercetin with 0.1 and 0 .05 mmol?L -1. Quercetin markedly inhibited the proliferation of HUVEC with 240,120,60 and 30 ?mol?L -1. The inhibition rate was 67.0%,58.1% ,39.7% and 20.7% respectively. Quercetin at the concentration of 240 ?mol? L -1 and 120 ?mol?L -1 resulted in S,G 2 arrest of HUVEC. Conclusion Quercetin has substantial inhibitory effects on angiogenesi s induced by VEGF and bFGF, and on proliferation of HUVEC.