According to the theory of traditional Chinese medicine, blood stasis is a main pathological mechanism in the development of vascular diseases. Supplementing Qi and activating blood circulation, as the therapeutic principle for the blood stasis, has been adapted. Studies demonstrated that the supplementing Qi and activating blood circulation recipe could regulate the expression of vasoactive peptides in vascular smooth muscle cells (VSMCs). The recipe inhibited the formation of neointima following arterial intimal lesions through down-regulating expression of proliferation-related genes and phenotypic modulation of VSMCs. The recipe also markedly inhibited the adhesion and migration of VSMCs and matrix remodelling by means of a mechanism that balances extracellular matrix turnover rate. The purpose of this review is to summarize the recent advances made in our understanding of new functions for the recipe in regulating VSMCs behaviours and their microenvironment relevant to vascular diseases and maintaining proper homeostasis.

The technique of genomics and proteomics is one of the fastest developments with the farest-reaching consequences in the high and new biotechnology in the world of today. It can be used to screen the target molecules of the action of traditional Chinese medicines, to identify the new effective components from traditional Chinese medicines, and to explore the mechanisms of the effects of traditional Chinese medicines. It meets the shortcomings of the conventional methodology being applied in the current studies of traditional Chinese medicine. Application of the theories and technique of genomics and proteomics in the study of traditional Chinese medicine would be of great significance for opening new research field of traditional Chinese medicine, for facilitating the integration of traditional Chinese medicine and modern biological science and technology, and for promoting the internationalization of traditional Chinese medicine.

Objective To study the relationship between the lipoprotein associated phospholipase A2 (LP-PLA2) with the carotid plaques cerebral infarction,and study the predictive value of LP-PLA2 in carotid artery plaque stability.Methods According to the results of color doppler ultrasound examination of carotid artery,169 patients with cerebral infarction were random divided into cerebral infarction with carotid plaques group (101 patients) and cerebral infarction without carotid plaques group(68 patients) groups.According to the nature of plaque stability of carotid plaques.101 cases of cerebral infarction with carotid plaques group was divided into plaques group 30 cases and 71 cases of unstable plaque group.Set healthy control groups at the same time.Then detected level of LP-PLA2 for each patient by the method of double antibody sandwich enzyme-linked immunosorbent (ELISA).To evaluate the predictive value of LP-PLA2 in carotid artery plaque stability by mapping the receiver-operating characteristic (ROC) curve.Results The level of LP-PLA2 (212.90± 117.69 ng/ml) in carotid plaques group were significantly higher than those without plaque group (127.70 ± 57.96 ng/ml,t=3.016,P ＜0.01).It was not show significantly difference between no plaque group and healthy control group (108.34 ± 42.58 ng/ml,t=0.779,P＞0.05).But it showed significantly different between the unstable plaque group (236.24 ± 128.33 ng/ml)and stability plaques group (157.65±59.27 ng/ml,t=3.442,P＜0.01).Conclusion The LP-PLA2 of plasma could be involved in the development of atherosclerosis plaques.The LP-PLA2 can certain correlation with cerebral infarction of carotid plaques,can well evaluate the stability of carotid plaques.

CD8-Positive T-Lymphocytes ; immunology ; Dendritic Cells ; immunology ; Hepatitis B ; immunology ; therapy ; Hepatitis B Surface Antigens ; immunology ; Humans

Objective: To construct a phage-displayed random combinatorial library of IgA affibodies and to analyze its directed in vitro evolution, so as to study the relationship of IgA affibody structure with its function. Methods: The coding sequences of two affibodies, ZA1 and ZA2, were generated by overlapping PCR. The affibodies with a random linking peptide coding sequence in the 3′ terminal were randomly ligated and cloned into the K pn I site of the phagemid pCANTAB5S to construct a combinatorial phage library. Totally four rounds of in vitro human IgA directed evolution were conducted, and selected phage clones were prepared individually to test the IgA binding activity by ELISA technology. Results: The combinatorial phage library was successfully constructed; it contained about 3.4 × 107 clones with a titer of 1.6 × 1012 TU/L, and the positive clones accounted for more than 79%. Sequence analysis showed that the two single affibodies were randomly linked by random linking peptides. The composition of the phage clones displaying three or four affibodies in tandem increased remarkably along with the rounds of selection, which indicated the successful IgA directed evolution. Three new arrangements of two, three or four affibodies in tandem were obtained. ELISA results demonstrated a significantly enhanced IgA binding activity of three or four affibodies in tandem. Conclusion: A series of new IgA binding recombinants have been obtained by directed in vitro evolution of combinatorial phage library displaying randomly linked IgA affibodies. The three or four affibodies in tandem have much higher IgA binding activity than others, indicating that the in vitro molecular evolution is an effective way to produce IgA binding proteins with high activity.

Objective:To investigate the effects of exenatide on podocyte in diabetic nephropathy mice.Methods:Diabetic nephropathy mice models were induced by using streptozocin-treated C57BL/6J mice on high fat diets, which were randomized by random number table to diabetic nephropathy control group (DN group, n=8) and exenatide treatment diabetic nephropathy group (DN+ Ex group, n=8). The C57BL/6J mice on normal chow diet were used as normal control group (NC group, n=8). After the intervention, blood glucose, renal function, and urine albumin/creatinine ratio were measured. Pathological glomerular changes were observed by pexiodic acid-Schiff stain (PAS) staining. The mRNA expression of profibrotic molecules Collagen Ⅳ, transforming growth factor-β (TGF-β), and Fibronectin in glomerular lysates were measured by realtime quantitative PCR (RT-PCR). Podocyte injury and apoptosis were evaluated by immunofluorescent staining and transmission electron microscopy. The expression of Nephrin, Cleaved caspase-3, protein kinase B (Akt), and phosphorylated Akt (p-Akt) in glomerular lysates were examined by western blotting. Results:Compared with the DN group, urine albumin/creatinine ratio was significantly decreased in the DN+ Ex group ( P<0.01). PAS staining and analysis found that exenatide administration ameliorated mesangial matrix expansion and glomerular hypertrophyin in DN group ( P<0.05). RT-PCR analyses showed that the glomerular expression for Fibronectin, TGF-β, and Collagen Ⅳ were significantly decreased in the DN+ Ex group compared with the DN group ( P<0.01). Immunofluorescent staining and transmission electron microscopy revealed that exenatide treatment improved podocyte injury and apoptosis in DN group. Western blotting analyses showed that exenatide increased the Nephrin expression, decreased the Cleaved caspase-3 expression, increased the p-Akt expression in glomerular lysatesin diabetic nephropathy mice ( P<0.01). Conclusion:Exenatide attenuates podocyte injury and apoptosis and proteinuria, and prevents the progression of diabetic nephropathy mice. Phosphatidylinositol 3-kinase (PI3K)/Akt pathway in glomerular lysates may be related to the protective effects of exenatide.

China ; Metals, Heavy ; Research Support as Topic ; statistics & numerical data

AIM: To investigate the effect of platelet-derived growth factor (PDGF) on ?_3 integrin gene expression and the role of ?_3 integrin on adhesion, migration and proliferation of vascular smooth muscle cells (VSMC) induced by PDGF. METHODS: ?_3 integrin gene expression was detected by RT-PCR. After ?_3 integrin extracellular domain was blocked, VSMC adhesion, migration and proliferation were measured by adhesion assay, a wound-culture model and [~3H]-TdR incorporation, respectively. RESULTS: After the interaction between ?_3 integrin and extracellular matrix was blocked, VSMC proliferation was inhibited in some degree and the rate of [~3H]-TdR incorporation into VSMC decreased 39%. The cell adhesion and migration were significantly inhibited when 10 mg/L anti-?_3 integrin antibody was added (P

AIM: To study the relationship between expression of ? 3 integrin, focal adhesion kinase (FAK) and migration of vascular smooth muscle cells (VSMC) stimulated by osteopontin (OPN) and fibronectin (FN).METHODS: VSMC migration was examined using a model of wounding injury of confluent cultured cells. The expression of ? 3 integrin, FAK and Gax genes in VSMC were detected using Western blotting and RT-PCR. RESULTS: OPN and FN induced the migration activity of VSMC in a time-dependent manner ( P

Objective To observe the effects of Xinshuaiheji (XSHJ) on cardiac function, plasma angiotensin Ⅱ (AngⅡ) and histomorphology in rats with heart failure after acute myocardial infarction. Methods A model of heart failure (HF) induced by myocardial infarction (MI) in rats was made, 10 days after MI, rats were treated for 4 weeks with bidist Water, Captopril, high dosage of XSHJ, low dosage of XSHJ. The effects of Xinshuaiheji on cardiac function (stroke volume, SV, cardiac output, CO, cardiac index, CI ) and AngⅡ were observed. We also observed and compared the changes of heart weight/body weight ratio (HW/BW), ratio of ventricular wall thinning in MI. Results After treatment with XSHJ, the cardiac function (SV, CO, CI) of HF rats improved (P