A new isoflavone from the stems of Derris eriocarpa How.

A preliminary screening test was performed to discover new antihyperlipidaemic active compounds from the leguminous plant Derris eriocarpa How. A new compound, derris-isoflavone F (1), and derrubone dimethyl ether (6), a known synthetic compound of natural origin, were isolated from the stems of D. eriocarpa alongside eight recognised compounds. To our knowledge, this is the first instance of documenting the identification of compounds 1-10 from this plant. The new compound were evaluated for their antihyperlipidemic and antiproliferative properties. Compound 1 evidently reduced the triglyceride (TG) content in oleic acid-treated HepG2 cells, which validated its efficacy as a potential TG-lowering agent.

Silencing profilin-1 inhibits gastric cancer progression via integrin ß1/focal adhesion kinase pathway modulation.

AIM: To investigate the role of profilin-1 (PFN1) in gastric cancer and the underlying mechanisms. METHODS: Immunohistochemical analysis, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to detect PFN1 expression in clinical gastric carcinoma and adjacent tissues, and the association of PFN1 expression with patient clinicopathological characteristics was analyzed. PFN1 was knocked down to investigate the role of this protein in cell proliferation and metastasis in the SGC-7901 cell line. To explore the underlying mechanisms, the expression of integrin ß1 and the activity of focal adhesion kinase (FAK) and the downstream proteins extracellular-regulated kinase (ERK)1/2, P38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K), AKT and mammalian target of rapamycin (mTOR) were measured through Western blot or qRT-PCR analysis. Fibronectin (FN), a ligand of integrin ß1, was used to verify the correlation between alterations in the integrin ß1/FAK pathway and changes in tumor cell aggressiveness upon PFN1 perturbation. RESULTS: Immunohistochemical, Western blot and qRT-PCR analyses revealed that PFN1 expression was higher at both the protein and mRNA levels in gastric carcinoma tissues compared with the adjacent tissues. In addition, high PFN1 expression (53/75, 70.4%) was correlated with tumor infiltration, lymph node metastasis and TNM stage in gastric cancer, but not with gender, age, location, tumor size, or histological differentiation. In vitro experiments showed that PFN1 knockdown inhibited the proliferation of SGC-7901 cells through the induction G0/G1 arrest. Silencing PFN1 inhibited cell migration and invasion and down-regulated the expression of matrix metalloproteinase (MMP)-2 and MMP9. Moreover, silencing PFN1 reduced the expression of integrin ß1 at the protein level and inhibited the activity of FAK, and the downstream effectors ERK1/2, P38MAPK, PI3K, AKT and mTOR. FN-promoted cell proliferation and metastasis via the integrin ß1/FAK pathway was ameliorated by PFN1 silencing. CONCLUSION: These findings suggest that PFN1 plays a critical role in gastric carcinoma progression, and these effects are likely mediated through the integrin ß1/FAK pathway.

[Path analysis of lifestyle habits to the metabolic syndrome].

OBJECTIVE: To evaluate the relationship between lifestyle habits and the components of metabolic syndrome (MS). METHODS: Based on the routine health check-up system in a certain Center for Health Management of Shandong Province, a longitudinal surveillance health check-up cohort from 2005 to 2010 was set up. There were 13 225 urban workers in Jinan included in the analysis. The content of the survey included demographic information, medical history, lifestyle habits, body mass index (BMI) and the level of blood pressure, fasting blood-glucose, and blood lipid, etc. The distribution of BMI, blood pressure, fasting blood-glucose, blood lipid and lifestyle habits between MS patients and non-MS population was compared, latent variables were extracted by exploratory factor analysis to determine the structure model, and then a partial least squares path model was constructed between lifestyle habits and the components of MS. RESULTS: Participants'age was (46.62 ± 12.16) years old. The overall prevalence of the MS was 22.43% (2967/13 225), 26.49% (2535/9570) in males and 11.82% (432/3655) in females. The prevalence of the MS was statistically different between males and females (χ(2) = 327.08, P < 0.01). Between MS patients and non-MS population, the difference of dietary habits was statistically significant (χ(2) = 166.31, P < 0.01) in MS patients, the rate of vegetarian, mixed and animal food was 23.39% (694/2967), 42.50% (1261/2967) and 34.11% (1012/2967) respectively, while in non-MS population was 30.80% (3159/10 258), 46.37% (4757/10 258), 22.83% (2342/10 258) respectively. Their alcohol consumption has statistical difference (χ(2) = 374.22, P < 0.01) in MS patients, the rate of never or past, occasional and regular drinking was 27.37% (812/2967), 24.71% (733/2967), 47.93% (1422/2967) respectively, and in non-MS population was 39.60% (4062/10 258), 31.36% (3217/10 258), 29.04% (2979/10 258) respectively. The difference of their smoking status was statistically significant (χ(2) = 115.86, P < 0.01) in MS patients, the rate of never or past, occasional and regular smoking was 59.72% (1772/2967), 6.24% (185/2967), 34.04% (1010/2967) respectively, while in non-MS population was 70.03% (7184/10 258), 5.35% (549/10 258), 24.61% (2525/10 258) respectively. Both lifestyle habits and the components of MS were attributable to only one latent variable. After adjustment for age and gender, the path coefficient between the latent component of lifestyle habits and the latent component of MS was 0.22 with statistical significance (t = 6.46, P < 0.01) through bootstrap test. Reliability and validity of the model:the lifestyle latent variable: average variance extracted was 0.53, composite reliability was 0.77 and Cronbach's a was 0.57. The MS latent variable: average variance extracted was 0.45, composite reliability was 0.76 and Cronbach's a was 0.59. CONCLUSION: Unhealthy lifestyle habits are closely related to MS. Meat diet, excessive drinking and smoking are risk factors for MS.