Objective To study the effects of puerarin on proliferation and apoptosis of human gastric cancer MGC-803 and AGS cells.Methods Human gastric cancer cells were treated with puerarin at different concentrations.MTT assay was used to test cell proliferation and FCM was used to detect cell apoptosis.Results The inhibition rates had upwarded trend with increasing concentrations (MGC-803:1.24 ％,2.80 ％,15.10 ％,18.55 ％,59.65 ％; AGS:15.59 ％,25.31％,30.25 ％,36.91％,64.47 ％),when treated with puerarin at different concentrations (1.5,3.0,6.0 12.0,24.0 mmol/L) for 48 hours.Apoptosis rates gradually increased with increasing concentrations (MGC-803:5.49 ％,9.53 ％,13.81％; AGS:6.23 ％,16.38 ％,25.99 ％),when treated with puerarin at different concentrations (0,12.0,24.0 mmol/L) for 24 hours.Conclusion Puerarin inhibits proliferation and induces apoptosis of human gastric cancer cells MGC-803 and AGS.

Objective To discuss the clinical application of coronary CT angiography(CCTA)-derived fractional flow reserve(CT-FFR)in evaluating the risk stratification of the coronary artery stenosis and atherosclerotic plaque quantitative parameters.Methods A total of 122 patients,who received CCTA examination at the Xuzhou Municipal Central Hospital of China,were enrolled in this study.The patients were divided into non-ischemia group(CT-FFR＞0.8,n=66)and ischemia group(CT-FFR0.8,n=56).The characteristics of atherosclerotic plaque were compared between the two groups.Logistic regression analysis was used to analyze the correlation between plaque characteristics and ischemic lesions.Results There were 218 vessels having a CT-FFR＞0.8 and 174 vessels having a CT-FFR ≤0.8.Statistically significant differences in the total plaque volume,calcified plaque volume,plaque length,and stenosis ratio＞50％existed between the two groups(all P＜0.05).Logistic regression analysis indicated that the total plaque volume,calcified plaque volume,plaque length,and stenosis ratio＞50％were the risk factors for myocardial ischemia.Conclusion CT-FFR can be used for the risk stratification of coronary stenosis and atherosclerotic plaque characteristics,which can evaluate the local myocardial blood supply condition from the anatomical stenosis and functional level so as to optimize the diagnosis and treatment measures.

Renal fibrosis, especially tubulointerstitial fibrosis, is the most common pathway of all chronic kidney diseases progressing to end-stage renal diseases. Several adaptive reactions occur in renal tubular epithelial cells after chronic injury, such as changes in glycolipid metabolism, unfolded protein response, autophagy and senescence, epithelial-to-mesenchymal transition and G2/M cell cycle arrest. Maladaptive repair mechanisms can induce tubulointerstitial fibrosis. This article will discuss the molecular mechanism of these adaptive responses of renal tubular epithelial cells driving renal tubulointerstitial fibrosis, and provide a basis for exploring new drug targets for renal tubulointerstitial fibrosis.