ABSTRACT
The teaching effect of "process management and evaluation" was assessed in resident standardization training plan in acupuncture-moxibustion department of hospital for postgraduates of non-acupuncture-moxibustion speciality. A total of 120 postgraduates of non-acupuncture-moxibustion speciality participating in resident standardization training were randomized into an observation group (60 cases) and a control group (60 cases, 1 case dropped off). In the control group, the conventional training mode was used. In the observation group, the "process management and evaluation" was adopted, in which, the syllabus was refined, various teaching modes were cooperated and the summary was conducted once a week. The training results were evaluated at the end of 1-month shift test and questionnaire was issued in all of the postgraduates of the two groups. In the observation group, the score for theory and the score of each of the items for technical ability, named differentiation and treatment, technical manipulation and physician-patient communication, as well as the total score were all higher than the control group successively (
Subject(s)
Humans , Acupuncture , Acupuncture Therapy , Hospitals , Moxibustion , Reference StandardsABSTRACT
Aim To clarify the role of autophagy in the regulation mechanism of epithelial-mesenchymal transition(EMT) in hepatocytes and the transition to myofibroblast. Methods BNL CL. 2, a mouse embryonic hepatocyte, and BNL CL. 2 cells knocked-down BECN1 genes were treated with TGF-β1(2 μg . L-1) and curcumin(10, 20, 30 jimol • L - 1 ) . Real-time PCR and Western blot were used to detect Beclin-1, LC3, Vimentin and α-SMA gene and protein expression in BNL cl. 2 cells. The optical microscope was used to observe the changes of cell morphology. And the changes in cell autophagy were detected by GFPLC3 plasmid transfection. Results After the intervention of TGF-β1, the expression of Vimentin and α-SMA, the mesenchymal marker, increased and the autophagy decreased. Curcumin could inhibit Vimentin and a-SMA expression in hepatocytes. Moreover, curcumin could increase the autophagy related genes and protein expression of Beclin-1 and LC3 in hepatocytes. Curcumin could increase the level of autophagy and inhibit the cell transformation to myofibroblast-like cells. After interfering with BECN1, the effect of curcumin inhibiting hepatic EMT was partially blocked. Conclusions Curcumin could inhibit the process of EMT of hepatocytes by increasing the level of autophagy. The occurrence and development of liver fibrosis was consequently inhibited.
ABSTRACT
Objective:To construct oxaliplatin (L-OHP) drug-resistant cell line HCT-116/L-OHP in human colon cancer, in order to observe the reversal effect of curcumin (cur) on its drug resistance, and preliminarily explore the possible drug resistance mechanism. Method:The concentration gradient increasing method was used to gradually increase the L-OHP concentration of HCT-116 in parental colon cancer cells, and the cell line HCT-116/L-OHP resistant to L-OHP was established. The cytotoxicity of L-OHP and curcumin to HCT-116 and HCT-116/L-OHP cells was detected by cell counting kit-8(CCK-8) method to observe whether curative resistance could be reversed. Western blot was used to detect the expressions of drug-resistance-related proteins. Real-time PCR was used to detect changes in related genes. Result:Human colon cancer cell line resistant to L-OHP were successfully established and named as HCT-116/L-OHP, with a drug resistance index of 12.6.Compared with HCT-116 cell lines, the expression levels of resected and repaired cross complementation gene 1 (ERCC1) protein and gene in HCT-116/L-OHP cell lines were significantly increased (PP-1), the expression of ERCC1 decreased (PPConclusion:HCT-116/L-OHP cell lines have a stable drug resistance, and its drug resistance mechanism may be up-regulated with the expression of ERCC1, which leads to the up-regulation of Bcl-2,GST-π,MRP,P-gp,Survivin and other related proteins, and enables tumor cells to acquire drug resistance. Curcumin can reverse the drug resistance of HCT-116/L-OHP, and its mechanism may be to reduce the expression of ERCC1, thereby down-regulating the expressions of Bcl-2,GST-π,MRP,P-gp,Survivin and other drug-resistant related genes and proteins, and increase the sensitivity of tumor to L-OHP, so as to reverse the drug resistance of tumor cells.