Objective To observe the clinical curative effect of Semen Cassiae application on navel in treating essential hypertension. Methods Totally 1674 cases of hypertension, according to visiting sequence, were randomly divided into treatment group (864 cases) and control group (810 cases). The control group was given hydrochloride enalapril 10 mg orally, 2 times a day. The treatment group was treated with Semen Cassiae application on navel, replaced per 24 h. The two groups were treated with moderate exercise, reasonable diet, and the course was 6 months. The clinical symptoms, blood pressure, blood lipid and blood rheology of the two groups were measured before and after treatment. Results To compare the symptoms efficacy, total effectiveness of treatment group was 95.14%(822/864), the control group was 71.11%(576/810), there was a significant difference (P<0.01). To compare antihypertensive effects, the total effective rate of the treatment group was 95.60% (826/864), the control group was 73.46% (595/810), there was a significant difference (P<0.01). The change of blood pressure in the treatment group was significantly better than the control group (P<0.01). TC, TG, HDL-C, LDL-C and blood rheology of the treatment group was significant different between before and after treatment (P<0.01). Conclusion On the basis of western medicine, Semen Cassiae application on navel played a double effect of acupoint and drug. It is more effective in lowering blood pressure, improving the clinical symptoms, blood lipid and blood rheology indexes.

This study was aimed to investigate the effect of intercellular adhesion molecule-1 (ICAM-1) on the migration in vitro of the murine mesenchymal stem cells (MSC) and its related mechanisms. The migration ability of murine MSC (C3H10T1/2), ICAM-1 transfected MSC (C3H10T1/2-MIGR1-ICAM-1) and empty vector-transfected MSC (C3H10T 1/2-MIGR1) were assayed in vitro by using the transwell system. Briefly, the cells were seeded on the membrane with 8 µm aperture and the fetal bovine serum was used as the chemotactic agent to induce MSC migration. The transmigrated cells were stained by crystal purple as well as DAPI for 8 h and 12 h respectively. The absolute cell numbers were counted and the migration rates of MSC were evaluated in each group. To explore the potential mechanisms which control the migration of MSC, the specific chemical inhibitors of MAPK pathway (SB203580, PD98059 and JNK inhibitor II) were added to the transwell system and the alteration of the MSC migration ability were evaluated at 12 h. The results showed that the migration ability at 8 h and 12 h of the ICAM-1-transfected MSC increased. Both absolute cell number and migration rate of MSC were significantly up-regulated by ICAM-1. Furthermore, the promoting effect of ICAM-1 on migration was partially suppressed by the inhibition of JNK/SAPK pathway. The transmigrated cell numbers and the migration rate decreased with the addition of JNK inhibitor II. However, the ICAM-1 promoting migration of MSC was not suppressed by the inhibitors for ERK/MAPK and p38/MAPK pathway did not work in the present study. It is concluded that ICAM-1 can induce mouse MSC migration in vitro, and the promoting effect is partially dependent on the activation of JNK/SAPK pathway.
Animals ; Cell Line ; Cell Movement ; Intercellular Adhesion Molecule-1 ; genetics ; metabolism ; MAP Kinase Signaling System ; Mesenchymal Stromal Cells ; cytology ; metabolism ; Mice ; Transfection