ABSTRACT
Objective To investigate the effect of berberine on glucose absorption and mRNA expression of 11 β-hydroxysteroid dehydrogenase type 1 ( 11β-HSD1 ) in insulin-resistant HepG2 cell model.Methods HepG2 cells were incubated with high-concentration insulin for 24 hours to build insulin-resistant cell model.In order to evaluate the cells for insulin resistance,the cells were cultured with different concentrations of insulin for 24 hours.The insulin-resistant cells were treated with different concentrations of berberine and insulin for 24 hours and the non insulin-resistant cells were used as a control.The glucose concentration in culture medium was detected by the method of glucose oxidase-peroxidase (GOD-POD).According to the glucose concentrations in blank medium and those in the medium of culturing cells 24 hours later,the rate of absorpting glucose by the cells was calculated.The mRNA expression of 11β-HSD1 in the insulin-resistant cells was detected by the reverse transcription polymerase chain reaction (RT-PCR).Results Incubated with 10-7mol/L insulin for 24 h,the insulin-resistant cell model had been built.The rate of glucose absorption of the model cell treated with high concentration berberine ( 10 μmol/L) was significantly improved [(42.53 ±1.99)％ vs (28.16±1.99)％,t =12.9457,P ＜0.01].High-concentration berberine showed a strong synergy with insulin on glucose absorption of the model cells.As the cells became resistant to insulin,the mRNA expression of 11β-HSD1 increased significantly compared to non insulin-resistant cells( relative expression quantity was (4.60 ±0.96 vs 0.67 ±0.42,t =4.9476,P ＜0.05 ).While the mRNA expression of 11β-HSD1 reduced in the insulin-resistant cells after treated with high-concentration berberine,and the relative expression quantity was not significantly different with non insulin-resistant cells ( 1.12 ±0.35 vs 0.67 ±0.42,P ＞0.05).However,low-concentration ( 1 μmol/L) of berberine had not the same role.Conclusions It is concluded that one of the acting mechanism of berberine improving the insulin sensitivity may be that the mRNA expression of 11β-HSD1 is downregulated in the insulin-resist-ant liver cell model depending on concentration.
ABSTRACT
Objective To evaluate the early and mid-term results of endovascular repair for acute and chronic type B aortic dissection, and to compare the clinical outcomes between the 2 groups. Methods From May 2002 to December 2006, 50 patients with type B aortic dissection were treated by endovascular stent-graft. There were 23 patients in the acute aortic dissection (AAD) group and 27 patients in the chronic aortic dissection (CAD) group. All patients were followed up from 1 to 54 months (average, 17±16 months).The immediate and follow-up clinical outcomes were documented and compared between the 2 groups. Results Placement of endovascular stent-grafts across the primary entry tears was technically successful in all 50 patients. Compared to the CAD group, the AAD group had a higher percentage of pleural effusion (17.4% vs. 0%,P=0.04) and visceral /leg ischemia (26.1% vs 3.7%, P=0.04). Procedure related complications, including endoleak and post-implantation syndrome, occurred more frequently in the AAD group than in the CAD group (21.7% vs 3.7% and 30.4% vs 11.1%, respectively; P=0.08 and P=0.04). Kaplan-Meier analysis showed no difference in the survival rate at 4 years between the 2 groups (86.4% vs 92.3%, P=0.42 by log-rank test). However, the event-free survival rate was higher in patients with chronic dissection than in patients with acute aortic dissection (96.2% vs 73.9%; P=0.02 by log-rank test). Conclusions Endovascular repair with stent-graft was safe and effective for the treatment of both acute and chronic type B aortic dissection. However, both immediate and long term major complications occurred more frequently in patients with acute dissection than in those with chronic dissection.