Efficacy and safety of Sancai powder in patients with type 2 diabetes mellitus: a randomized controlled trial.

OBJECTIVE: To assess the efficacy and safety of Sancai powder in patients with type 2 diabetes mellitus (T2DM) inadequately controlled with single oral metformin in a randomized controlled trial (RCT). METHODS: A total of 132 patients with T2DM were enrolled in the study, who only took metformin (500-1000 mg/day) for at least three months and with inadequate glycemic control (7.0% ≤ hemoglobin A1c ≤ 9.0% ) in the past three months. The patients stopped taking metformin with lifestyle interventions for three weeks, and 105 patients qualified for the program. They were randomly divided into the Sancai powder group and the metformin group (1500 mg/day). The follow-up period was for 12 weeks. Comparisons of several variables were analyzed. RESULTS: No significant differences were found between the two groups in hemoglobin A1c (HbA1c), fasting plasma glucose (FPG) and 2 h post-meal glucose (2hPG), although they had decreased significantly (P < 0.01). Homeostasis model assessment of beta cell function index was significantly improved in Sancai powder group (P < 0.01), and there were significant differences in the changes of homeostasis model assessment of insulin resistance and insulin sensitivity index in the two groups (P < 0.05). Sancai powder significantly reduced triglyceride level (P < 0.05), although there was no significant difference in the body weight and body mass index in the two groups. CONCLUSION: In this 12-week study, Sancai powder could significantly reduce hemoglobin A1c, FPG and 2hPG levels, improved beta-cell function and insulin resistance of the T2DM inadequately controlled with metformin.

High glucose induces activation of NF-κB inflammatory signaling through IκBα sumoylation in rat mesangial cells.

The posttranslational modification of proteins by small ubiquitin-like modifiers (SUMOs) has emerged as an important regulatory mechanism for the alteration of protein activity, stability, and cellular localization. The latest research demonstrates that sumoylation is extensively involved in the regulation of the nuclear factor κB (NF-κB) pathway, which plays a critical role in the regulation of inflammation and contributes to fibrosis in diabetic nephropathy (DN). However, the role of sumoylation in the regulation of NF-κB signaling in DN is still unclear. In the present study, we cultured rat glomerular mesangial cells (GMCs) stimulated by high glucose and divided GMCs into six groups: normal glucose group (5.6mmol/L), high glucose groups (10, 20, and 30mmol/L), mannitol group (i.e., osmotic control group), and MG132 intervention group (30mmol/L glucose with MG132, a proteasome inhibitor). The expression of SUMO1, SUMO2/3, IκBα, NF-κBp65, and monocyte chemotactic protein 1 (MCP-1) was measured by Western blot, reverse-transcription polymerase chain reaction, and indirect immunofluorescence laser scanning confocal microscopy. The interaction between SUMO1, SUMO2/3, and IκBα was observed by co-immunoprecipitation. The results showed that the expression of SUMO1 and SUMO2/3 was dose- and time-dependently enhanced by high glucose (p<0.05). However, the expression of IκBα sumoylation in high glucose was significantly decreased compared with the normal glucose group (p<0.05). The expression of IκBα was dose- and time-dependently decreased, and NF-κBp65 and MCP-1 were increased under high glucose conditions, which could be mostly reversed by adding MG132 (p<0.05). The present results support the hypothesis that high glucose may activate NF-κB inflammatory signaling through IκBα sumoylation and ubiquitination.