RESUMO
Objective: To observe the effect of Shenqi compound recipe on glucose and lipid metabolism in patients with Qi and Yin deficiency and blood stasis syndrome newly diagnosed type 2 diabetes mellitus (T2DM), and its intervention effect on intestinal microecology and serum proinflammatory factors. Method: The 106 eligible patients were divided into the observation group (54 cases) and the control group (52 cases) by random number table method. Another 40 healthy volunteers in physical examination center of the hospital during the same period were enrolled as health control group. On the basis of Guidelines for the Prevention and Treatment of Type 2 Diabetes in China(2013 edition), control group was provided lifestyle interventions, such as reasonable diet, weight control, moderate exercise, salt restriction, tobacco control, alcohol restriction and psychological balance. In addition to the therapy of the control group, the observation group was given Shengi compound for oral administration, 2 times/days. Both groups were treated for 8 weeks. The fasting blood glucose (FBG), postprandial 2 h blood glucose (PBG), glycosylated hemoglobin (HbA1c), homeostasis model assessment-insulin resistance index (HOMA-IR), total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) before and after treatment were evaluated. The structure and quantity of intestinal flora before and after treatment were detected. The traditional Chinese medicine(TCM)symptom was scored. The levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α) were measured before and after treatment. Result: FBG, PBG, HbA1c and HOMA-IR levels in observation group were lower than those in control group (PPPPβ, IL-6, IL-8 and TNF-α levels in observation group were lower than those in control group (PZ=2.134, PConclusion: Shenqi compound can regulate blood glucose and blood lipid in patients with newly diagnosed T2DM (Qi and Yin deficiency and blood stasis syndrome), improve IR, intestinal microecology imbalance, and reduce non-specific inflammatory response, with a good clinical efficacy on intestinal microecology of patients with Qi and Yin deficiency and blood stasis syndrome newly diagnosed type 2 diabetes mellitus.
RESUMO
<p><b>OBJECTIVE</b>To explore the possible neurophysiologic mechanisms of propofol and N-methyl-D- aspartate (NMDA) receptor antagonist against learning-memory impairment of depressed rats without olfactory bulbs.</p><p><b>METHODS</b>Models of depressed rats without olfactory bulbs were established. For the factorial design in analysis of variance, two intervention factors were included: electroconvulsive shock groups (with and without a course of electroconvulsive shock) and drug intervention groups [intraperotoneal (ip) injection of saline, NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed rats without olfactory bulbs were randomly divided into 6 experimental groups (n=10 per group): ip injection of 5 ml saline; ip injection of 5 ml of 10 mg/kg MK-801; ip injection of 5 ml of 10 mg/kg MK-801 and a course of electroconvulsive shock; ip injection of 5 ml of 200 mg/kg propofol; ip injection of 5 ml of 200 mg/kg propofol and a course of electroconvulsive shock; and ip injection of 5 ml saline and a course of electroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water maze test. The content of glutamic acid in the hippocampus was detected by high-performance liquid chromatography. The expressions of p-AT8Ser202 in the hippocampus were determined by Western blot analysis.</p><p><b>RESULTS</b>Propofol, MK-801 or electroconvulsive shock alone induced learning-memory impairment in depressed rats, as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up-regulated by electroconvulsive shock and down-regulated by propofol, but MK-801 had no significant effect on glutamic acid content. Levels of phosphorylated Tau protein p-AT8Ser202 in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8Ser202 levels induced by electroconvulsive shock.</p><p><b>CONCLUSION</b>Electroconvulsive shock might reduce learning-memory impairment caused by protein Tau hyperphosphorylation in depressed rats by down-regulating glutamate content.</p>