Objective:To investigate the effect of compound Sanggou granules on the activity of Fib, AT-Ⅲ, t-PA, PAI-1 and t-PA/ PAI-1 in hyperlipidemic rats. Methods: The hyperlipidemic rat model was established by feeding high fat diet to SD male rats. Sixty healthy SD rats were randomly divided into five groups: the normal diet control group, high fat control group, high dose drug group, low dose drug group and fluvastatin sodium group. Four weeks after the administration, the blood samples were withdrawn for the determination of the levels of blood lipid, Fib, A-Ⅲ, t-PA, PAI-1 and t-PA/ PAI-1. Results:Compared with those of the normal diet control group, the levels of TC, LDL-C, Fib and PAI-1 were increased and the levels of HDL-C, t-PA , AT-Ⅲand t-PA/ PAI-1 were decreased significantly (P<0. 01) in the high fat control group. Compared with those of the high fat control group, the levels of TC, LDL-C, PAI-1 and Fib were decreased(P<0. 01 or P<0. 05),and the levels of HDL-C, t-PA AT-Ⅲ and t-PA/PAI-1 were in-creased significantly in the high dose drug group (P<0. 05 or P<0. 01). The similar effects were shown in the fluvastatin sodium group with the stability of AT-Ⅲ. The levels of TC, LDL-C and PAI-1 were decreased and the levels of t-PA/PAI-1 were increased no-tably in the low dose drug group. Conclusion: Compound Sanggou granules exhibit hypolipidemic effect in hyperlipidemic rats, and can improve hypercoagulability and enhance anticoagulation and fibrinolytic activity in hyperlipidemic rats. Furthermore, compound Sanggou granules at high dose show the same effect as fluvastatin sodium, even in anticoagulation, the granules are superior to fluvasta-tin sodium.

Objective To investigate the effect of resveratrol on miRNA-106b in Alzheimer′s disease ( AD ) animal model.Methods Fifty Kunming male mice were divided into five groups by completely randomized block sampling.The five groups included three dosage resveratrol groups , an AD model group and a control group.The AD models were established in one month prior to treatments. Subsequently, from the 31st day various doses of resveratrol were provided intragastricly for 60 days.Then the memory function was observed by the step-down test.Meanwhile, the varying expressions of APP , P62, ApoA1, miRNA-106b, ABCA1 were tested in each group to determine whether there is the binding site for miRNA-106b in APP 3′UTR sequence.Results Compared with the control group by step-down test, the memory function of the AD model group mice decreased in different degree , which in the drug treatment group was higher than that in the model group (P<0.05).Compared with the AD group, the expression of APP (1.131 ±0.035) in the drug treatment group was higher than that in the model group (0.652 ± 0.026), while the P62 (0.412 ±0.022) and ApoA1 (0.534 ±0.032) were lower than the model group ( all P<0.05 ).High and medium dose groups of resveratrol treatment reduced varying degrees of APP (0.733 ±0.018,0.929 ±0.019,F=177.733) levels, and increased P62(0.954 ±0.035,0.633 ±0.015, F=434.5 ) and ApoA1 ( 1.042 ±0.051, 0.824 ±0.034, F=286.582 ) levels ( all P<0.05 ).The expression of miRNA-106b (0.464 ±0.313) and ABCA1(0.293 ±0.042) in the model group was lower than that in the control group (miRNA-106b 1.064 ±0.032, F=238.159; ABCA1 0.781 ±0.027,F=341.61;both P<0.05).The miRNA-106b (0.843 ±0.034, 0.601 ±0.012) and ABCA1 (0.882 ± 0.025, 0.624 ±0.036) levels in the high, medium dose resveratrol treatment groups increased to different extent ( both P<0.05 ).After the drug treatment , luciferase reporter vector experiments showed that the APP 3′UTR sequence contains the binding site of miRNA-106b.Conclusions APP is one of the target genes of miRNA-106b.Resveratrol is capable of improving AD by enhancing the expression of miRNA-106b and down-regulating the target genes including APP , P62 and ApoA1.This provides a new theoretical basis for the clinical treatment of AD.

Aim To establish the rat model of Spleen-Qi deficiency, analyse the metabolic pathways and investigate the connection between the changed urinary metabolites and Spleen-Qi deficiency, in order to explore the potential mechanisms of Spleen-Qi deficiency.Methods With the binding methods of diarrhea induced by bitter and cold, abnormal of starvation and excessive tiredness, the rat Spleen-Qi deficiency model was established.Then the activity of creatine phosphokinase(CPK) was detected.The endogenous metabolites in the urine were detected by NMR, and the data were analyzed with multivariate and statistical methods.Then the metabolites were selected that could be clearly distinct in the two groups with the fold change value(>1.2) and the P<0.05 of Student′s t-test.Both the pathway analysis and enrichment analysis were performed with Metabo Analyst 3.0.Results Compared with the normal rats, the activity of CPK decreased significantly in model rats(P<0.05).A significant separation appeared in the principal components analysis(PCA) score plot when the control group and the model group were compared, indicating that the Spleen-Qi deficiency model was successfully duplicated.The 33 differential metabolites, which mainly involved in the metabolic pathways, were distinguished from the comparision of Spleen-Qi deficiency model group and control group.The metabolic pathways was related to energy metabolism, amino acid metabolism, nucleotide metabolism and disturbance of gut microbes.Conclusions The main energy metabolic pathways (tricarboxylic acid cycle, glycolysis and liquid oxidation) may be disturbed in Spleen-Qi deficiency rats.The energy supply function is suppressed, which leads to the fatigue and weight loss in rats.

About 80％ of the patients with pancreatic cancer have glucose metabolism alterations,which suggests an association between diabetes and the occurrence and development of pancreatic cancer.Studies have shown that diabetes and hypoglycemic agents are closely related to the occurrence risk,clinical manifestation and prognosis of pancreatic cancer.Recent findings demonstrate that insulin resistance,hyperinsulinemia,the expression level of insulin-like growth factor related protein and inflammatory reaction are the possible mechanisms of the interaction between diabetes and pancreatic cancer.However,the definite mechanism still remains unclear,and further researches are still needed.