The high and continuing soaring incidence of diabetes may become a huge obstacle to China's development. The antidiabetic drug development is one way to solve the problem. Animal model is a powerful tool for drug development. This paper compares and analyzes the three kinds of animal models for antidiabetic drug development in replicating principle, methods and characteristic, then summarized the application in the research of traditional Chinese medicine. At the same time, the analysis of the market, application and clinical advantages of hypoglycemic medicine from traditional Chinese medicine, is given in this paper, based on the literature analysis. From the point of the clinic advantage embodiment and new drug development, this paper will provide advisory and assistance support for the anti-diabetic fighting with traditional Chinese medicine.

Notch signaling, a highly conserved pathway, is wide-ly found in invertebrates and vertebrates. By mediating cell com-munication, it can regulate many physiological and pathological processes in various kinds of cells, including cell proliferation, differentiation and apoptosis in multi-cellular organism. Accu-mulating evidence shows that abnormality in Notch signaling is highly related to diabetes mellitus and its complications. Accord-ingly, this paper reviews the molecular basis of Notch signaling and the relations between its abnormal expression and diabetes mellitus, and focuses on the impact of key elements in the Notch signaling pathway on diabetic complications as well as correlative mechanisms.

[ ABSTRACT] AIM: To investigate the protective effect of mesenchymal stem cell ( MSC)-conditioned medium (MSCCM) on myocardial cell line H9c2 and its mechanism.METHODS:Verification of MSC was performed by flow cy-tometry analysis, followed by MTT assay to determine the optimal incubation time of MSCCM with myocardial cells.The cells were divided into 4 groups:normal ( N) group, model ( M) group, M+MSCCM group and MSCCM group.The cells in M+MSCCM group and MSCCM group were pre-incubated with MSCCM for 24 h.The cells in M group and M+MSCCM group were treated with 300 μmol/L H2 O2 for 4 h to imitate oxidative injury of myocardial cells.Mitochondrial membrane potential and apoptotic rate of injured myocardial cells were detected by flow cytometry.The ROS production was measured by fluorescence microscopy.The nuclear translocation of Nrf2 and expression of HO-1 was examined by Western blot.RE-SULTS:No difference of mitochondrial membrane potential, apoptotic rate or ROS production between MSCCM group and N group was observed (P>0.05).The mitochondrial membrane potential depolarization, apoptotic rate and ROS produc-tion in M+MSCCM group were significantly lower than those in M group ( P<0.01 ) .The nuclear translocation of Nrf2 and expression of HO-1 in the myocardial cells were increased with MSCCM incubation time prolonged.CONCLUSION:MSCCM protects the myocardial cells against oxidative injury induced by H2 O2 .The anti-oxidative mechanism would be as-sociated with the activation of Nrf2/ARE pathway.

With the advanced development of information technology, there is a huge impact on various industries for the arrival of big data. In the biomedical field, innovative genome sequencing technology enables low-cost, high-throughput, and high-speed to become a reality, which leads to an explosive growth in data and also appeared in an urgent need to process those massive biological information. High performance computing (HPC) along with effective methods is one of the best ways to deal with the problem of big data in biomedical field which could serve the biomedical development best. We discussed the issues faced in biomedical big data processing and concluded that the bioinformatics is an indispensable component of biomedical technologies.

Micro RNA (miRNA)were small RNAs encoded by the non-coding RNA genes,which functioned through degrada-tion of mRNA or inhibition of mRNA translation.The miRNA was involved in numerous biological processes,including cell proliferation,apoptosis,development and differentiation.And ectopic expression of miRNA could result in diseases,such as neoplastic hematologic disorder and solid tumor.miR-1 06b-25 cluster contained miR-1 06b,miR-93 and miR-25.These miR-NAs were correlated with the development of tumor.Therefore, we reviewed recent articles on the relationship of miR-1 06b-25 cluster with tumor.

OBJECTIVE:To study the effect and its possible mechanism of Xuezhiping capsule on blood lipid levels of high blood lipid model golden hamsters. METHODS:Golden hamsters were randomly divided into normal control group,model group, atorvastatin group (3 mg/kg),combination group (Xuezhiping capsule 1.3 g/kg+atorvastatin 1.5 mg/kg),Xuezhiping capsule low-dose,medium-dose,high-dose groups(Xuezhiping capsule 1.3,2.6,5.2 g/kg),10 in each group. Hamsters in normal control group received normal diet,the other groups were given high-fat diet to establish high blood lipid model. Then relevant drugs were intragastrically given 2 weeks later. Normal control group and model group were intragastrically given equal volume of distilled wa-ter,once a day,for 4 weeks. After last administration,blood lipid indexes(TG,TC,HDL-C,LDL-C,FFA),mRNA and protein expressions of lipid metabolism related genes (PPAR-α,CYP7A1,ACOX,SREBP-1c,ACC1) were detected. RESULTS:Com-pared with normal control group,serum contents of TC,TG,LDL-C,FFA in model group increased,HDL-C content decreased;PPAR-α,CYP7A1,ACOX mRNA and protein expressions were weakened,SREBP-1c,ACC1 mRNA and protein expressions were enhanced(P<0.05). Compared with model group,above-mentioned indexes were obviously improved in Xuezhiping capsule high-dose group,atorvastatin group and combination group (except for HDL-C in Xuezhiping capsule high-dose group)(P<0.05);TC,TG,FFA contents,and PPAR-α,CYP7A1,ACOX,ACC1 mRNA,and CYP7A1,SREBP-1c,ACC1 protein were obviously improved in Xuezhiping capsule medium-dose group(P<0.05);TC,TG contents,and PPAR-α mRNA,and CYP7A1, SREBP-1c protein were obviously improved in Xuezhiping capsule low-dose group (P<0.05). CONCLUSIONS:Xuezhiping cap-sule has a promising effect of lowering blood lipid,the mechanism may be related to activating PPAR-α and inhibiting SREBP-lc signaling pathway.

Arsenic trioxide has a significantly positive effect on the treatment of acute promyelocyte leukemia( APL) , and it also has been proved that arsenic trioxide can protect against some other kinds of malignant tumors in recent years. However, with the further research about arsenic trioxide, the reports about car-diac toxicity of arsenic trioxide are increasing. Currently, the possible mechanisms of As2 O3-induced cardiotoxicity are mainly considered to be associated with changes in cardiac ion chan-nels, oxidative stress injury and apoptosis. Research advances on cardiac toxicity of arsenic trioxide and some ways of preven-tion are summarized.

Aim To investigate the protective effect of isorhamnetin on H9 C2 myocardial cell line and its mechanisms. Methods The toxicity and optimal pro-tective concentration of isorhamnetin were determined by MTT assay. The experimental subjects were divided into four groups:group N ( normal ) , group M ( mod-el) , group M + ISO ( model + isorhamnetin ) , and group ISO ( isorhamnetin only ) . Group M +ISO and ISO were pre-incubated with isorhamnetin for 12 hours while other groups with plain DMEM. Group M and M+ ISO were treated with 300μmol · L-1 H2 O2 for 4 hours after pre-incubation. Mitochondrial membrane potential depolarization of H9 C2 was measured by fluo-rescence microscope. Apoptotic rate and ROS produc-tion of injured myocardial cell line were detected using
flow cytometry. The oxidative indictors were measured by spectrophotometry. The expressions of cytoplasmic cytochrome C, caspase-9, caspase-3, Bcl-2, Bax, Nrf2 and HO-1 were examined by Western blot. Result There was no difference in mitochondrial membrane potential depolarization, apoptotic rate, ROS produc-tion, oxidative indictors production and expressions of cytoplasmic cytochrome C, caspase-9,caspase-3, Bcl-2 , Bax between groups ISO and N ( P>0. 05 ) . Apop-totic rate, ROS production, expressions of cytoplasmic cytochrome C, caspase-9, caspase-3, Bax, MDA pro-duction of group M+ISO were significantly lower than those of group M ( P < 0. 01 ) . And mitochondrial membrane potential, Bcl-2, CAT, SOD and GSH-Px of group M + ISO were increased compared to group M .
Nuclear translocation of Nrf2 and expression of HO-1 in myocardial cell line were increased with the prolonged isorhamnetin incubation time. Conclusion Isorham-netin could protect myocardial cell line against H2 O2-induced oxidative injury and apoptosis through the in-
terruption of mitochondrial dependent apoptotic path-way and activation of Nrf2/ARE pathway.

This study is to report the study of protective effects of myricitrin against oxidative stress-induced apoptosis of vascular endothelial cells and the investigation of the possible mechanisms of action of myricitrin. The model of H2O2-induced apoptosis of vascular endothelial cells was used to determine the protective effects of myricitrin. The levels of LDH, MDA and the activities of SOD, NO were measured using the respective kits. The H2O2-induced apoptosis of vascular endothelial cells was detected using MTT reduction, TUNEL assay, JC-1 and ROS staining. The activation of Caspase-3 was also measured by fluorometry. The expression of apoptosis-related proteins was determined with Western blotting assay. Myricitrin had significant protective effects against H2O2-induced apoptosis of vascular endothelial cells in a time- and dose-dependent manner. The results show that myricitrin could attenuate H2O2-induced decrease in the activities of SOD (P < 0.01). Myricitrin could decrease the levels of LDH, MDA and increase cell viability and the mitochondrial membrane potential (P < 0.01). Myricitrin had protective effects in a dose-dependent manner between 32 micromol x L(-1) to 64 micromol x L(-1). Myricitrin pretreatment could attenuate H2O2-induced increase of p-ERK. Moreover, myricitrin pretreatment could up-regulate the expression of the anti-apoptotic protein Bcl-2, down-regulate the expression of the pro-apoptotic protein Bax, and decrease the expression of Caspase-3, 9. In conclusion, myricitrin had significant protective effects against H2O2-induced apoptosis of vascular endothelial cells. Myricitrin can enhance the activities of anti-oxidative enzymes and decrease the production of free radicals. The possible mechanisms of action of myricitrin are due to myricitrin-mediated inhibition of phosphorylation of the apoptosis signaling pathways-related kinase ERK, up-regulation of the expression of the anti-apoptotic protein, and down-regulation of the expression of the pro-apoptotic protein.

Myocardial ischemia/reperfusion injury ( MI/RI) is a pathophysiological phenomenon commonly seen during thromboly-sis, percutaneous transluminal coronary angioplasty ( PTCA ) , and coronary artery bypass grafting ( CABG ) . It is defined as restoration of blood flow to a previously ischemic region followed by complex pathological events leading to tissue injury greater than the original ischemic insult. Many experimental interven-tions have been reported to protect the ischemic myocardium in experimental animals; however, with the exception of early reperfusion, none has been translated into clinical practice. The root of Panax notoginseng ( Burk. ) F. H. Chen ( PN) is one of the iconic herbs in traditional Chinese medicine. Traditional pharmacopeia recommended it among the most efficacious herbs for‘promoting blood circulation ’ and hemostasis. Inspired by this, in the last decade, a large number of modern investigators made substantial efforts to search the PN activities against a vari-ety of MIRI. The systematic review was performed according to the protecting drug of the MIRI development guidelines.