This paper reviews some problems from five aspects such as being good at querying to enlighten students to think on their own,giving examples skillfully to arouse study interesting,summarizing timely to improve study efficiency,linking with clinic to cultivate the practice capability and using multimedia reasonably.

This paper introduces the comparative approach including its implication,implementing ways and values in efferent nervous pharmacological teaching from characteristics of efferent nervous pharmacology.It can be concluded that comparative approach is the suitable teaching method in the teaching of efferent nervous pharmacology.

AIM:To investigate the effect of insulin and selenium in combination on the apoptosis and the ex-pression of Ku70, acetylated Ku70, Bax and cytochrome C in myocardial cells of the rats with diabetic cardiomyopathy (DCM), and to explore the mechanism of insulin and selenium in their synergistic anti-DCM effect.METHODS:SD rats (n=50) were randomly grouped into control, DCM, DCM with insulin treatment (DCM+In) group, DCM with selenium treatment (DCM+Se) group, and DCM with insulin and selenium combination treatment (DCM+In+Se) group.Mito-chondrial membrane potential ( MMP) was measured by flow cytometry .The cell apoptosis was observed by terminal-deoxy-nucleotidyl transferase mediated nick end labeling (TUNEL).The levels of Ku70, Bax and cytochrome C were examined by Western blot .The acetylation status of Ku 70 was detected by co-immunoprecipitation .RESULTS: The rats in DCM group showed marked cell apoptosis compared with the control rats .The levels of Ku70 and acetylated Ku70 declined sig-nificantly compared with control group .Bax significantly translocated from cytoplasm into mitochondria and cytochrome C translocated from mitochondria into cytoplasm compared with control group .Compared with DCM +In group or DCM +Se group, insulin and selenium in combination significantly inhibited the apoptosis , down-regulated Ku70 and acetylated Ku70 levels, and prevented Bax and cytochrome C translocation .CONCLUSION: Insulin and selenium synergistically inhibits myocardial apoptosis by regulating Ku 70 acetylation and inhibiting Bax translocation .

Aim To explore the mechanism of insulin in combination with selenium preventing myocardial apoptosis in diabetic cardiomyopathy rats .Methods SD rats ( n =50 ) were randomly divided into five groups: control , diabetic cardiomyopathy ( DCM ) , DCM with insulin treatment , DCM with selenium treat-ment, and DCM with insulin and selenium combination treatment .The cell apoptosis was observed by TUNEL . The levels of Bcl-2, caspase-3, PARP, Cbl-b and p38 MAPK were examined by Western blot .The inter-actions of Cbl-b-p38 MAPK and Ku70-Bax were detec-ted by immunoprecipitation .Results Insulin in com-bination with selenium synergistically inhibited apopto-sis, up-regulated Cbl-b, down-regulated p38MAPK ex-pressions and increased the interactions of Cbl-b-p38MAPK and Ku70-Bax.Conclusion Insulin and selenium synergistically inhibit myocardial apoptosis by regulating Cbl-b-inhibited p38 MAPK and preventing Bax translocation .

Diversified teaching methods including traditional teaching,problem based learning,interactive teaching and team cooperation teaching were adopted in the process of teaching.Problem based learning can stimulate students' learning interests; interactive teaching can improve the students' hands-on ability and team cooperation teaching can cultivate students' cooperation spirits.Diversified teaching mode made different teaching methods integrated and complemented each other,forming a special teaching mode for the course of functional experiment.

OBJECTIVETo investigate the changes of cholinergic nerves in doxorubicin (DOX)-induced rat failing heart and tumor necrosis factor-α (TNF-α) in the heart tissue and serum.

METHODSAdult Sprague-Dawley rats were randomized into control (n=10) and DOX-induced chronic heart failure (CHF) groups (n=15), and in the latter group, the rats were given intraperitoneal injections of 2.5 mg/kg DOX once a week for 6 weeks, with a total cumulative dose of 15 mg/kg. The control rats were injected with normal saline (1 ml/week). Karnovsky-Roots histochemical staining combined with point counting was used to demonstrate the distribution of cholinergic nerves in the heart. The expression levels of TNF-α in the heart tissue and serum were determined with ELISA.

RESULTSPositively stained cholinergic nerves were found in all the rat hearts in the two groups, but in CHF group, the point counts of cholinergic nerves were significantly lower than that of the control group (P<0.01). Compared with the control rats, those with DOX-induced CHF showed elevated levels of TNF-α both in the heart tissue and in the serum (P<0.01).

CONCLUSIONIn rats with DOX-induced CHF, the parasympathetic nervous system is down-regulated in the failing heart, and the diminished cholinergic anti-inflammatory pathway may play an important role in the progression of CHF.

Animals ; Cholinergic Agents ; pharmacology ; Cholinergic Fibers ; drug effects ; Doxorubicin ; pharmacology ; Heart ; drug effects ; innervation ; Heart Failure ; chemically induced ; metabolism ; Male ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo investigate the effect of xy2004, a centchroman derivative, on the proliferation of MCF-7 cells and the mechanisms.

METHODSThe effects of xy2004 on MCF-7 cell proliferation and apoptosis were evaluated with MTT assay and flow cytometry, respectively. The expressions of the apoptosis-related proteins were examined with Western blotting. Competitive estrogen-receptor binding assay was used to investigate the affinity of xy2004 to estrogen receptors (ER).

RESULTSxy2004 induced proliferation of MCF-7 cells at low concentrations but inhibited cell proliferation at high concentrations. The application of tamoxifen inhibited xy2004-induced proliferation of MCF-7 cells. The relative binding affinity of xy9906 to ERα and ERβ, presented as the IC50 value, was 7.38 × 10⁻³ mol/L and 4.12 × 10⁻⁷ mol/L, respectively. Treatment of MCF-7 cells with high-concentration xy2004 reduced the cellular expression of Bcl-2 protein and increased Bax protein expression.

CONCLUSIONAt low concentrations, xy2004 directly stimulates the proliferation of MCF -7 cells through ligand-receptor binding, and at high concentrations, it inhibits the cell proliferation by regulating the expression levels of the apoptosis-related proteins.

Apoptosis ; Breast Neoplasms ; pathology ; Cell Proliferation ; Centchroman ; pharmacology ; Estrogen Receptor alpha ; metabolism ; Estrogen Receptor beta ; metabolism ; Humans ; MCF-7 Cells ; drug effects ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Tamoxifen ; bcl-2-Associated X Protein ; metabolism

【Objective】 To observe the uric acid-lowering effect of 3,4-dihydroxy-5-nitrobenzaldehyde (DHNB) on hyperuricemia models in mice and quails so as to improve the pharmacodynamic validation on hyperuricemia models. 【Methods】 The mouse hyperuricemia animal model was prepared by intraperitoneal injection of potassium oxonate 300 mg/kg; 30 g/(kg·d) yeast powder mixed feed (yeast powder∶feed, 1∶4) was used to prepare the quail hyperuricemia animal model. DHNB, 100 mg/kg, was intraperitoneally injected into the mice 1 hour prior to modeling; DHNB, 100 mg/kg, was intragastrically administered for two days consecutively into the quail hyperuricemia models. Control groups in mice and quails were set up respectively. Biochemical kits were used to detect serum uric acid, aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), creatinine (Cr), and blood urea nitrogen (BUN) in mouse and quail serum. Heart, lung, liver and kidney tissues of mice and quails were stained with HE. 【Results】 The serum uric acid in the mouse and quail hyperuricemia model groups was higher than that in the control group [(277.37±94.89) μmol/L vs. (176.49±44.83) μmol/L, P<0.05; (313.58±191.87) μmol/L vs. (167.26±66.56) μmol/ L, P<0.05)], indicating that the modeling was successful. DHNB could not reduce serum uric acid in hyperuricemia mouse model [(277.37±94.89) μmol/L vs. (238.72±63.43) μmol/L, P>0.05]. However, it significantly decreased serum uric acid in the quail model of hyperuricemia (313.58±191.87) μmol/L vs. (160.44±49.90)μmol/L, P<0.05]. Administration of DHNB 100 mg/kg one or two times had no effect on the liver and kidney functions of mice and quails, and had no toxicity to the heart, lung, liver or kidney tissues of mice and quails. 【Conclusion】 DHNB has a uric acid-lowering effect on the hyperuricemia quail model, and a single dose that caused the uric acid-lowering effect has no obvious toxicity to mouse or quail viscera. The quail hyperuricemia model is more suitable for the validation of the uric acid-lowering efficacy of DHNB than the mouse hyperuricemia model.