AIM and METHOD To investigate the antibacterial activity (ED 50 value) of cefoperazonesodium and tazobactam sodium (4∶0 5) in vivo using minor modified Karbers method,which will offer some important evidences for clinical trial and therapy RESULTS The ED 50 value of cefoperazone sodium and tazobactam sodium(4∶0 5) and Cefoperazone sodium and sulbactam sodium (1∶1) in vivo protested against zymogenic staphylococcus aureus and Escherichia coli in mice infected by these bacteria were 92 0 mg?kg -1 and 3 4 mg?kg -1 ,164 0 mg?kg -1 and 6 9 mg?kg -1 ,respectively,and 256 5 mg?kg -1 and 38 9 mg?kg -1 in single composed compound of cefoperazone sodium,cefoperazone sodium and tazobactam sodium (4∶0 5) in vivo had more potent antibacterial activity compared with cefoperazone sodium and sulbactam sodium (1∶1) and single composed compound of cefoperazone sodium. The ED 50 value of cefoperazone sodium and tazobactam sodium (4∶0 5) protested against pseudomonas aeruginosa in mice infected was lower than that of Cefoperazone sodium and sulbactam sodium and single composed compound of cefoperazone sodium CONCLUSION Cefoperazone sodium and tazobactam sodium made in China has an markedly therapeutic effect on antibacterial activity protected against zymogenic staphylococcus aureus and Escherichia coli and pseudomonas aeruginosa in mice infected by these bacteria

OBJECTIVE:To study the percutaneous absorption of 0.03% Tacrolimus ointment,and to compare the difference of domestic test preparation and imported reference preparation. METHODS:Modified Franz diffusion cells were adopted in trans-dermal test in vitro;HPLC-MS method was used to determine permeation amount and rate in vitro,delay time of domestic test preparation and imported reference preparation 0.03%Tacrolimus ointment. RESULTS:24 h in vitro permeation amount of test and reference preparations were(3 907±1 191)and(3 896±1 064)ng/cm2;permeation rates were 186.7 and 182.9 ng/(cm2·h);de-lay time were 1.95 and 2.00 h,respectively(P>0.05). CONCLUSIONS:Test preparation shows good percutaneous property,and is similar to reference preparation in penetration absorbency through nude mice skin.

AIM To study the effects of apomorphine hydrochloride on the sexual function of rate. METHODS Male rats were grouped at random and respectively intraperitoneally injected with different dosages of apomorphine hydrochloride (4 32, 2 16 and 1 08 mg?kg -1 ), These male rats were put into cages respectively with a female rat to conduct the copulation experiment,including the latent periods of their seizure and ejaculation and the times of their seizing of the female rats and ejaculation within twenty minutes on the first and the eighth day during the injection. Radioimmunoassay(RIA) was used to determine the contents of luteinizing hormone(LH) ,prolactin(PRL) ,testosterone(T) and estradiol(E 2) in the venous blood on the fourth and the eighth day during the injection. RESULTS Apomorphine hydrochloride(4 32 and 2 16 mg?kg -1 ) can significantly increas the copulatory capability of male rats on the first and the eighth day during the injection, obviously reduce the latent periods of their seizing of the female rats and ejaculation when male and female rats were caged together, and increase the times of their seizure and ejaculation within twenty minutes after being caged together,but it had no obvious effects on the contents of luteinizing hormone(LH), prolactin (PRL), testosterone(T) and estradiol(E 2) in the venous blood. CONCLUSION Apomorphine hydrochloride can significantly increase the sexual function of male rats.

AIM To investigate the influence on change of SOD and MDA in the blood of rats which had cellular immunoreactive colitis by Fengliao Changweikang Granule (CWKG). METHODS Male Wistar rats were divided into six groups. Numbers of each group were 32. Animal model of rat cellular iumynoreactive colitis was made by TNBS and ethanol mixed liguid enema. Rats were killed at the 1st, 3rd, 7th and 21st day respectively. Gross morphologic observation of intestinal wall was made, SOD vitality and MDA content in blood were determined. RESULTS At day 7 and 21, the intestinal wall damage criterion value of large dosage group was lower than model group ( P

OBJECTIVE： To study the effects of ivermectin on the migration and invasion of human gastric cancer cell lines BGC-823 and MGC-803 and its mechanism. METHODS： After treated with 0， 2.5， 5， 10， 20， 40 μmol/L ivermectin for 24 h， inhibitory rate of human gastric cancer cell lines BGC-823 and MGC-803 were detected by MTT assay. Effects of 5 μmol/L ivermectin and phosphate buffercontaining 0.67‰ dimethyl sulfoxide （control group） for 24 h on the migration and invasion of` gastric cancer cells BGC-823 and MGC-803 were observed by Transwell chamber invasion assay.Western blot assay was used to detect the protein expression of TGF-β1， TGF-βR， Smad2 and Smad3 in epithelial-mesenchymal transition （EMT） markers E-cadherin， N-cadherin， Vimentin， Snail and EMT transduction pathway TGF-β/smad of BGC-823 and MGC-803 cells after treated with 5， 10 μmol/L ivermectin and phosphate buffercontaining 0.67‰ dimethyl sulfoxide （control group） for 24 h. RESULTS： Ivermectin could inhibit the growth of BGC-823 and MGC-803， inhibitory rate of it was positively correlated with its concentration. Compared with control group， the number of migration and invasion BGC-823 and MGC-803 cells were decreased significantly after treated with 5 μmol/L ivermectin （P＜0.01 or P＜0.001）； the expression of E-cadherin protein was enhanced significantly in BGC-823 and MGC-803 cells after treated with 5 and 10 μmol/L ivermectin （P＜0.05 or P＜0.01 or P＜0.001）； the protein expression of N-cadherin， Vimentin， Snail， TGF-βR， Smad2 and Smad3 were decreased significantly （P＜0.05， P＜0.01 or P＜0.001）； protein expression of TGF-β1 was decreased significantly after treated with 10 μmol/L ivermectin （P＜0.05）. CONCLUSIONS： Ivermectin can significantly inhibit the migration and invasion of gastric cancer cells BGC-823 and MGC-803， and inhibiting the biological activity of EMT by reducing the expression of TGF-β/smad pathway is one of the mechanisms that inhibit the migration and invasion of gastric cancer cells.