Objective:To investigate the effect of Epibueropyridinium A(EA),extracted from Scrophularia ningpoensis,in prevention of D-galactose-induced cataract in rats.Methods: SD rats were randomly divided into 5 groups (n=10),namely,the normal control,cataract model,20 mg/kg EA,10 mg/kg EA,and positive control groups.The cataract model was induced by intraabdominal administration of D-galactose into rats.Rats of the 2 EA groups received corresponding amount of EA and those in the positive control group received epalrestat(10 mg/kg) or VitE(30 mg/kg).The changes of the lens were examined with slit lamp microscope at defined time points.The activities of superoxide dismutase(SOD) and the content of malonaldehyde(MDA) and sorbitol were determined in the lens 3 and 6 weeks later.Results: EA obviously improved the lens opacification in the 2 EA groups compared to cataract model group,and the improvement in high EA group was more obvious than that in the low EA group(P

We found that the platelet aggregation rates induced by ADP, arachidonic acid (AA), collagen and A23187 had an apparent decreasing after injection of berberine into the vein of rabbits, and also found that berberine had an apparent inhibition of calcium influx into platelet induced by A23187 at lower concentrations. We demonstrated that berberine had no obvious effect on cAMP level in the intact platelet of rabbits.

Objective:To investigate the inhibitory effect of Epibueropyridinium A on aldose reductase.Methods: Aldose reductase was extracted from cattle crystalline lens.Besides Epibueropyridinium A,the reactive system also contained DL-glyceraldehyde,aldose reductase,and NADPH.The activity changes of aldose reductase were detected at 340 nm.Epalrestat was taken as the positive control.The inhibitory type,Ki and IC_(50) were determined by double reciprocal plot,quadratic drawing,and drawing of inhibitor's concentration to inhibitory ratio,respectively.Results: Epibueropyridinium A significantly inhibited the activity of aldose reductase in a competitive manner,with IC_(50) being 4.2 ?g/ml and Ki being 4.88 ?g/ml.Conclusion: Epibueropyridinium A is competitive inhibitor of aldose reductase.

Objective:To study the pharmacokinetics,thissue distribution and secretion of nerve growth factor(NGF)in mice.Methods:The conecntration of NGF in various body fluids and tissue were determined by isotope tracer combined SDSPAGE method.Results:The plasma concenmtration-time curve was in accordance with the two-compartment pharmacokinetic model.The elimation half-life(t1/2β)was 3.1.The half-life of distribution(t1/2ka)was 5min.Tpeak was 25 min.AUC was 72.4 mg·kg-1·h-1.The concentrations of NGF were high in thyroid,blood,submaxillary glands,superior cervical ganglion,adrenasl and kidneys.Conclusion:NGF has a wide distribution,high tissue concentrationa nd excrtet mainly through the urine.

Objective ToinvestigatemechanismofWentilactoneA (WA)inhibitionofsmallcelllungcancer(SCLC)cell line NCI-H1688 migration .Methods The migration and proliferation were analyzed by wounding-healing assay and MTT assay [3-(4 ,5-Dimethylthiazol-2-yl)-2 ,5-diphenyltetrazolium bromide ,MTT] .Immunofluorescence was used to confirm the ex-pression of ATF3 protein after WA treatment .Western blot was used to examine the expression of key proteins in ATF3/Nrf2/AKR1C1 signal pathway .Results WA inhibits the proliferation and migration of SCLC .MTT analysis showed WA in-hibits the proliferation of NCI-H1688 cell line in a time-dependent manner .The number of migrated cells in WA treatment group was (8 .73 ± 1 .06) mm ,which was lower than that of control group (15 .63 ± 3 .11) mm ,The number of migrated cells in AKR1C1 expression group was (24 .37 ± 0 .90) mm ,the number of migrated cells in AKR1C1 expression and WA treatment group was (14 .17 ± 1 .31) mm ,with significant difference (P<0 .05) .WA enhances the nuclear expression of ATF3 ,and then reduces the expression of p-Nrf2 and AKR1C1 .Conclusion WA inhibits the proliferation and migration of SCLC through ATF3/Nrf2/AKR1C1 signal pathway .

Objective To evaluate the genetic toxicity of Wentilactone A. Methods The classical genotoxicity test combination (Ames test, in vitro CHO cell chromosome aberration test and mouse bone marrow micronucleus test) was used to detect the genotoxicity of Wentilactone A. Results Ames test suggested that Wentilactone A was not mutagenic against Salmonella typhimurium with or without the metabolic activation system (S9) at five doses of 5 000, 500, 50, 5, and 0.5 μg/dish. CHO cell chromosome aberration test suggested that the CHO cells cultured in 4 h and 24 h did not induce chromosomal aberrations in three dose groups at the final concentration of 23.74, 47.48, 94.96 μg/ml, with and without S9. The mouse bone marrow micronucleus test showed no significant difference in the bone marrow micronucleus induction rate of cells at three doses of 100, 200, and 400 mg/kg treated for 24 h and at dose of 400 mg/kg treated for 48 h compared with the solvent control group (P>0.05). Conclusion These results indicated that Wentilactone A did not exhibit genetic toxicity based on the Ames test, CHO chromosomal aberration test and micronucleus assay. It was suggested that Wentilactone A had no genetic toxicity and potential carcinogenicity.