RESUMO
Objective: To investigate the effect of water-soluble components from Salvia miltiorrhiza on liver sinusoid endothelial cell function and angiogenesis. Methods: Different dosages of water-soluble components from S. miltiorrhiza were incubated for 24 h with HHSEC cell line, and the toxicity of HHSEC cells was assayed by CCK-8 method. The proliferation of HHSEC cells was induced by endothelial cell growth supplements (ECGS), with receptor tyrosine kinase inhibitor sorafenib as positive control, cell proliferation was analyzed by EdU DNA cell proliferation kit; Fluorescence probe method was used to assay the intracellular NO level and NOS activity; Immunofluorescence method was performed to observe the expression of CD31; The transgenic zebrafishes were incubated for 24 h with each component. The fluorescence vessels, the number of functional blood vessels, and intersegmental vessel changes were observed; Chicken chorioallantoic membranes were incubated for 24 h with each component, Image Analysis Software was used to analyze the vessel area changes. Results: Compared with control group, the proliferation of HHSEC cells induced by ECGS increased, the level of NO and NOS activity reduced and the expression of CD31 increased; Compared with the model group, salvianolic acid A, salvianolic acid B, salvianolic acid C, and sorafenib inhibited the proliferation of HHSEC cells induced by ECGS, reduced the level of NO, NOS activity, and expression of CD31. The vessel area of chicken chorioallantoic membranes was decreased in sorafenib, salvianolic acid A, salvianolic acid B and caffeic acid. Salvianolic acid C also significantly inhibited the intersegmental vessel changes of transgenic zebrafish. Conclusion: Salvianolic acid A, salvianolic acid B, and salvianolic acid C have the potential effects on function of endothelial cell proliferation and angiogenesis.
RESUMO
Objective To investigate the anti-oxidant effect and the possible mechanisms ofpicrodide II in cerebral ischemia/reperfusion injuries in rats. Methods A total of 90 adult, healthy, mmale Wistar rats were used to established the middle cerebral artery occlusion reperfusion (MCAO/R) models by intraluminal monofilament suture on the left external-internal carotid artery. The treatment group and the positive control group were respectively injected with 1.0％ picroside II (10 mg/kg, 250 μl) and salvianic acid A sodium (10 mg/kg, 250 μl) via the tail vein, and the negative control group and sham-surgery group were injected with 0.1mol/L phosphate buffer saline (PBS) 250 μl. The neurological deficit scores were evaluated with Bederson's test. The cerebral infarction volume was observed with tetrazolium (TTC) staining. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase dUTP nick-end labeling and the expressions of inducible nitric oxide synthase (iNOS) and superoxide dismutase (SOD) were detected with immunohistochemical assay.The concentration of iNOS and SOD proteins in brain tissue was detected by enzyme linked immunosorbent assay.Results Neurological behavioral malfunction appeared in all the rats with MCAO/R. The infarction focuses emerged in the ischemic hemisphere following the MCAO/R injuries. The number of apoptotic cells and the expression of iNOS increased while the SOD reduced after MCAO/R. After the treatment of picrodide Ⅱ, the nervous behavioral function (1.28±0.38)improved, the infarction volume(68.73±4.46)％ reduced, the number of apoptosis positive cells(6.10± 1.26), the expressions and the concentrations in brain tissue of iNOS(4.67+0.51)decressed while those of SOD (0.53 ±0.14) increased significantly compared with the negative control groups(t=3.16、 2.51、 4.15、3.12、 3.25, P＜0.05). Conclusion PicrodideⅡ might play a neuroprotective effect by inhibiting the neuronal apoptosis and the expressions of iNOS and SOD after cerebral ischemia/reperfusion injuries.