ABSTRACT
Aim To investigate the therapeutic effects of total saponins of Panax notoginseng( PNS) on ather-osclerosis( AS) in ApoE knockout mice. Methods According to TC level, ApoE knockout mice were ran-domly assigned into six groups. Control group was fed with normal diet, and the other groups were fed with high-fat diet. After 16 weeks, mouse serum and aortas were harvested. The formation of atherosclerotic plaque was analyzed by oil red staining, the proportion of pathological lesion and the apoptosis of endothelial cells in left ventricular outflow tract were analyzed by HE staining and TUNEL. The serum level of lipids profiles, oxLDL-C were detected, and the mRNA ex-pressions of ICAM-1, VCAM-1, iNOS, eNOS, IL-1, IL-6 and TNF-α were detected by qPCR. Results In model group, the serum content of TC, LDL-C and HDL-C significantly increased(P<0.01); the area of atherosclerotic plaque significantly increased ( P <0.01) ; and the apoptosis of endothelial cells and the proportion of pathological lesion of left ventricular out- flow tract significantly increased(P<0.01). Also, the mRNA expression of ICAM-1, VCAM-1, iNOS, IL-1, IL-6 and TNF-α in model group increased. Compared with model group, the serum content of TC, LDL-C and HDL-C decreased after administration of PNS. The serum content of oxLDL-C was significantly reduced in PNS groups( P <0.01, P <0.05 ) . The apoptosis of endothelial cells significantly declined as well ( P <0.01, P <0.05 ) . The area of atherosclerotic plaque decreased after administration of PNS. The mRNA ex-pression of ICAM-1, VCAM-1, iNOS, IL-1, IL-6 and TNF-α in PNS groups were down-regulated. Conclu-sions In ApoE-KO mouse model, PNS plays a role in the therapy of AS, which may be due to its modulating lipid metabolism, protecting vascular endothelium, de-creasing inflammation and inhibiting adhesion of im-mune cells.
ABSTRACT
<p><b>OBJECTIVE</b>To study on the drug release characteristics and mechanism of gastrodin ion-activated nasal in situ gel in vitro.</p><p><b>METHOD</b>Regularity and mechanism of the drug release of gastrodin nasal in situ gel were studied by using the diffusion cell model and the membrane-less dissolution model, respectively. A novel kinesis diffusion cell model was designed according to the characteristics of release environment of nasal cavity. It was used to investigate the effect of adhesiveness on the release of the in situ gel.</p><p><b>RESULT</b>Drug release of gastrodin nasal in situ gel followed the one order release model. Erosion rate of the gel was low and not linearly correlated with the release rate. Compared with gastrodin solution, the nasal in situ gel could increase release time and release amount.</p><p><b>CONCLUSION</b>Gastrodin in the nasal in situ gel is released mainly by diffusion rather than erosion. Release amount of the in situ gel in nasal cavity may be obviously increased because of its adhesiveness.</p>