Antiangiogenic effect of celastrol on the growth of human glioma: an in vitro and in vivo study / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Celastrol is a major active component of Tripterygium wilfordii named "Thunder God Vine", which is widely used to treat rheumatoid arthritis in China. The present study aims to demonstrate that celastrol has potent anticancer activity against glioma in vitro and in vivo.</p><p><b>METHODS</b>Proliferation, migration, and tube formation of ECV-304 cells were determined by MTT and matrigel assays. The antiangiogenesis effect of celastrol was assessed by the chick chorioallantoic membrane assay and the in vivo matrigel plug assay. Tumor microvessels (MVD) were determined immunohistochemically with anti-CD34 antibody. Vascular endothelial growth factor (VEGF) expression was defined as positive if distinct staining of the cytoplasm was observed in at least 10% of tumor cells at the deepest invasive site, central portion and superficial part of the tumor. MVD was estimated by averaging the counts of three times at a x 200 field in the most vascularized area of the deepest invasive site.</p><p><b>RESULTS</b>Celastrol purified from T. wilfordii inhibited the proliferation of vascular endothelial cells (ECV-304) with an IC50 value of 1.33 microg/ml. Celastrol, at the concentration of 0.2 microg/ml, significantly inhibited cell migration and tube formation. Celastrol inhibited angiogenesis in a dose-dependent manner both in vitro and in vivo. Subcutaneous administration of celastrol 5 days a week for 4 consecutive weeks significantly reduced tumor volume in a dose-dependent manner in the SHG-44 xenograft model. Celastrol at each different dose level lowered the density of MVD significantly in tumor bearing nude mice compared to the control group. Immunohistochemistry experiments further revealed that celastrol also decreased the level of VEGFR-1 and VEGFR-2 expression, but not the level of VEGF expression.</p><p><b>CONCLUSIONS</b>Celastrol elicits antiangiogenic effects in vitro and in vivo, and could be of potential use in the treatment of malignant cancers such as glioblastoma.</p>

The duplication blepharoplasty with the multiple ring incisions / 中国基层医药

Objective To explore the clinic effects in duplication blepharoplasty with the multiple tiny inci- sions.Methods The line of drooping blepharon was set in routine in 183 patients,the incisions with 3～4mm long would be made in middle and the both canthi sides on the line,cutting 1.5～2mm long flaps of the muscle orbicularis oculi off in the down rim of the incisions.Excessive fats also released form the orbital septum in patients with swelling blepharon.Then put up the muscle tendon of blepharon and sutured with the slcin on the up rim of tarsal plate.Results The reaction of tissue after operation was very light,swelling in the incision could disappear after 7～23 days and the incision scars weretiny and unclear,tbe double-fold eyelids had a good appearance in long time.Con- clusion It is an effective and usable procedure to the patients without skin loosening or serious swelling blepharon by means of multiple tiny incisions in blepharoplasty.

Celastrol in the inhibition of neovascularization / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the inhibition effect of celastrol on neovascularization.</p><p><b>METHODS</b>The effect of celastrol on the in vitro proliferation of endothelial cell of vessel (ECV) was examined by MTT assay. The effect of celastrol on endothelial cell migration, tube formation on Matrigel and Chick chorioallantoic membrane angiogenesis was also examined. Matrigel plug assay was used to evaluate the effect of celastrol on angiogenesis in vivo.</p><p><b>RESULTS</b>The proliferation of ECV was inhibited significantly by celastrol with IC(50) being 1.33 microg/ml. Celastrol inhibited endothelial cell migration and tube formation in a dose-dependent manner. Celastrol also inhibited angiogenesis both in Matrigel plug of mouse model and in chick chorioallantoic membranes.</p><p><b>CONCLUSION</b>Celastrol, which can inhibit angiogenesis, could be developed as an antiangiogenic drug.</p>