RESUMO
Aim To study the therapeutic effect of helicid on osteoarthritis (OA) of joint instability model, and explore the mechanism of helicid in the treatment of OA. Methods A rat knee model of OA was established by the medial meniscectomy (MMx) method. After treatment with helicid, HE and safranin O/fast green staining methods were used to observe the his-topathological changes of rat knee articular cartilage; Western blot was used to detect the protein expression level of Trpvl in rat synovial tissue. Immunohistochemical staining was used to examine the expression of Trpvl in rat knee articular cartilage and synovial tissues. Results Helicid significantly slowed down the degeneration of rat knee articular cartilage as shown by HE and safranin O/fast green staining. Western blot results showed that helicid down-regulated the expression of Trpvl in rat synovial tissue examined. Immunohistochemical results showed that helicid significantly reduced the expression of Trpvl in both of knee articular cartilage and synovial tissues. Conclusions Helicid prominently decreases MMx-induced articular cartilage damage and cartilage matrix loss, thereby exerting a therapeutic effect on OA.
RESUMO
Objective To observe the inhibitory effect of ginsenoside RG3 on choroidal neovascularization in vitro and in vivo.Methods MTT assay was used to evaluate the inhibitory effect of ginsenoside RG3 on human umbilical vein endothelial cells (HUVEC) proliferation in vitro,and HUVEC were divided into normal group,in which the cells were cultured in DMEM/F-12 medium containing 10％ fetal bovine serum,control group with its medium containing 2 g · L-1 dimethyl sulfoxide (DMSO) and different concentrations of ginsenoside RG3 administration group (12.5 μmol · L-1,25.0 imol · L-1,50.0 μmol · L-1,100.0 μmol · L-1).Then the absorbance value was measured after 6 h.Then,a small amount of HUVEC was collected again and divided into control group with its medium containing 2 g · L-1 DMSO and 100.0 μrnol · L-1 ginsenoside RG3 group for detecting the inhibitory effect of ginsenoside RG3 on tubular formation and vascular endothelial growth factor (VEGF) protein expression by Western blots.In vivo,20 male C57BL/6J mice were collected and randomly divided into control group and ginsenoside RG3 group.After 2 weeks,followed by establishment of model with a semiconductor laser,fundus fluorescein angiography was performed on the 1 st day and 21 st days after treatment.Results MTT results showed that absorbance value of the normal group,control group,12.5 μnol · L-1,25.0 μmol · L-1,50.0 μmol · L-1,100.0 μmol · L-1 ginsenoside RG3 group was 0.43 +0.17,0.43 ±0.05,0.33 +0.02,0.24 +0.02,0.18 ±0.01,0.15 ±0.01 accordingly,and there was no significant difference between the control group and the normal group (all P ＞ 0.05),but the difference between the other group and control group was statistically significant (all P ＜ 0.05).Tubular formation assay showed that the number of tubular formation in the control group and 100.0 μmol · L-1 ginsenoside RG3 group was 72.5 + 5.56 and 11.33 ± 3.71,respectively,and the difference was statistically significant (P ＜ 0.01).Western blots showed that the relative expression of VEGF in 100.0 μmol · L-1 ginsenoside RG3 group (0.14 ±0.01) was significantly lower than that in the control group (0.46 ±0.01),and the difference was statistically significant (P ＜0.01).In vivo fundus fluorescein anglography showed that the fluorescein leakage area of ginsenoside RG3 group was lower than that of the control group.Conclusion Ginsenosid RG3 can inhibit the formation of choroidal neovascularization by inhibiting the expression of VEGF in vitro and in vivo.
RESUMO
Objective To observe the inhibitory effect of ginsenoside RG3 on choroidal neovascularization in vitro and in vivo.Methods MTT assay was used to evaluate the inhibitory effect of ginsenoside RG3 on human umbilical vein endothelial cells (HUVEC) proliferation in vitro,and HUVEC were divided into normal group,in which the cells were cultured in DMEM/F-12 medium containing 10％ fetal bovine serum,control group with its medium containing 2 g · L-1 dimethyl sulfoxide (DMSO) and different concentrations of ginsenoside RG3 administration group (12.5 μmol · L-1,25.0 imol · L-1,50.0 μmol · L-1,100.0 μmol · L-1).Then the absorbance value was measured after 6 h.Then,a small amount of HUVEC was collected again and divided into control group with its medium containing 2 g · L-1 DMSO and 100.0 μrnol · L-1 ginsenoside RG3 group for detecting the inhibitory effect of ginsenoside RG3 on tubular formation and vascular endothelial growth factor (VEGF) protein expression by Western blots.In vivo,20 male C57BL/6J mice were collected and randomly divided into control group and ginsenoside RG3 group.After 2 weeks,followed by establishment of model with a semiconductor laser,fundus fluorescein angiography was performed on the 1 st day and 21 st days after treatment.Results MTT results showed that absorbance value of the normal group,control group,12.5 μnol · L-1,25.0 μmol · L-1,50.0 μmol · L-1,100.0 μmol · L-1 ginsenoside RG3 group was 0.43 +0.17,0.43 ±0.05,0.33 +0.02,0.24 +0.02,0.18 ±0.01,0.15 ±0.01 accordingly,and there was no significant difference between the control group and the normal group (all P ＞ 0.05),but the difference between the other group and control group was statistically significant (all P ＜ 0.05).Tubular formation assay showed that the number of tubular formation in the control group and 100.0 μmol · L-1 ginsenoside RG3 group was 72.5 + 5.56 and 11.33 ± 3.71,respectively,and the difference was statistically significant (P ＜ 0.01).Western blots showed that the relative expression of VEGF in 100.0 μmol · L-1 ginsenoside RG3 group (0.14 ±0.01) was significantly lower than that in the control group (0.46 ±0.01),and the difference was statistically significant (P ＜0.01).In vivo fundus fluorescein anglography showed that the fluorescein leakage area of ginsenoside RG3 group was lower than that of the control group.Conclusion Ginsenosid RG3 can inhibit the formation of choroidal neovascularization by inhibiting the expression of VEGF in vitro and in vivo.