The inhibitory effect of astilbin on transplant arteriosclerosis in murine model of thoracic aorta transplantation was examined. Model of rat thoracic aorta transplantation was established. Ninety rats were divided in...The inhibitory effect of astilbin on transplant arteriosclerosis in murine model of thoracic aorta transplantation was examined. Model of rat thoracic aorta transplantation was established. Ninety rats were divided into three groups. In isograft group, the thoracic aorta of Brown Norway （BN） rat was anastomosed with the abdominal aorta of another BN rat. In allograft group, the thoracic aorta of BN rat was anastomosed with the abdominal aorta of Lewis rat. In astilbin group, the rats receiving allo-transplantation were given astilbin 5 mg/kg per day for a time of 28 days. The donor thoracic aorta and the recipient abdominal aorta were anastomosed by means of a polyethylene can- nula （inner diameter： 1.5 mm, length： 3 mm length）. The grafts were histologically examined for structural changes. The areas of arterial lumen and endatrium were calculated. Our results showed that, in the allograft group, 28 days after allografting, conspicuous proliferation of smooth muscles and infiltration with a great number of inflammatory cells were found in the tunica intima and tunica media. Astilbin significantly inhibited the proliferation of smooth muscles and ameliorated the infiltration of inflammatory cells thereyby prevent against the development of transplant arteriosclerosis. It is concluded that asltilbin can effectively prevent the development of arteriosclerosis in allotransplant by inhibiting the proliferation of smooth muscles and inhibit the proliferation of smooth muscles in tunica of intima and media and reducing infiltration of the inflammatory cells.展开更多
This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (AngⅡ) and explored the possible mechanisms. Cell proliferation model of RASMCs was...This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (AngⅡ) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngⅡ. Cells were randomly divided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngⅡ model group, cells were treated with AngⅡ at 10–7 mol/L; in three astilbin groups, cells were treated with 10, 15, 30 mg/L of astilbin; in three AngⅡ+astilbin groups, cells were treated with AngⅡ (at 10–7 mol/L) and astilbin at 10, 15, 30 mg/L. Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined. The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR), and the expression of NF-κB in RASMCs was immunocytochemically observed. Our results showed that MTT metabo-lism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G0/G1 phase were increased and that of G2/S phase were decreased markedly. Not only highly expression of c-myc gene stimulated by AngⅡ could be inhibited by Astilbin significantly, but also the expression of NF-κB protein can be down regulated by Astilbin. We are led to conclude that astilbin astilbin can inhibit the AngⅡ-mediated proliferation of RASMCs by blocking the transition of RASMCs from G0/G1 phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.展开更多
Objective:To investigate the osteoblastogenic activity of the ethyl acetate(EtOAc)extract of Smilax glabra Roxb roots and its major active compound astilbin.Methods:Astilbin was isolated from EtOAc extract using silic...Objective:To investigate the osteoblastogenic activity of the ethyl acetate(EtOAc)extract of Smilax glabra Roxb roots and its major active compound astilbin.Methods:Astilbin was isolated from EtOAc extract using silica gel chromatography combined with fraction crystallization.Chemical structure of astilbin was determined by analysis of the spectroscopic data in comparison with the literature.MTT method was used to detect the toxicity.Alkaline phosphatase(ALP)activity was determined by the spectrophotometric method at 405 nm using p-nitrophenyl phosphate as a substrate.Calcium deposition was stained with alizarin red-S,distained with cetylpyridium chloride,and quantified at 562 nm.In silico model for astilbin-ALP interaction was analyzed using AutoDock 4.2.6.The changes in expression of osteoblast differentiation related genes were determined using quantitative real-time PCR.Results:Both the EtOAc extract and astilbin had no toxicity toward osteoblast MC3T3-E1 cells at 5.0,10,25,and 50μg/mL.At 25μg/mL,they enhanced ALP activity and mineralization of osteoblasts up to 30%and 55%for the EtOAc extract and 22%and 41%for astilbin,respectively.Molecular docking analysis of astilbin-ALP interaction revealed Arg167,Asp320,His324,and His437 were key residues participating in hydrophobic interaction;meanwhile,His434 and Thr436 residues were involved in hydrogen bond formation in the active site of human tissue-nonspecific ALP.Moreover,the expression level of genes opn,col1,osx,and runx2 were up-regulated in astilbin treated samples with the fold changes as 2.2;3.7;4.1;2.3,respectively at 10μg/mL(P<0.05).Conclusions:The EtOAc extract and its major compound astilbin exhibit osteoblastogenic activity by up-regulating important markers for bone cell differentiation.It could be a new and promising osteogenic agent with dual actions for therapeutic applications.展开更多
基金supported by a grant from the National Natural Sciences Foundation of China (No.30500656)
文摘The inhibitory effect of astilbin on transplant arteriosclerosis in murine model of thoracic aorta transplantation was examined. Model of rat thoracic aorta transplantation was established. Ninety rats were divided into three groups. In isograft group, the thoracic aorta of Brown Norway （BN） rat was anastomosed with the abdominal aorta of another BN rat. In allograft group, the thoracic aorta of BN rat was anastomosed with the abdominal aorta of Lewis rat. In astilbin group, the rats receiving allo-transplantation were given astilbin 5 mg/kg per day for a time of 28 days. The donor thoracic aorta and the recipient abdominal aorta were anastomosed by means of a polyethylene can- nula （inner diameter： 1.5 mm, length： 3 mm length）. The grafts were histologically examined for structural changes. The areas of arterial lumen and endatrium were calculated. Our results showed that, in the allograft group, 28 days after allografting, conspicuous proliferation of smooth muscles and infiltration with a great number of inflammatory cells were found in the tunica intima and tunica media. Astilbin significantly inhibited the proliferation of smooth muscles and ameliorated the infiltration of inflammatory cells thereyby prevent against the development of transplant arteriosclerosis. It is concluded that asltilbin can effectively prevent the development of arteriosclerosis in allotransplant by inhibiting the proliferation of smooth muscles and inhibit the proliferation of smooth muscles in tunica of intima and media and reducing infiltration of the inflammatory cells.
基金supported by agrant from the National Natural Science Foundation of China(No.30500656)
文摘This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (AngⅡ) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngⅡ. Cells were randomly divided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngⅡ model group, cells were treated with AngⅡ at 10–7 mol/L; in three astilbin groups, cells were treated with 10, 15, 30 mg/L of astilbin; in three AngⅡ+astilbin groups, cells were treated with AngⅡ (at 10–7 mol/L) and astilbin at 10, 15, 30 mg/L. Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined. The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR), and the expression of NF-κB in RASMCs was immunocytochemically observed. Our results showed that MTT metabo-lism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G0/G1 phase were increased and that of G2/S phase were decreased markedly. Not only highly expression of c-myc gene stimulated by AngⅡ could be inhibited by Astilbin significantly, but also the expression of NF-κB protein can be down regulated by Astilbin. We are led to conclude that astilbin astilbin can inhibit the AngⅡ-mediated proliferation of RASMCs by blocking the transition of RASMCs from G0/G1 phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.
基金supported by the the Vietnam Academy of Science and Technology under grant NCCC 08.10/20-20the Institute of Biotechnology under grant CS20-01。
文摘Objective:To investigate the osteoblastogenic activity of the ethyl acetate(EtOAc)extract of Smilax glabra Roxb roots and its major active compound astilbin.Methods:Astilbin was isolated from EtOAc extract using silica gel chromatography combined with fraction crystallization.Chemical structure of astilbin was determined by analysis of the spectroscopic data in comparison with the literature.MTT method was used to detect the toxicity.Alkaline phosphatase(ALP)activity was determined by the spectrophotometric method at 405 nm using p-nitrophenyl phosphate as a substrate.Calcium deposition was stained with alizarin red-S,distained with cetylpyridium chloride,and quantified at 562 nm.In silico model for astilbin-ALP interaction was analyzed using AutoDock 4.2.6.The changes in expression of osteoblast differentiation related genes were determined using quantitative real-time PCR.Results:Both the EtOAc extract and astilbin had no toxicity toward osteoblast MC3T3-E1 cells at 5.0,10,25,and 50μg/mL.At 25μg/mL,they enhanced ALP activity and mineralization of osteoblasts up to 30%and 55%for the EtOAc extract and 22%and 41%for astilbin,respectively.Molecular docking analysis of astilbin-ALP interaction revealed Arg167,Asp320,His324,and His437 were key residues participating in hydrophobic interaction;meanwhile,His434 and Thr436 residues were involved in hydrogen bond formation in the active site of human tissue-nonspecific ALP.Moreover,the expression level of genes opn,col1,osx,and runx2 were up-regulated in astilbin treated samples with the fold changes as 2.2;3.7;4.1;2.3,respectively at 10μg/mL(P<0.05).Conclusions:The EtOAc extract and its major compound astilbin exhibit osteoblastogenic activity by up-regulating important markers for bone cell differentiation.It could be a new and promising osteogenic agent with dual actions for therapeutic applications.
