目的探讨雷公藤多苷对Ig A肾病（Ig A nephropathy,Ig AN）患者血清离子及β2糖蛋白I（β2-glycoprotein,β2-GPI）/氧化低密度脂蛋白（oxidized low density lipoprotein,ox-LDL）的影响。方法收集丽水市人民医院肾内科2014年1月~2015...目的探讨雷公藤多苷对Ig A肾病（Ig A nephropathy,Ig AN）患者血清离子及β2糖蛋白I（β2-glycoprotein,β2-GPI）/氧化低密度脂蛋白（oxidized low density lipoprotein,ox-LDL）的影响。方法收集丽水市人民医院肾内科2014年1月~2015年4月收治的原发性Ig AN患者54例,随机分为对照组和实验组,每组27例,对照组患者常规给予盐酸贝那普利片10 mg,1次/天口服;给予双嘧达莫片50 mg,3次/天口服,实验组在对照组基础上给予雷公藤多苷片20 mg,3次/天口服。2组患者均治疗6个月。治疗结束后,对所有患者的血清Ca、P、β2-GPI/ox-LDL水平及肾功能相关指标进行检测。结果与对照组治疗后比较,实验组患者血清Ca水平较高,血清P水平较低（P〈0.05）;实验组患者的血清β2-GPI/ox-LDL水平较低（P〈0.05）;实验组患者的血清Scr、BUN水平较低（P〈0.05）。结论雷公藤多苷能够显著降低Ig AN患者血清P、β2-GPI/ox-LDL、Scr及BUN水平,提高血清Ca水平,改善肾功能。展开更多
[Objectives] To explore the protective effect and possible mechanisms of the coenzyme Q10( CoQ 10) on the human umbilical vein endothelial cell( HUVEC) injury induced by the oxidized low-density lipoprotein( ox-LDL). ...[Objectives] To explore the protective effect and possible mechanisms of the coenzyme Q10( CoQ 10) on the human umbilical vein endothelial cell( HUVEC) injury induced by the oxidized low-density lipoprotein( ox-LDL). [Methods]With the human umbilical vein endothelial cells( HUVECs) cultured in vitro as the test target,the HUVECs were randomly divided into 5 groups: normal control group; model group; low concentration CoQ10 group( 12. 5); medium concentration CoQ10 group( 25); high concentration CoQ10 group( 50). The CCK-8 method was used to test the cell viability,and the drug concentration was screened in 60 μM of CoQ 10 toxic concentration; the total protein was extracted and Western blot was used to detect the protein expression of c-fos,c-jun and PON2; the RT-PCR method was used for determination of the content of c-fos,c-jun and PON2 mRNA. [Results]Compared with the normal group,the cell viability was significantly reduced in the 35 μg/m L high ox-LDL model group,and the cell injury was induced; compared with model group,after 12 h pre-protection,12. 5 μM,25 μM,50 μM CoQ10 could all significantly improve the survival of injured cells( P < 0. 05); compared with the normal group;the protein and mRNA levels of c-fos,c-jun,PON2 in the model group all declined; compared with the model group,the protein level and mRNA expression of c-fos,c-jun,PON2 in different CoQ10 groups increased to varying degrees( P < 0. 05). [Conclusions] CoQ 10 could reduce the HUVEC injury induced by high ox-LDL,and possible mechanism was achieved by upregulating the expression of AP-1 and PON2.展开更多
Objectives Bone morphogenetic protein-2 (BMP-2) plays an key role both in vascular development and pathophysiological processes. However, the mechanisms of oxidized low density lipoprotein (ox-LDL) and combinated with...Objectives Bone morphogenetic protein-2 (BMP-2) plays an key role both in vascular development and pathophysiological processes. However, the mechanisms of oxidized low density lipoprotein (ox-LDL) and combinated with atorvastatin or probucol on BMP-2 expression are entirely unknown in human umbilical vein cells. Methods The HUVECs were treated by ox-LDL and combinated with atorvastatin, probucol. The expression of BMP-2, NF-κB65, PPARγ mRNA was examined by RT-PCR analysis and ELISA method. The MDA and SOD were detected by routine methods. Results Ox-LDL can induced BMP-2 mNRA expression, associated with NF-κB65 mNRA expression activation. Both atorvastatin and probucol can suppress BMP-2 and NF-κB65 expression induced by oxLDL and upregulate the expression of PPARγ. Furthermore, the increase of supernatant MDA levels and decrease of supernatant SOD levels resulted from oxLDL treatment can be reversed by probucol or atorvastatin. Conclusions OxLDL-induced BMP-2 mNRA expression can be suppressed by atorvastatin and probucol, which may be accomplished by activating NF-κB65 expression and upregulating the expression of PPARγ. Our findings also indicate that that BMP-2 mNRA expression includes the activation of reactive oxygen species.展开更多
基金Supported by Project of National Natural Science Foundation(81274126)
文摘[Objectives] To explore the protective effect and possible mechanisms of the coenzyme Q10( CoQ 10) on the human umbilical vein endothelial cell( HUVEC) injury induced by the oxidized low-density lipoprotein( ox-LDL). [Methods]With the human umbilical vein endothelial cells( HUVECs) cultured in vitro as the test target,the HUVECs were randomly divided into 5 groups: normal control group; model group; low concentration CoQ10 group( 12. 5); medium concentration CoQ10 group( 25); high concentration CoQ10 group( 50). The CCK-8 method was used to test the cell viability,and the drug concentration was screened in 60 μM of CoQ 10 toxic concentration; the total protein was extracted and Western blot was used to detect the protein expression of c-fos,c-jun and PON2; the RT-PCR method was used for determination of the content of c-fos,c-jun and PON2 mRNA. [Results]Compared with the normal group,the cell viability was significantly reduced in the 35 μg/m L high ox-LDL model group,and the cell injury was induced; compared with model group,after 12 h pre-protection,12. 5 μM,25 μM,50 μM CoQ10 could all significantly improve the survival of injured cells( P < 0. 05); compared with the normal group;the protein and mRNA levels of c-fos,c-jun,PON2 in the model group all declined; compared with the model group,the protein level and mRNA expression of c-fos,c-jun,PON2 in different CoQ10 groups increased to varying degrees( P < 0. 05). [Conclusions] CoQ 10 could reduce the HUVEC injury induced by high ox-LDL,and possible mechanism was achieved by upregulating the expression of AP-1 and PON2.
文摘Objectives Bone morphogenetic protein-2 (BMP-2) plays an key role both in vascular development and pathophysiological processes. However, the mechanisms of oxidized low density lipoprotein (ox-LDL) and combinated with atorvastatin or probucol on BMP-2 expression are entirely unknown in human umbilical vein cells. Methods The HUVECs were treated by ox-LDL and combinated with atorvastatin, probucol. The expression of BMP-2, NF-κB65, PPARγ mRNA was examined by RT-PCR analysis and ELISA method. The MDA and SOD were detected by routine methods. Results Ox-LDL can induced BMP-2 mNRA expression, associated with NF-κB65 mNRA expression activation. Both atorvastatin and probucol can suppress BMP-2 and NF-κB65 expression induced by oxLDL and upregulate the expression of PPARγ. Furthermore, the increase of supernatant MDA levels and decrease of supernatant SOD levels resulted from oxLDL treatment can be reversed by probucol or atorvastatin. Conclusions OxLDL-induced BMP-2 mNRA expression can be suppressed by atorvastatin and probucol, which may be accomplished by activating NF-κB65 expression and upregulating the expression of PPARγ. Our findings also indicate that that BMP-2 mNRA expression includes the activation of reactive oxygen species.
