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11.
YAN Jin-chuan WU Zong-gui ZHANG Ling-zhen LI Li FAN Jie LING Ling HAN Wen-yu ZHANG Suo-long 《园艺学报》2002,18(4):344-347
AMI:To clarify whether OX-LDL and simvastatin can induce the changes of PKC activity and cytosolic free Ca2+ in rat aortic smooth muscle cells (ASMC). METHODS:PKC activity and cytosolic free Ca2+ were measured by its ability to transfer phosphate from [32P]ATP to lysine-rich histone and flow cytometric analysis after loading with the Ca2+dye fluo-3/Am, respectively. RESULTS:OX-LDL increased PKC total activity in a dose-dependent manner and induced translocation of PKC from the cytosolic to membrane, while OX-LDL induced biphasic [Ca2+]i responses including the rapid initial transient phase and the sustained phase. When simvastatin was added, the translocation of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but significantly reduced the subsequent plateau phase. CONCLUSSION:OX-LDL can induce dynamic changes of signal transduction of PKC and cytosolic free Ca2+ in ASMC and these two events are closely linked. 相似文献
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AIM:To observe the effect of simvastatin on the proliferation of vascular smooth muscle cells(VSMCs) induced by serum and growth factor PDGF-BB and the effect of simvastatin on the expression of PTEN,a important regulator of G1/S cell cycle transition. METHODS:The DNA synthesis was determined by [3H]-TdR incorporation, cell cycle was examined with flow cytometry, the protein level of PTEN was measured by Western blot method. RESULTS: (1)Simvastatin inhibited [3H]-TdR incorporation in a dose dependent manner. (2) Flow cytometric DNA analysis revealed that simvastatin induced significantly enhancement of G0/G1 phase and decrease in S phase VSMCs.(3)Simvastatin increased protein level of PTEN and mevalonate, a metabolite of HMG-COA, reversed the effect of simvastatin on PTEN protein expression. CONCLUSION:Simvastatin may inhibit proliferation of VSMCs and retarded cell cycle in G0/G1 phase by increasing PTEN expression through inhibiting synthesis of mevalonate. 相似文献
13.
目的观察辛伐他汀对野百合碱（MCT）诱导的肺动脉高压大鼠核因子NF-κB的表达及血清C反应蛋白和TNF-α水平的影响,探讨辛伐他汀治疗肺动脉高压的作用机制。方法将30只健康雄性SD大鼠随机分为正常对照组,MCT诱导的肺动脉高压组（模型对照组）,辛伐他汀干预治疗组（治疗组）。注射野百合碱建立动物模型,右心导管法检测大鼠平均肺动脉压（mPAP）,测量右心室肥大指数（RVHI）。采用Western blot法检测各组大鼠IKKα,IκBα和NF-κB p65蛋白表达情况。结果治疗组大鼠的mPAP和RVHI均显著低于模型对照组;治疗组大鼠肺组织NF-κB p65蛋白表达及血清C反应蛋白和TNF-α水平均明显低于模型对照组,差异均有统计学意义（P＜0.01或0.05）。结论辛伐他汀可有效降低MCT诱导肺动脉高压模型大鼠的肺动脉压、改善肺血管重构,其机理可能与抑制肺组织核因子NF-κB的表达及炎症因子的释放有关。 相似文献
14.
AIM To investigate the effects of simvastatin （SIM） on the proliferation of esophageal cancer Eca109 cells through NF-κB p65 pathway. METHODS Esophageal cancer Eca109 cells were cultured in vitro and treated with SIM at different concentrations （2 , 4, 8, 16 and 32 μmol/L）. The proliferation of Eca109 cells was measured by MTT assay and plate colony formation assay. The proliferation-related protein levels of cyclin D1, c-Myc, NF-κB p65 （p65） and IκB-α in the esophageal cancer Eca109 cells were determined by Western blot. ELISA was used to detect the levels of tumor necrosis factor α （TNF-α） and interleukin-6 （IL-6） in the culture supernatant of Eca109 cells. RESULTS Compared with control group, the inhibitory effects of SIM at 2 , 4 , 8 and 16 μmol/L on the viability of Eca109 cells were increased in a concentration-dependent and time-dependent manners （P <0.05）. Simultaneously, the inhibitory rates of SIM at 16 and 32 μmol/L on the viability of Eca109 cells showed no significant difference （P >0.05）. The inhibitory rates of SIM at 16 μmol/L on the viability of esophageal cancer cells was 50.61% at 48 h, which was closed to half of the inhibitory dose IC50, and it was used as the optimum concentration and time for follow-up experiments. Compared with control group, the plate colony formation rate of Eca109 cells, the protein levels of cyclinD1, c-Myc, nuclear p65, TNF-α and IL-6 in 8 and 16 μmol/L groups were decreased, while the levels of cytosolic p65 and IκB-α proteins were increased （P <0.05）. No significant difference of plate colony formation rate in Eca109 cells, and the protein levels of cyclin D1, c-Myc, nuclear and cytoplasmic p65, IκB-α, TNF-α and IL-6 between 16 μmol/L SIM group and 32 μmol/L SIM group was observed （P >0.05）. CONCLUSION Simvastatin inhibits the proliferation of esophageal cancer Eca109 cells, and its mechanism may be related to up-regulation of IκB-α, down-regulation of cyclinD1 and c-myc, inhibition of p65 nuclear translocation, and the expression of TNF-α and IL-6 downstream of NF-κB p65 pathway. 相似文献
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本文以色谱柱SUPELCOSIL LC-18-DB,33＊4.6 mm,3μm,流速3.0 mL/min,柱温25℃,检测波长238nm,以乙腈-0.1%磷酸（50∶50）和0.1%的磷酸作为流动相。建立一种高效液相色谱测定辛伐他汀咀嚼片中辛伐他汀含量的方法,并对此法进行考察。结果表明辛伐他汀在浓度为0.195 2 mg/mL-0.608 1 mg/mL（浓度水平50%-150%）范围内具有良好的线性,平均回收率为99.3%,RSD为0.64%（n=9）。 相似文献
16.
AIM: To explore the effect of gypenosides (GPs) on PCSK9 gene expression in hyperlipidemic rat liver and the blood lipids lowered by simvastatin.METHODS: Healthy male SD rats (n=60) were randomized into 5 groups:normal control group, hyperlipidemic model group, simvastatin group, GPs group and GPs combined with simvastatin group (combined group). The rats in all groups were fed high-fat diet except normal control group which were fed with ordinary diet. The rats in control group and hyperlipidemic model group were gavaged with 0.3% CMC-Na every day. The rats in GPs group were gavaged with GPs at 160 mg·kg-1·d-1. The rats in simvastatin group were gavaged with simvastatin at 5 mg·kg-1·d-1. The rats in combined group were gavaged with GPs and simvastatin. The experiment lasted for 8 weeks. The rats were anesthetized with chloral hydrate, and abdominal arterial blood samples were collected to detect the total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C). The body weight and the wet weight of the livers were measured, and the liver index was calculated. The pathological changes of the livers were observed under microscope with HE staining. The expression of PCSK9 and low-density lipoprotein receptor (LDLR) at mRNA and protein levels was determined by real-time PCR and Western blot. RESULTS: The model of hyperlipidemia rats was established successfully. Compared with model group, the levels of TC, TG and LDL-C in simvastatin group, GPs group and combined group were obviously decreased (P<0.05), and the HDL-C levels were obviously upregulated (P<0.05). Compared with model group, the liver indexes in simvastatin group, GPs group and combined group were obviously decreased (P<0.05). The pathological changes of the liver tissues showed that hepatic adipose appeared in model group, and that in simvastatin group and GPs group had different degrees of relief, especially in combined group. Compared with model group, the mRNA expression levels of PCSK9 and LDLR in simvastatin group were obviously increased, while the mRNA expression levels of PCSK9 in GPs group and combined group were obviously decreased (P<0.05), and the mRNA expression of LDLR in combined group was obviously increased (P<0.05). Compared with model group, the protein expression of PCSK9 and LDLR in simvastatin group was obviously increased, while the protein expression levels of PCSK9 in GPs group and combined group were obviously reduced, and the LDLR protein levels were obviously increased (P<0.05). CONCLUSION: Gypenosides inhibit the expression of PCSK9 and increase the expression of LDLR in the liver. The combination of gypenosides and simvastatin promotes the lipid-lowering effect of simvastatin and attenuates hepatic steatosis, which may be related to inhibiting the expression of PCSK9 in the liver. 相似文献
17.
JING Jiao MA Hai-ling YAN Wen-sheng ZHANG Yong-zhong ZHANG Yu-qing JIAO Zong-wei 《园艺学报》2017,33(12):2274-2277
AIM: To observe the effect of simvastatin on myocardial tissue after renal ischemia-reperfusion injury and its mechanism. METHODS: A rat model of renal ischemia-reperfusion injury was prepared by clamping the bilateral renal arteries for 45 min. The rats (n=36) were randomly divided into sham operation group, renal ischemia-reperfusion (I/R) group and simvastatin group with 12 rats in each group. The content of serum creatinine (SCr), blood urea nitrogen (BUN) and myocardial tissue malondialdehyde (MDA), the myocardial activity of lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD), and the myocardial protein expression of Bcl-2 and Bax were detected. RESULTS: Compared with sham operation group, the content of SCr, BUN and myocardial MDA, and the myocardial activity of LDH and CK in I/R group were significantly increased (P<0.05), and the activity of SOD was significantly decreased (P<0.05). Compared with I/R group, the content of SCr, BUN and myocardial MDA, and the myocardial activity of LDH and CK in simvastatin group were significantly decreased (P<0.05), while SOD activity was enhanced (P<0.05). The protein expression of Bcl-2 and Bax in sham operation group was less than that in I/R group (P<0.05), and the protein level of Bax in simvastatin group was significantly lower than that in I/R group (P<0.05), while the protein level of Bcl-2 was increased (P<0.05). CONCLUSION: Simvastatin has a protective effect on the myocardium of the rats with renal ischemia-reperfusion injury, and the protective mechanism may be related to the elimination of free radicals by simvastatin, increase in the protein expression of Bcl-2 and decrease in the protein expression of Bax. 相似文献