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AIM: To observe the effect of microRNA-19a (miR-19a) on the lipid catabolism of hepatocyte LO2, and to explore the potential mechanism. METHODS: miR-19a was over-expressed or silenced by transfection of miR-19a mimics or miR-19a inhibitor into LO2 cells, then the mRNA level of miR-19a was detected by real-time PCR. The potential target of miR-19a was found by the method of bioinformatics through internet website. The effect of miR-19a on the 3' UTR of peroxisome proliferator-activated receptor α (PPARα) was measured by dual luciferase reporter assay, and the protein level of PPARα and its 2 major downstream rate-limiting enzymes involved in lipid catabolism, acyl-coenzyme a dehydrogenase (ACADM) and carnitine palmitoyltransferase 1A (CPT1A), were detected by Western blotting. Meanwhile, the effect of miR-19a on the generation of ketone body was measured by beta-hydroxybutyric acid (β-OHB) detection assay. RESULTS: The mRNA level of miR-19a was dramatically elevated by the transfection of miR-19a mimics, and sharply decreased by the transfection of miR-19a inhibitor (P<0.05). PPARα was found as a potential target of miR-19a, and dual luciferase reporter assay and Western blotting confirmed the regulatory effect of miR-19a on the expression of PPARα, with the protein level changes of ACADM and CPT1A. miR-19a mimics down-regulated, while miR-19a inhibitor up-regulated the concentration of β-OHB in LO2 cells (P<0.05). CONCLUSION: miR-19a regulates the lipid catabolism of hepatocytes by targeting the PPARα and its 2 downstream rate-limiting enzymes. 相似文献
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AIM: To investigate the changes of peroxisome proliferator-activated receptors (PPAR)α/peroxisome proliferator activated receptor coactivator 1 alpha (PGC-1α) in doxorubicin (DOX) induced dilated cardiomyopathy (DCM) and its effect on the energy metabolism and myocardial function in mice. METHODS: Forty mice were randomly divided into 4 groups: control group, DOX group, PPARα inhibitor group and PPARα agonist group. The DCM model was established by injection of DOX. The protein levels of PPARα/PGC-1α were detected. The PPARα inhibitor and PPARα agonist were used 2 weeks beforeinjection of DOX. The contents of adenine acid and phosphocreatine (Pcr) in the mitochondria were measured by high-performance liquid chromatography (HPLC). The ANT activity was analyzed by the atractyloside-inhibitor stop technique. The changes of the echocardiography and hemodynamics were also observed. RESULTS: DOX induced DCM model was successfully established. The protein levels of PPARα and PGC-1α in control group were significantly higher than those in DOX group (P<0.05). Both of the high-energy phosphate contents and the transport activity of ANT were decreased in DOX group (P<0.05), and the hemodynamic parameters were disordered (P<0.01). Compared with DOX group, PPARα inhibitor pre-treatment significantly reduced the PPARα/PGC-1α expression. Meanwhile, high-energy phosphate contents in the mitochondria and the ANT transport activity of the mitochondria decreased, as well as the left ventricular function (P<0.05). On the other hand, PPARα agonist significantly increased the expression of PPARα and PGC-1α, and improved the transport activity of ANT. In addition, the hemodynamic parameters were ameliorated, but the high-energy phosphate contents of the mitochondria did not significantly change. CONCLUSION: PPARα/PGC-1α plays an important role in the regulation of ANT transport activity in dilated cardiomyopathy induced by DOX, and the activation of PPARα/PGC-1α has protective effects on the DCM induced by DOX. 相似文献
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HUANG Jin-xian LUO Jia-ni LIU Pei-qing CHEN Shao-rui HUANG Qiu-ju PAN Xue-diao ZANG Lin-quan ZHOU Si-gui 《园艺学报》2014,30(5):769-778
AIM：To study the effect of short-chain acyl-coenzyme A dehydrogenase (SCAD）on cardiac hypertrophy and to explore the role of adenosine monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor α (PPARα） signal pathway in the regulation of SCAD during the development of cardiac hypertrophy. METHODS：The optimal sequence of SCAD interference was chosen by Western blotting and real-time PCR. The cardiomyocytes were treated with fenofibrate (10 μmol/L) for 24 h and subsequently stimulated with the optimal sequence of SCAD interference. The changes of SCAD expression at mRNA and protein levels, the enzyme activity of SCAD, the cardiomyocyte surface area and free fatty acids were determined. Using real-time PCR for analyzing the markers of cardiac hypertrophy, the mRNA expression of atrial natriuretic factor (ANF） and brain natriuretic peptide (BNP) was detected to judge the development of cardiac hypertrophy. The cardiomyocytes were treated with fenofibrate (10 μmol/L) or AMPK activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR, 0.5 mmol/L) for 30 min and subsequently stimulated with phenylephrine (PE, 20 μmol/L) for 24 h. The changes of cardiomyocyte surface area, free fatty acids, and the expression of SCAD, PPARα and p-AMPKα (T172) at mRNA and protein levels were observed. RESULTS：The effect of optimal sequence siRNA-1186 and PE on the cardiomyocytes was the same. Compared with control group, the expression of ANF and BNP at mRNA level, the cardiomyocyte surface area and free fatty acids were increased obviously in siRNA-1186 group. After pretreated with fenofibrate (10 μmol/L), the expression of PPARα and SCAD, and the enzyme activity of SCAD were significantly increased, while the free fatty acids were decreased, indicating that fenofibrate prevented the development of cardiac hypertrophy induced by knockdown of SCAD. Compared with control group, the expression of SCAD, PPARα and p-AMPKα (T172) at mRNA and protein levels was significantly down-regulated, and the enzyme activity of SCAD was obviously decreased in PE group. Compared with PE group, the expression of SCAD, PPARα and p-AMPKα (T172) was significantly up-regulated, and the cardiomyocyte surface area and the content of free fatty acids were obviously decreased in the cardiomyocytes pretreated with fenofibrate or AICAR for 30 min. CONCLUSION：Down-regulation of SCAD is related to the cardiac hypertrophy and energy metabolism. AMPK/PPARα/SCAD signaling pathway may regulate cardiac hypertrophy directly. 相似文献
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HUANG Qiu-ju HUANG Jin-xian LUO Jia-ni LIU Pei-qing CHEN Shao-rui PAN Xue-diao ZANG Lin-quan ZHOU Si-gui 《园艺学报》2014,30(8):1427-1432
AIM：To investigate the different effects of ERK1/2/PPARα/SCAD (short-chain acyl-CoA dehydrogenase) signal pathways on the cardiac hypertrophy induced by insulin-like growth factors 1 (IGF-1) or phenylephrine (PE). METHODS：The neonatal rat cardiomyocytes induced by IGF-1 were used as the model of physiological cardiac hypertrophy, and those induced by PE were used as the model of pathological cardiac hypertrophy. The surface area of the cardiomyocytes, the expression of p-ERK1/2, PPARα and SCAD, the activity of SCAD and the content of free fatty acid in the cardiomyocytes were measured. RESULTS：Compared with the control cells, the surface area of the cardiomyocytes induced by IGF-1 and PE were both increased. Compared with the controls, the expression of SCAD and PPARα, and the activity of SCAD in the cardiomyocytes induced by IGF-1 were increased, while the expression of p-ERK1/2 was decreased. However, the cardiomyocytes treated with PE showed decreased expression of SCAD and PPARα, decreased activity of SCAD and increased expression of p-ERK1/2. Meanwhile, the decrease in free fatty acid in IGF-1-induced cardiomyocytes and the increase in PE-induced cardiomyocytes indicated that the fatty acid utilization was increased in the cardiomyocytes induced by IGF-1, but decreased in the cardiomyocytes induced by PE. CONCLUSION：The changes of p-ERK1/2, PPARα and SCAD in the cardiac hypertrophy induced by IGF-1 or PE indicate that the effects of ERK1/2/PPARα/SCAD signal pathways are different between physiological cardiac hypertrophy and pathological cardiac hypertrophy, and that SCAD may be a molecular marker of these 2 different cardiac hypertrophies and a potential therapeutic target for pathological cardiac hypertrophy. 相似文献
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AIM: To observe the effect of Tangshenfang (TS) on the liver protection and the levels of silent information regulator 1 (SIRT1) and peroxisom proliferator-activated receptor γ coactivator-1α (PGC-1α) in the liver tissue. METHODS: The rat model of diabetes mellitus (DM) was established by intravenous injection of streptozotocin (STZ;30 mg/kg) after having the high fat/high glucose diets for 1 month. The diabetic rats were randomly divided into DM group, DM with high-dose TS (TSHi) group, medium-dose TS (TSMed) group and low-dose TS (TSLow)group. The normal rats were served as control group. There were 8 rats in each group. After treatment with TS for 12 weeks, the serum biochemical indices including fasting blood glucose (FBG), triglyceride (TG), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were tested. Fasting insulin (FINS) was also detected by radioimmunoassay, and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. The serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) were measured by ELISA. The activity of SOD and content of MDA in the liver tissues were measured by the methods of hydroxylamine and thiobarbituric acid. The liver pathological changes were observed under light microscope with HE and Masson staining. The protein expression of SIRT1and PGC-1α in the liver tissues was determined by Western blot. RESULTS: In DM group, serum FBG, TG, ALT, AST, FINS, HOMA-IR, TNF-α and IL-1 were obviously increased compared with the control group (P<0.01). The fatty changes, local necrosis, inflammation and fibrosis in the liver tissues were observed. The content of MDA in liver increased, while the activity of SOD decreased markedly. The protein expression of SIRT1 and PGC-1α was decreased (P<0.05). In TS treatment groups, all these changes in DM rats were markedly reversed by TS, and the protein expression of SIRT1 and PGC-1α in the liver tissues was markedly increased. CONCLUSION: TS may protect the rats from diabetic liver injury by increasing the expression of SIRT1 and PGC-1α, and thereby improving insulin resistance and oxidative stress. 相似文献
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AIM: To investigate the effect of over-expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) on mitochondrial morphology and cell apoptosis in the cortical neurons with oxygen glucose deprivation/reoxygenation (OGD/R). METHODS: The whole gene sequence of PGC-1α was obtained from the cerebral cortex of C57BL/6 mice by RT-PCR and cloned into the eukaryotic expression vector pEGFP-N1. The pEGFP-N1-PGC-1α was identified by PCR, and transfected into cortical neurons. The level of PGC-1α expression was identified by Western blot. The cortical neurons transfected with pEGFP-N1 and pEGFP-N1-PGC-1α vectors were treated with OGD/R. The mitochondrial mass, reactive oxygen species (ROS) and ATP production, cell apoptosis and changes of cleaved caspase-3 were detected by MitoTracker Red staining, flow cytometry, ATP metabolic assay kit and TUNEL. RESULTS: Over-expression of PGC-1α inhibited the decrease in mitochondrial biogenesis capacity and the ROS formation of OGD/R neurons (P<0.05), enhanced the ability of ATP synthesis (P<0.01), inhibited neuronal apoptosis (P<0.01) and decreased the activation of caspase-3 (P<0.01). CONCLUSION: PGC-1α over-expression inhibits neuronal apoptosis with OGD/R treatment by promoting mitochondrial biogenesis, inhibiting the production of ROS and maintaining mitochondrial function. PGC-1α may be used as a target for the development of cerebral ischemia/reperfusion injury drugs. 相似文献
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HU Qin ZHANG Yun ZHANG Xian-jun FENG Jin-bo LIU Chun-xi JIANG Hong JIANG Gui-hua WANG Rong 《园艺学报》2006,22(12):2289-2295
AIM: To investigate the relationship of PPARγ gene expression with the composition of aortic plaque in apoE-knock out mice. METHODS: PPARγ gene and protein in aortic area of 20-week-old and 40-week-old apoE-knock out mice were investigated using RT-PCR and immunoblotting. The same aged wild type mice (C57BL/6J) were served as control (n=10). The composition of aortic plaques was analyzed by Movat method and oil red O staining. The expression of antigens such as PPARγ, SM-actin and MOMA-2 in aortic plaque were compared using immunohistochemistry. The relationship of PPARγ with macrophage, smooth muscle cells (SMC), lipid, elastic fiber, collagen and proteoglycan in aortic plaque were analyzed using immunofluorescence. RESULTS: PPARγ gene and protein in aortic wall and plaque of apoE-knock out mice were more significant than that in the same aged C57BL/6J mice (P<0.05). PPARγ expression at 40-week-old apoE-knock out mice was most significant and very low in C57BL/6J mice. More PPARγ expression of gene and protein at 20-week-old C57BL/6J mice than 40-week-old C57BL/6J mice were observed. Compared with 20-week-old apoE-/- mice, the lipid pool in aortic plaque at 40-week-old apoE-/- mice were increased remarkably, while elastic fiber, collagen and proteoglycan in plaque were decreased and aortic remodeling was very significant. Even, upregulation of MOMA-2 and downregulation of SM-actin were also detected in latter (P<0.05). In addition to SMC of aortic tunica media, PPARγ also expressed in SMC and macrophages in the aortic plaque of apoE-/- mice. PPARγ was very enriched in lipid pool of the plaque. CONCLUSION: PPARγ expression level decreases with aging in C57BL/6J mice, while increases with plaque progression in apoE-knock out mice. There is positive correlation between PPARγ expression and lipid composition in plaque. The observed upregulation of PPARγ gene expression in aortic plaque may be a compensatory behavior and protective mechanism in apoE-knock out mice. 相似文献
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AIM:To investigate the effects of resveratrol (RSV) on cardiac dysfunction and acid sphingomyelinase (ASMase)-ceramide pathway in diabetic rats. METHODS:Type 2 diabetes mellitus (T2DM) model was established by a high-fat diet combined with STZ intraperitoneac injection (30 mg/kg). SD rats (n=20) were randomly divided into control group, T2DM group; T2DM+RSV group (diabetic rats were given resveratrol at 100 mg·kg·d-1 by intragastric administration for the treatment) and RSV group (some of control rats were selected to give the same dose of RSV for drug control group). The M-mode Doppler ultrasonography was performed to observe the changes of cardiac function and structure in the rats. The levels of serum glucose, lipid and superoxide dismutase (SOD) activity, malondialdehyde (MDA) content in heart tissues were measured. Oil red O staining and Sirius red staining were performed to observe lipid accumulation and cardiac fibrosis in heart tissues. The cardiac ceramide concentration in diabetic rats was analyzed by high-performance liquid chromatography. The protein expression of ASMase and peroxisome proliferator-activated receptor-γ co-activator 1α (PGC-1α) in the hearts was determined by Western blot. RESULTS:Compared with the control group, the levels of fasting blood glucose, total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) were significantly elevated in T2DM group. The values of ±dp/dtmax, fractional shortening and ejection fraction were declined, and the left ventricle internal dimension at end-systole (LVIDs) and left ventricle internal at end-diastole (LVIDd) were increased. Furthermore, increased MDA content and more lipid accumulation were also observed in diabetic hearts, while the SOD activity, ATP content and PGC-1α expression were reduced in diabetic hearts. However, all these parameters were reversed by addition of RSV, concomitant with decreased ASMase expression and ceramide content. CONCLUSION:RSV dramatically alleviates diabetes-induced cardiac dysfunction and cardiac fibrosis, which may attribute to inhibition of ASMase-ceramide activation. 相似文献
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ZHANG Ling SUN Meng SHI Bo TANG Li-li WU Cun-zao CAI Yong XIA Peng ZHENG Shao-ling YANG Yi-rong CHEN Bi-cheng 《园艺学报》2014,30(8):1363-1367
AIM：To investigate the effect of immunosuppressant FK506 on serum glucose in rats and to explore its mechanism. METHODS：Sprague-Dawley rats (n=12) were randomly divided into drug group and normal group. The rats in drug group were intraperitoneally injected with FK506 at dose of 1 mg·kg-1·d-1 and the rats in normal group received saline (1 mL·kg-1·d-1, ip) for 14 d. The fasting weight and fasting glucose were regularly measured every 2 d. Visceral fat was isolated from the rats at the end of experiment. The mRNA expression of adiponectin, leptin, visfatin, resistin, retinol-binding protein 4 (RBP4) and peroxisome proliferator-activated receptors γ (PPAR-γ) was determined by real-time fluorescence quantitative PCR. The protein expression of PPAR-γ and adiponectin was measured by Western blotting. RESULTS：Compared with normal group, the concentration of fasting blood glucose in model group was significantly increased from the 10th day (P<0.05). At day 14, the fasting blood glucose of the model group increased from (5.10±062) mmol/L to (7.73 ± 0.73) mmol/L. No significant change of blood glucose in normal group between the 10th day and the 14th day ［from (4.66 ± 0.32) mmol/L to (5.80±0.10) mmol/L］ was observed. Compared with normal group, the mRNA expression of PPAR-γ, adiponectin and leptin in the adipose tissue of model group was significantly decreased (P<001), whereas the expression of visfatin, resistin and RBP4 was significantly increased (P<005). Compared with normal group, the expression of PPAR-γ and adiponectin in model group was decreased (P<001). CONCLUSION：FK506 may decrease the expression of PPAR-γ to change the expression of adipocytokines and induce hyperglycemia in rats. 相似文献
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AIM:To investigate the effect of diosgenin (Dio) on the proliferation, apoptosis and expression of peroxisome proliferator-activated receptor γ (PPARγ) in human glioblastoma U87MG cells and its possible mechanism. METHODS:Human astrocytes (HA) and U87MG cells were cultured in vitro and treated with Dio (0, 10, 20, 30, 40 and 50 μmol/L) and GW9662 (5 μmol/L) for 48 h, and then the cell viability was detected by CCK-8 assay. Cell colony formation assay was used to assess the proliferation potential. Flow cytometry was used to analyze the cell cycle distribution and apoptosis. The mRNA expression level of PPARγ was measured by RT-PCR. Western blot was used to determine the protein levels of PPARγ, cyclin D1, cyclin E1, Bcl-2 and Bax. RESULTS:Dio had no significant influence on the viabi-lity of HA (P>0.05). However, Dio remarkably reduced the viability of U87MG cells in a dose-dependent manner (P<0.05) with IC50 of 24.31 μmol/L. Meanwhile, Dio remarkably diminished colony formation ability (P<0.05), induced G0/G1 phase arrest of the cell cycle and apoptosis (P<0.05), up-regulated the expression of PPARγ at mRNA and protein levels, increased the protein level of Bax (P<0.05), and down-regulated the protein levels of cyclin D1, cyclin E1 and Bcl-2 (P<0.05) in a dose-dependent manner. However, these effects induced by Dio were inhibited by GW9662 (P<0.05), a specific inhibitor of PPARγ. CONCLUSION:Dio may inhibit proliferation and induce apoptosis in human glioblastoma U87MG cells most likely via up-regulating the expression of PPARγ, and then down-regulating the protein levels of cyclin D1, cyclin E1 and Bcl-2, and up-regulating the protein level of Bax. 相似文献
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AIM: To investigate the effect of ryanodine receptor 1 (RYR1) down-regulation on mitochondria in mouse myoblast C2C12 cell line and to explore the possible mechanism. METHODS: The expression of RYR1 in the C2C12 cells was knocked down by the targeted small interfering RNA (siRNA). The mitochondrial number and morpholo-gical changes were evaluated by transmission electron microscopy and the stereoscopic analysis. Real-time PCR and Western blot were used to determine the mRNA and protein levels of mitofusin 2 (Mfn2), peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) and extracellular signal-regulated kinase 1/2 (ERK1/2), respectively. RESULTS: The expression of RYR1 was significantly down-regulated by siRNA transfection (P<0.01), with fragmentized mitochondria in the C2C12 cells in knock-down (KD) group. Although no statistical difference of the mitochondrial number was observed, the mitochondria area and circumference were significantly lowered in KD group (P<0.05). In KD group, the mRNA and protein expression of Mfn2 was significantly reduced (P<0.01). The mRNA level of PGC-1α was also reduced (P<0.01), but no significant change at protein level was observed. No change of ERK1/2 expression and phosphorylated ERK1/2 level was detected. CONCLUSION: Knock-down of RYR1 expression leads to morphological changes of mitochondria, and down-regulation of Mfn2 expression may be involved in the underlying mechanism. While PGC-1α and ERK1/2-associated oxidative stress pathway may not play an important role in the process. 相似文献
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AIM: To investigate the role of Rho-kinase signal pathway in rat cardiac fibroblasts (CFBs) proliferation and collagen synthesis induced by angiotensinⅡ (AngⅡ). METHODS: CFBs of neonatal Sprague-Dawley (SD) rats were isolated with the method of trypsin digestion and differential anchoring velocity. The CFBs were stimulated with AngⅡto induce fibrosis. Proliferation of CFBs was observed by MTT coloricmetric assay. Synthesis of collagen was detected by the hydroxyproline. The expression of Rho-kinase mRNA was examined using RT-PCR analysis. The extent of phosphorylation of myosin-binding subunit (MBS-P) of myosin phosphatase was quantified by Western blotting analysis, which was used to evaluate the activity of Rho-kinase.RESULTS: (1) Stimulation of neonatal SD rat CFBs with AngⅡ (10-7 mol/L) significantly increased CFBs proliferation and collagen synthesis (P<0.01). (2）Stimulation of neonatal SD rat CFBs with AngⅡ (10-7 mol/L) significantly increased the expression of Rho-kinase mRNA and rapidly activated Rho-kinase in a time-dependent manner. (3) Within a concentration coverage, hydroxyfasudil (H4413), a Rho-kinase inhibitor, effectively inhibited AngⅡ-induced CFBs proliferation and collagen synthesis (P<0.05 or P<0.01).CONCLUSION: Rho-kinase signal pathway may be one of the most important signal transducter for AngⅡ-induced CFBs proliferation and collagen synthesis in neonatal SD rats. 相似文献
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WANG Pei-jian WANG Qiu-lin YANG Zhen WANG Fang PU Chun-hua LI Wen-zhang LIANG Deng-pan ZHOU Peng 《园艺学报》2015,31(1):49-53
AIM: To explore the effects of PPARγ on the elevated level of reactive oxygen species (ROS) induced by high glucose and its mechanism. METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured with DMEM containing high glucose (33 mmol/L D-glucose), and DMEM containing lower glucose (5.5 mmol/L D-glucose) was used as control. Superoxide anion and nitric oxide fluorescence probes were used to observe the effects of PPARγ agonist on ROS and NO productions in the HUVECs. The uncoupling protein 2 (UCP2) protein level in the HUVECs was detected by Western blotting. RESULTS: PPARγ agonist pioglitazone inhibited the ROS generation and prevented the decrease in NO level under high glucose condition, and these effects were reversed by pretreatment with PPARγ antagonist GW9662. The results of Western blotting indicated that PPARγ agonist pioglitazone up-regulated the UCP2 expression under high glucose condition, and this effect was also blocked by GW9662. Inhibition of UCP2 by genipin attenuated the effect of pioglotazone on the ROS production. CONCLUSION: Activation of PPARγ inhibits ROS generation under high glucose condition, and this effect may mediate by up-regulation of UCP2. 相似文献
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AIM To observe the changes of liver lipid metabolism-related peroxisome proliferator-activated receptor-γ (PPAR-γ)/liver X receptor-α (LXR-α)/ATP-binding cassette transporter G1 (ABCG1) signaling pathways and inflammatory factors in mice with atherosclerosis (AS), and to investigate the effects of Huayu-Qutan recipe (HYQT) on hepatic lipid metabolism and inflammatory response and the mechanisms. METHODS
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AIM: To explore the protective effect of phytosterol ester (PSE) on aortic aging in rats. METHODS: The female SD rats (12 months old, n=42) were randomly divided into control group, model group and PSE group. During the experiment, the rats in control group, model group and PSE group were treated with basic feed, high-fat diet (HFD) and HFD with 2% PSE (W/W) for 6 months, respectively. The morphological changes of the aorta were observed by HE staining and Masson staining, and the absolute area of smooth muscle cells and collagen fiber in the vascular wall were measured by image analysis. The levels of advanced glycosylation end products (AGEs), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) in the plasma were detected. The expression of silent information regulator 1 (SIRT1) and peroxisome proliferator-activated receptor γ (PPARγ) at mRNA and protein levels in the vascular tissue was determined by real time PCR and Western blot, respectively. RESULTS: PSE significantly lowered plasma TC and LDL-C, and increased plasma HDL-C level (P<0.05), but had no effect on plasma TG level. PSE significantly attenuated the thickening of intima and media of aging aortic, and decreased the migration of vascular smooth muscle cells (VSMC) and the amount of VSMC and collagen fiber in the aorta (P<0.05). PSE significantly reduced the contents of AGEs and MDA (P<0.05), but had no effect on the activity of SOD and CAT in the plasma. PSE also down-regulated the expression of PPARγ and up-regulated the expression of SIRT1 (P<0.05). CONCLUSION: PSE is able to attenuate the senescence process in the aorta by reducing the production of reactive oxygen species in plasma, and activating SIRT1, or inhibiting the expression of PPARγ in vascular tissues. 相似文献
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AIM: To investigate the inhibitory effect of peroxisome proliferator-activated receptor δ (PPARδ) agonist GW501516 on the apoptosis induced by oxidized low-density lipoprotein(ox-LDL) or high concentration of glucose in human umbilical vein endothelial cells (HUVECs). METHODS: Cell apoptosis was induced by ox-LDL or high concentration of glucose in HUVECs and was examined by flow cytometry.The HUVECs were treated with GW501516 at different concentrations. The viability of HUVECs was analyzed by MTT assay. RESULTS: The apoptosis rate of HUVECs treated with ox-LDL was 21.3%, while those of HUVECs treated with ox-LDL combined with low, medium and high concentrations of GW501516 were 17.47%, 9.72% and 3.94%, respectively. The apoptosis rate of HUVECs treated with glucose was 22.60%, while those of HUVECs treated with glucose combined with different concentrations of GW501516 were 20.23%, 17.01% and 9.38%, respectively.The results indicated that ox-LDL or glucose induced apoptosis of HUVECs and GW501516 decreased the apoptotic rates induced by ox-LDL or glucose in a dose-dependent manner. The results of MTT assay showed that glucose or ox-LDL decreased the viability of HUVECs and GW501516 attenuated the effect of glucose or ox-LDL on HUVECs. CONCLUSION: GW501516 inhibits the apoptotic effects of ox-LDL and glucose on HUVECs and increases the viability of the cells. 相似文献