红景天苷抗动脉粥样硬化机制研究进展
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摘要
动脉粥样硬化(As)是冠心病、脑卒中、外周血管疾病的主要致病原因。如今有多种学说对其发病机制进行阐述,均未阐明具体致病机理。目前临床药物治疗主要以抗血小板聚集、降脂、抗凝及溶栓为主,但对血管内皮的保护却鲜有作用,特异性不佳。中药红景天苷(SAL)在动物模型实验中具有显著的抗As作用。大量机制研究也证实SAL能明显减轻血管内皮细胞损伤、抑制内皮凋亡、延缓内皮衰老、抑制炎症及应激反应、抗泡沫细胞形成并抑制其凋亡的发生、防止血管平滑肌细胞过度增殖、降低血液黏稠度、阻止血栓形成、稳定斑块,从而保护血管系统,抑制As的发生、发展。因此,SAL有望成为阻止As从发生、发展到恶化的整个进程的重要治疗手段。本文综合了近年来SAL干预As的机制研究进展,旨在为进一步的科研和临床应用提供参考价值。
Atherosclerosis(As) is the main cause of coronary heart disease, stroke and peripheral vascular disease. Nowadays, there are many theories to explain its pathogenesis, but none of them has clarified the specific pathogenesis. Anti-platelet aggregation, lipid-lowering, anticoagulation and thrombolysis are the main clinical drugs treatment at present, but they have little effect on the protection of vascular endothelium and have poor specificity. The traditional Chinese medicine salidroside(SAL) has significant anti-As effect in animal model experiments. A large number of mechanism studies have also confirmed that SAL can significantly reduce vascular endothelial cell injury, inhibit endothelial apoptosis, delay endothelial senescence, inhibit inflammation and stress response, prevent foam cell formation and the occurrence of apoptosis, prevent vascular smooth muscle cells from overproliferation, reduce blood viscosity, prevent thrombosis and stabilize plaque, thereby protecting the vascular system and inhibiting the occurrence and development of As. Therefore, SAL is expected to become an important treatment for preventing the entire process of As from occurrence, development to deterioration. This article summarizes the research progress of the mechanism of SAL intervening As in recent years, aiming to provide reference value for further research and clinical application.
Atherosclerosis(As) is the main cause of coronary heart disease, stroke and peripheral vascular disease. Nowadays, there are many theories to explain its pathogenesis, but none of them has clarified the specific pathogenesis. Anti-platelet aggregation, lipid-lowering, anticoagulation and thrombolysis are the main clinical drugs treatment at present, but they have little effect on the protection of vascular endothelium and have poor specificity. The traditional Chinese medicine salidroside(SAL) has significant anti-As effect in animal model experiments. A large number of mechanism studies have also confirmed that SAL can significantly reduce vascular endothelial cell injury, inhibit endothelial apoptosis, delay endothelial senescence, inhibit inflammation and stress response, prevent foam cell formation and the occurrence of apoptosis, prevent vascular smooth muscle cells from overproliferation, reduce blood viscosity, prevent thrombosis and stabilize plaque, thereby protecting the vascular system and inhibiting the occurrence and development of As. Therefore, SAL is expected to become an important treatment for preventing the entire process of As from occurrence, development to deterioration. This article summarizes the research progress of the mechanism of SAL intervening As in recent years, aiming to provide reference value for further research and clinical application.
引文
[1] Zhang J,Liu A,Hou R,et al.Salidroside protects cardiomyocyte against hypoxia-induced death:a HIF-1alpha-activated and VEGF-mediated pathway[J].Eur J Pharmacol,2009,607(1-3):6-14.
[2] Wang XL,Wang X,Xiong LL,et al.Salidroside improves doxorubicin-induced cardiac dysfunction by suppression of excessive oxidative stress and cardiomyocyte apoptosis[J].J Cardiovasc Pharmacol,2013,62(6):512-523.
[3] Li D,Fu Y,Zhang W,et al.Salidroside attenuates inflammatory responses by suppressing nuclear factor-kappa B and mitogen activated protein kinases activation in lipopolysaccharide-induced mastitis in mice[J].Inflamm Res,2013,62(1):9-15.
[4] Mao G,Wang Y,Qiu Q,et al.Salidroside protects human fibroblast cells from premature senescence induced by H2O2 partly through modulating oxidative status[J].Mech Ageing Dev,2010,131(11-12):723-731.
[5] Sun K,Xia H,Xia R.Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway[J].Int J Clin Exp Pathol,2015,8(1):615-621.
[6] Zheng T,Yang X,Wu D,et al.Salidroside ameliorates insulin resistance through activation of a mitochondria-associated AMPK/PI3K/Akt/GSK3 beta pathway[J].Br J Pharmacol,2015,172(13):3284-3301.
[7] De Bock K,Eijnde BO,Ramaekers M,et al.Acute Rhodiola rosea intake can improve endurance exercise performance[J].Int J Sport Nutr Exerc Metab,2004,14(3):298-307.
[8] Shevtsov VA,Zholus BI,Shervarly VI,et al.A randomized trial of two different doses of a SHR-5 Rhodiola rosea extract versus placebo and control of capacity for mental work[J].Phytomedicine,2003,10(2-3):95-105.
[9] Panossian A,Wikman G,Sarris J.Rosenroot (Rhodiola rosea):traditional use,chemical composition,pharmacology and clinical efficacy[J].Phytomedicine,2010,17(7):481-493.
[10] Zhang BC,Li WM,Guo R,et al.Salidroside decreases atherosclerotic plaque formation in low-density lipoprotein receptor-deficient mice[J].Evid Based Complement Alternat Med,2012,2012(5):607508.
[11] 张立平,郑曦,马双陶,等.红景天甙对间歇性低压低氧诱导的ApoE-/-小鼠动脉粥样硬化的影响[J].中国动脉硬化杂志,2014,22(7):675-679.
[12] 阙肖冬,孙岩,吕若谷,等.红景天苷对大鼠实验性血栓形成的影响及其作用机制[J].中国医药指南,2011,9(24):40-41.
[13] Vita JA,Keaney JF Jr.Endothelial function:a barometer for cardiovascular risk?[J].Circulation,2002,106(6):640-642.
[14] Bobermin LD,Wartchow KM,Flores MP,et al.Ammonia-induced oxidative damage in neurons is prevented by resveratrol and lipoic acid with participation of heme oxygenase 1[J].Neurotoxicology,2015,49:28-35.
[15] Park SY,Park DJ,Kim YH,et al.Upregulation of heme oxygenase-1 via PI3K/Akt and Nrf-2 signaling pathways mediates the anti-inflammatory activity of Schisandrin in porphyromonas gingivalis LPS-stimulated macrophages[J].Immunol Lett,2011,139(1-2):93-101.
[16] Zhu Y,Zhang YJ,Liu WW,et al.Salidroside suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway[J].Molecules,2016,21(8):1033.
[17] Xing SS,Yang X,Li W,et al.Salidroside stimulates mitochondrial biogenesis and protects against H2O2-induced endothelial dysfunction[J].Oxid Med Cell Longev,2014,2014(12):904834.
[18] Leung SB,Zhang H,Lau CW,et al.Salidroside improves homocysteine-induced endothelial dysfunction by reducing oxidative stress[J].Evid Based Complement Alternat Med,2013,2013(1):679635.
[19] 刘磊,张舒,张明谦.红景天苷对高糖致内皮细胞表面损伤的保护作用及机制研究[J].中药材,2017,40(4):949-952.
[20] Xu MC,Shi HM,Wang H,et al.Salidroside protects against hydrogen peroxide-induced injury in HUVECs via the regulation of REDD1 and mTOR activation[J].Mol Med Rep,2013,8(1):147-153.
[21] Alameddine A,Fajloun Z,Bourreau J,et al.The cardiovascular effects of salidroside in the Goto-Kakizaki diabetic rat model[J].J Physiol Pharmacol,2015,66(2):249-257.
[22] Sano R,Reed JC.ER stress-induced cell death mechanisms[J].Biochim Biophys Acta,2013,1833(12):3460-3470.
[23] Zhu L,Jia F,Wei J,et al.Salidroside protects against homocysteine-induced injury in human umbilical vein endothelial cells via the regulation of endoplasmic reticulum stress[J].Cardiovasc Ther,2017,35(1):33-39.
[24] 朱琳,王彦军,俞天虹,等.红景天苷通过抑制内质网应激减少高同型半胱氨酸诱导的人脐静脉内皮细胞损伤[J].中国动脉硬化杂志,2015,23(1):5-10.
[25] Zernecke A,Weber C.Chemokines in the vascular inflammatory response of atherosclerosis[J].Cardiovasc Res,2010,86(2):192-201.
[26] 苏燕青,汪旭雯,王颖峥,等.红景天苷对人脐静脉内皮细胞氧糖剥夺/复氧损伤的保护作用[J].中国药理学通报,2018,34(6):831-836.
[27] Choy JC,Granville DJ,Hunt DW,et al.Endothelial cell apoptosis:biochemical characteristics and potential implications for atherosclerosis[J].J Mol Cell Cardiol,2001,33(9):1673-1690.
[28] Zhao X,Jin L,Shen N,et al.Salidroside inhibits endogenous hydrogen peroxide induced cytotoxicity of endothelial cells[J].Biol Pharm Bull,2013,36(11):1773-1778.
[29] Tan CB,Gao M,Xu WR,et al.Protective effects of salidroside on endothelial cell apoptosis induced by cobalt chloride[J].Biol Pharm Bull,2009,32(8):1359-1363.
[30] Zhang Y,Huang S,Leng Y,et al.Effect of DcR3-specific siRNA on cell growth suppression and apoptosis induction in glioma cells via affecting ERK and AKT[J].Onco Targets Ther,2016,9:5195-5202.
[31] Yin Y,Liu H,Wang F,et al.Transplantation of cryopreserved human umbilical cord blood-derived endothelial progenitor cells induces recovery of carotid artery injury in nude rats[J].Stem Cell Res Ther,2015,6(1):1-12.
[32] Tang Y,Vater C,Jacobi A,et al.Salidroside exerts angiogenic and cytoprotective effects on human bone marrow-derived endothelial progenitor cells via Akt/mTOR/p70S6K and MAPK signalling pathways[J].Br J Pharmacol,2014,171(9):2440-2456.
[33] Nazari-Shafti TZ,Cooke JP.Telomerase therapy to reverse cardiovascular senescence[J].Methodist Debakey Cardiovasc J,2015,11(3):172-175.
[34] Sun L,Dou F,Chen J,et al.Salidroside slows the progression of EA.hy926 cell senescence by regulating the cell cycle in an atherosclerosis model[J].Mol Med Rep,2018,17(1):257-263.
[35] Zhang D,Sun X,Liu J,et al.Homocysteine accelerates senescence of endothelial cells via DNA hypomethylation of human telomerase reverse transcriptase[J].Arterioscler Thromb Vasc Biol,2015,35(1):71-78.
[36] Roos CM,Hagler M,Zhang B,et al.Transcriptional and phenotypic changes in aorta and aortic valve with aging and MnSOD deficiency in mice[J].Am J Physiol Heart Circ Physiol,2013,305(10):H1428-H1439.
[37] Xing SS,Li J,Chen L,et al.Salidroside attenuates endothelial cellular senescence via decreasing the expression of inflammatory cytokines and increasing the expression of SIRT3[J].Mech Ageing Dev,2018,175:1-6.
[38] Xing SS,Yang XY,Zheng T,et al.Salidroside improves endothelial function and alleviates atherosclerosis by activating a mitochondria-related AMPK/PI3K/Akt/eNOS pathway[J].Vascul Pharmacol,2015,72(B11):141-152.
[39] Zhang P,Li Y,Guo R,et al.Salidroside protects against advanced glycation end products-induced vascular endothelial dysfunction[J].Med Sci Monit,2018,24:2420-2428.
[40] Fang S,Xu Y,Zhang Y,et al.Irgm1 promotes M1 but not M2 macrophage polarization in atherosclerosispathogenesis and development[J].Atherosclerosis,2016,251:282-290.
[41] Cho W,Kang JL,Park YM.Corticotropin-releasing hormone (CRH) promotes macrophage foam cell formation via reduced expression of ATP binding cassette transporter-1 (ABCA1)[J].PLoS One,2015,10(6):e0130587.
[42] Thakkar S,Wang X,Khaidakov M,et al.Structure-based design targeted at LOX-1,a receptor for oxidized low-density lipoprotein[J].Sci Rep,2015,5:16740.
[43] Ni J,Li Y,Li W,et al.Salidroside protects against foam cell formation and apoptosis,possibly via the MAPK and AKT signaling pathways[J].Lipids Health Dis,2017,16(1):198.
[44] Zhuang X,Maimaitijiang A,Li Y,et al.Salidroside inhibits high-glucose induced proliferation of vascular smooth muscle cells via inhibiting mitochondrial fission and oxidative stress[J].Exp Ther Med,2017,14(1):515-524.
[45] Zheng TP,Liu YH,Yang LX,et al.Increased plasma dipeptidyl peptidase-4 activities are associated with high prevalence of subclinical atherosclerosis in Chinese patients with newly diagnosed type 2 diabetes:a cross-sectional study[J].Atherosclerosis,2015,242(2):580-588.
[46] Fernandez-Velasco M,Ruiz-Hurtado G,Gomez AM,et al.Ca2+ handling alterations and vascular dysfunction in diabetes[J].Cell Calcium,2014,56(5):397-407.
[47] Tousoulis D,Papageorgiou N,Androulakis E,et al.Diabetes mellitus-associated vascular impairment:novel circulating biomarkers and therapeutic approaches[J].J Am Coll Cardiol,2013,62(8):667-676.
[48] Beckman JA,Creager MA,Libby P.Diabetes and atherosclerosis:epidemiology,pathophysiology,and management[J].JAMA,2002,287(19):2570-2581.
[49] Srivastava SP,Shi S,Koya D,et al.Lipid mediators in diabetic nephropathy[J].Fibrogenesis Tissue Repair,2014,7(1):12-12.
[50] Li F,Tang H,Xiao F,et al.Protective effect of salidroside from Rhodiolae Radix on diabetes-induced oxidative stress in mice[J].Molecules,2011,16(12):9912-9924.
[51] Li HB,Ge YK,Zheng XX,et al.Salidroside stimulated glucose uptake in skeletal muscle cells by activating AMP-activated protein kinase[J].Eur J Pharmacol,2008,588(2-3):165-169.
[52] Ju L,Wen X,Wang C,et al.Salidroside,a natural antioxidant,improves beta-cell survival and function via activating AMPK pathway[J].Front Pharmacol,2017,8:749.
[53] Ono K,Horie T,Nishino T,et al.MicroRNAs and high-density lipoprotein cholesterol metabolism[J].Int Heart J,2015,56(4):365-371.
[54] Iliopoulos D,Drosatos K,Hiyama Y,et al.MicroRNA-370 controls the expression of microRNA-122 and Cpt1 alpha and affects lipid metabolism[J].J Lipid Res,2010,51(6):1513-1523.
[55] Zhang XR,Fu XJ,Zhu DS,et al.Salidroside-regulated lipid metabolism with down-regulation of miR-370 in type 2 diabetic mice[J].Eur J Pharmacol,2016,779:46-52.
[2] Wang XL,Wang X,Xiong LL,et al.Salidroside improves doxorubicin-induced cardiac dysfunction by suppression of excessive oxidative stress and cardiomyocyte apoptosis[J].J Cardiovasc Pharmacol,2013,62(6):512-523.
[3] Li D,Fu Y,Zhang W,et al.Salidroside attenuates inflammatory responses by suppressing nuclear factor-kappa B and mitogen activated protein kinases activation in lipopolysaccharide-induced mastitis in mice[J].Inflamm Res,2013,62(1):9-15.
[4] Mao G,Wang Y,Qiu Q,et al.Salidroside protects human fibroblast cells from premature senescence induced by H2O2 partly through modulating oxidative status[J].Mech Ageing Dev,2010,131(11-12):723-731.
[5] Sun K,Xia H,Xia R.Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway[J].Int J Clin Exp Pathol,2015,8(1):615-621.
[6] Zheng T,Yang X,Wu D,et al.Salidroside ameliorates insulin resistance through activation of a mitochondria-associated AMPK/PI3K/Akt/GSK3 beta pathway[J].Br J Pharmacol,2015,172(13):3284-3301.
[7] De Bock K,Eijnde BO,Ramaekers M,et al.Acute Rhodiola rosea intake can improve endurance exercise performance[J].Int J Sport Nutr Exerc Metab,2004,14(3):298-307.
[8] Shevtsov VA,Zholus BI,Shervarly VI,et al.A randomized trial of two different doses of a SHR-5 Rhodiola rosea extract versus placebo and control of capacity for mental work[J].Phytomedicine,2003,10(2-3):95-105.
[9] Panossian A,Wikman G,Sarris J.Rosenroot (Rhodiola rosea):traditional use,chemical composition,pharmacology and clinical efficacy[J].Phytomedicine,2010,17(7):481-493.
[10] Zhang BC,Li WM,Guo R,et al.Salidroside decreases atherosclerotic plaque formation in low-density lipoprotein receptor-deficient mice[J].Evid Based Complement Alternat Med,2012,2012(5):607508.
[11] 张立平,郑曦,马双陶,等.红景天甙对间歇性低压低氧诱导的ApoE-/-小鼠动脉粥样硬化的影响[J].中国动脉硬化杂志,2014,22(7):675-679.
[12] 阙肖冬,孙岩,吕若谷,等.红景天苷对大鼠实验性血栓形成的影响及其作用机制[J].中国医药指南,2011,9(24):40-41.
[13] Vita JA,Keaney JF Jr.Endothelial function:a barometer for cardiovascular risk?[J].Circulation,2002,106(6):640-642.
[14] Bobermin LD,Wartchow KM,Flores MP,et al.Ammonia-induced oxidative damage in neurons is prevented by resveratrol and lipoic acid with participation of heme oxygenase 1[J].Neurotoxicology,2015,49:28-35.
[15] Park SY,Park DJ,Kim YH,et al.Upregulation of heme oxygenase-1 via PI3K/Akt and Nrf-2 signaling pathways mediates the anti-inflammatory activity of Schisandrin in porphyromonas gingivalis LPS-stimulated macrophages[J].Immunol Lett,2011,139(1-2):93-101.
[16] Zhu Y,Zhang YJ,Liu WW,et al.Salidroside suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway[J].Molecules,2016,21(8):1033.
[17] Xing SS,Yang X,Li W,et al.Salidroside stimulates mitochondrial biogenesis and protects against H2O2-induced endothelial dysfunction[J].Oxid Med Cell Longev,2014,2014(12):904834.
[18] Leung SB,Zhang H,Lau CW,et al.Salidroside improves homocysteine-induced endothelial dysfunction by reducing oxidative stress[J].Evid Based Complement Alternat Med,2013,2013(1):679635.
[19] 刘磊,张舒,张明谦.红景天苷对高糖致内皮细胞表面损伤的保护作用及机制研究[J].中药材,2017,40(4):949-952.
[20] Xu MC,Shi HM,Wang H,et al.Salidroside protects against hydrogen peroxide-induced injury in HUVECs via the regulation of REDD1 and mTOR activation[J].Mol Med Rep,2013,8(1):147-153.
[21] Alameddine A,Fajloun Z,Bourreau J,et al.The cardiovascular effects of salidroside in the Goto-Kakizaki diabetic rat model[J].J Physiol Pharmacol,2015,66(2):249-257.
[22] Sano R,Reed JC.ER stress-induced cell death mechanisms[J].Biochim Biophys Acta,2013,1833(12):3460-3470.
[23] Zhu L,Jia F,Wei J,et al.Salidroside protects against homocysteine-induced injury in human umbilical vein endothelial cells via the regulation of endoplasmic reticulum stress[J].Cardiovasc Ther,2017,35(1):33-39.
[24] 朱琳,王彦军,俞天虹,等.红景天苷通过抑制内质网应激减少高同型半胱氨酸诱导的人脐静脉内皮细胞损伤[J].中国动脉硬化杂志,2015,23(1):5-10.
[25] Zernecke A,Weber C.Chemokines in the vascular inflammatory response of atherosclerosis[J].Cardiovasc Res,2010,86(2):192-201.
[26] 苏燕青,汪旭雯,王颖峥,等.红景天苷对人脐静脉内皮细胞氧糖剥夺/复氧损伤的保护作用[J].中国药理学通报,2018,34(6):831-836.
[27] Choy JC,Granville DJ,Hunt DW,et al.Endothelial cell apoptosis:biochemical characteristics and potential implications for atherosclerosis[J].J Mol Cell Cardiol,2001,33(9):1673-1690.
[28] Zhao X,Jin L,Shen N,et al.Salidroside inhibits endogenous hydrogen peroxide induced cytotoxicity of endothelial cells[J].Biol Pharm Bull,2013,36(11):1773-1778.
[29] Tan CB,Gao M,Xu WR,et al.Protective effects of salidroside on endothelial cell apoptosis induced by cobalt chloride[J].Biol Pharm Bull,2009,32(8):1359-1363.
[30] Zhang Y,Huang S,Leng Y,et al.Effect of DcR3-specific siRNA on cell growth suppression and apoptosis induction in glioma cells via affecting ERK and AKT[J].Onco Targets Ther,2016,9:5195-5202.
[31] Yin Y,Liu H,Wang F,et al.Transplantation of cryopreserved human umbilical cord blood-derived endothelial progenitor cells induces recovery of carotid artery injury in nude rats[J].Stem Cell Res Ther,2015,6(1):1-12.
[32] Tang Y,Vater C,Jacobi A,et al.Salidroside exerts angiogenic and cytoprotective effects on human bone marrow-derived endothelial progenitor cells via Akt/mTOR/p70S6K and MAPK signalling pathways[J].Br J Pharmacol,2014,171(9):2440-2456.
[33] Nazari-Shafti TZ,Cooke JP.Telomerase therapy to reverse cardiovascular senescence[J].Methodist Debakey Cardiovasc J,2015,11(3):172-175.
[34] Sun L,Dou F,Chen J,et al.Salidroside slows the progression of EA.hy926 cell senescence by regulating the cell cycle in an atherosclerosis model[J].Mol Med Rep,2018,17(1):257-263.
[35] Zhang D,Sun X,Liu J,et al.Homocysteine accelerates senescence of endothelial cells via DNA hypomethylation of human telomerase reverse transcriptase[J].Arterioscler Thromb Vasc Biol,2015,35(1):71-78.
[36] Roos CM,Hagler M,Zhang B,et al.Transcriptional and phenotypic changes in aorta and aortic valve with aging and MnSOD deficiency in mice[J].Am J Physiol Heart Circ Physiol,2013,305(10):H1428-H1439.
[37] Xing SS,Li J,Chen L,et al.Salidroside attenuates endothelial cellular senescence via decreasing the expression of inflammatory cytokines and increasing the expression of SIRT3[J].Mech Ageing Dev,2018,175:1-6.
[38] Xing SS,Yang XY,Zheng T,et al.Salidroside improves endothelial function and alleviates atherosclerosis by activating a mitochondria-related AMPK/PI3K/Akt/eNOS pathway[J].Vascul Pharmacol,2015,72(B11):141-152.
[39] Zhang P,Li Y,Guo R,et al.Salidroside protects against advanced glycation end products-induced vascular endothelial dysfunction[J].Med Sci Monit,2018,24:2420-2428.
[40] Fang S,Xu Y,Zhang Y,et al.Irgm1 promotes M1 but not M2 macrophage polarization in atherosclerosispathogenesis and development[J].Atherosclerosis,2016,251:282-290.
[41] Cho W,Kang JL,Park YM.Corticotropin-releasing hormone (CRH) promotes macrophage foam cell formation via reduced expression of ATP binding cassette transporter-1 (ABCA1)[J].PLoS One,2015,10(6):e0130587.
[42] Thakkar S,Wang X,Khaidakov M,et al.Structure-based design targeted at LOX-1,a receptor for oxidized low-density lipoprotein[J].Sci Rep,2015,5:16740.
[43] Ni J,Li Y,Li W,et al.Salidroside protects against foam cell formation and apoptosis,possibly via the MAPK and AKT signaling pathways[J].Lipids Health Dis,2017,16(1):198.
[44] Zhuang X,Maimaitijiang A,Li Y,et al.Salidroside inhibits high-glucose induced proliferation of vascular smooth muscle cells via inhibiting mitochondrial fission and oxidative stress[J].Exp Ther Med,2017,14(1):515-524.
[45] Zheng TP,Liu YH,Yang LX,et al.Increased plasma dipeptidyl peptidase-4 activities are associated with high prevalence of subclinical atherosclerosis in Chinese patients with newly diagnosed type 2 diabetes:a cross-sectional study[J].Atherosclerosis,2015,242(2):580-588.
[46] Fernandez-Velasco M,Ruiz-Hurtado G,Gomez AM,et al.Ca2+ handling alterations and vascular dysfunction in diabetes[J].Cell Calcium,2014,56(5):397-407.
[47] Tousoulis D,Papageorgiou N,Androulakis E,et al.Diabetes mellitus-associated vascular impairment:novel circulating biomarkers and therapeutic approaches[J].J Am Coll Cardiol,2013,62(8):667-676.
[48] Beckman JA,Creager MA,Libby P.Diabetes and atherosclerosis:epidemiology,pathophysiology,and management[J].JAMA,2002,287(19):2570-2581.
[49] Srivastava SP,Shi S,Koya D,et al.Lipid mediators in diabetic nephropathy[J].Fibrogenesis Tissue Repair,2014,7(1):12-12.
[50] Li F,Tang H,Xiao F,et al.Protective effect of salidroside from Rhodiolae Radix on diabetes-induced oxidative stress in mice[J].Molecules,2011,16(12):9912-9924.
[51] Li HB,Ge YK,Zheng XX,et al.Salidroside stimulated glucose uptake in skeletal muscle cells by activating AMP-activated protein kinase[J].Eur J Pharmacol,2008,588(2-3):165-169.
[52] Ju L,Wen X,Wang C,et al.Salidroside,a natural antioxidant,improves beta-cell survival and function via activating AMPK pathway[J].Front Pharmacol,2017,8:749.
[53] Ono K,Horie T,Nishino T,et al.MicroRNAs and high-density lipoprotein cholesterol metabolism[J].Int Heart J,2015,56(4):365-371.
[54] Iliopoulos D,Drosatos K,Hiyama Y,et al.MicroRNA-370 controls the expression of microRNA-122 and Cpt1 alpha and affects lipid metabolism[J].J Lipid Res,2010,51(6):1513-1523.
[55] Zhang XR,Fu XJ,Zhu DS,et al.Salidroside-regulated lipid metabolism with down-regulation of miR-370 in type 2 diabetic mice[J].Eur J Pharmacol,2016,779:46-52.