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Chen Yan - One of the best experts on this subject based on the ideXlab platform.
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Vinpocetine protects against the development of experimental abdominal aortic aneurysms.
Clinical science (London England : 1979), 2020Co-Authors: Chongyang Zhang, Chia George Hsu, Amy Mohan, Hangchuan Shi, Chen YanAbstract:Abdominal aortic aneurysm (AAA), commonly occurring in the aged population, is a degenerative disease that dilate and weaken infrarenal aorta due to progressive degeneration of aortic wall integrity. Vinpocetine, a derivative of alkaloid vincamine, has long been used for cerebrovascular disorders and cognitive impairment in the aged population. Recent studies have indicated that Vinpocetine antagonizes occlusive vascular disorders such as intimal hyperplasia and atherosclerosis. However, its role in vascular degenerative disease AAA remains unexplored. Herein, we determined the effect of Vinpocetine on the formation of AAA as well as the intervention of pre-existing moderate AAA. AAA was induced by periaortic elastase application in C57BL/6J mice. Systemic Vinpocetine treatment was applied daily via intraperitoneal injection. We showed that Vinpocetine pre-treatment remarkably attenuated aneurysmal dilation assessed by diameter and volume. More importantly, Vinpocetine also significantly suppressed the progression of pre-existing moderate AAA in a post-intervention model. Vinpocetine improved multiple cellular and molecular changes associated with AAA, such as elastin degradation, media smooth muscle cell depletion, collagen fibers remodeling and macrophage infiltration in aneurysmal tissues. Vinpocetine potently suppressed tumor necrosis factor-α-induced nuclear factor kappa-light-chain-enhancer of activated B cells activation and proinflammatory mediator expression in primary cultured macrophages in vitro, as well as in the aorta wall in vivo, suggesting Vinpocetine conferred anti-AAA effect at least partially via the inhibition of inflammation. Taken together, our findings reveal a novel role of Vinpocetine in AAA formation, development and progression. Given the excellent safety profile of Vinpocetine, the present study suggests Vinpocetine may be a novel therapeutic agent for AAA prevention and treatment.
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Updates of Recent Vinpocetine Research in Treating Cardiovascular Diseases.
Journal of cellular immunology, 2020Co-Authors: Chongyang Zhang, Chen YanAbstract:Vinpocetine is a derivative of vincamine. It has been used to prevent and treat cerebrovascular disorders such as stoke and dementia, and remains widely available in dietary supplements that often marketed as nootropics. Due to its excellent safety profile at therapeutic dose regimen, Vinpocetine has raised research interest in its new applications in various experimental disease models. Here we review recent studies that uncovered novel functions of Vinpocetine in cardiovascular diseases, including atherosclerosis, obesity, neointimal hyperplasia, vasoconstriction, pathological cardiac remodeling and ischemia stroke. Molecular mechanisms underlined the protective effects of Vinpocetine are also discussed. These novel findings may suggest a broadened usage of Vinpocetine against relevant cardiovascular diseases in human.
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An update on Vinpocetine: New discoveries and clinical implications.
European journal of pharmacology, 2017Co-Authors: Yi-shuai Zhang, Chen YanAbstract:Vinpocetine, a derivative of the alkaloid vincamine, has been clinically used in many countries for treatment of cerebrovascular disorders such as stroke and dementia for more than 30 years. Currently, Vinpocetine is also available in the market as a dietary supplement to enhance cognition and memory. Due to its excellent safety profile, increasing efforts have been put into exploring the novel therapeutic effects and mechanism of actions of Vinpocetine in various cell types and disease models. Recent studies have revealed a number of novel functions of Vinpocetine, including anti-inflammation, antagonizing injury-induced vascular remodeling and high-fat-diet-induced atherosclerosis, as well as attenuating pathological cardiac remodeling. These novel findings may facilitate the repositioning of Vinpocetine for preventing or treating relevant disorders in humans.
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Vinpocetine attenuates lipid accumulation and atherosclerosis formation
Biochemical and biophysical research communications, 2013Co-Authors: Yujun Cai, Chen YanAbstract:Atherosclerosis, the major cause of myocardial infarction and stroke, is a chronic arterial disease characterized by lipid deposition and inflammation in the vessel wall. Cholesterol, in low-density lipoprotein (LDL), plays a critical role in the pathogenesis of atherosclerosis. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. Recent study indicated that Vinpocetine is a potent anti-inflammatory agent. However, its role in the pathogenesis of atherosclerosis remains unexplored. In the present study, we show that Vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet. In cultured murine macrophage RAW264.7 cells, Vinpocetine markedly attenuated oxidized LDL (ox-LDL) uptake and foam cell formation. Moreover, Vinpocetine greatly blocked the induction of ox-LDL receptor 1 (LOX-1) in cultured macrophages as well as in the LOX-1 level in atherosclerotic lesions. Taken together, our data reveal a novel role of Vinpocetine in reduction of pathogenesis of atherosclerosis, at least partially through suppressing LOX-1 signaling pathway. Given the excellent safety profile of Vinpocetine, this study suggests Vinpocetine may be a therapeutic candidate for treating atherosclerosis.
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Vinpocetine suppresses pathological vascular remodeling by inhibiting vascular smooth muscle cell proliferation and migration
Journal of Pharmacology and Experimental Therapeutics, 2012Co-Authors: Yujun Cai, Walter E Knight, Shujie Guo, Peter A Knight, Chen YanAbstract:Abnormal vascular smooth muscle cell (SMC) activation is associated with various vascular disorders such as atherosclerosis, in-stent restenosis, vein graft disease, and transplantation-associated vasculopathy. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. However, its role in pathological vascular remodeling remains unexplored. Herein, we show that systemic administration of Vinpocetine significantly reduced neointimal formation in carotid arteries after ligation injury. Vinpocetine also markedly decreased spontaneous remodeling of human saphenous vein explants in ex vivo culture. In cultured SMCs, Vinpocetine dose-dependently suppressed cell proliferation and caused G1-phase cell cycle arrest, which is associated with a decrease in cyclin D1 and an increase in p27Kip1 levels. In addition, Vinpocetine dose-dependently inhibited platelet-derived growth factor (PDGF)-stimulated SMC migration as determined by the two-dimensional migration assays and three-dimensional aortic medial explant invasive assay. Moreover, Vinpocetine significantly reduced PDGF-induced type I collagen and fibronectin expression. It is noteworthy that PDGF-stimulated phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2), but not protein kinase B, was specifically inhibited by Vinpocetine. Vinpocetine powerfully attenuated intracellular reactive oxidative species (ROS) production, which largely mediates the inhibitory effects of Vinpocetine on ERK1/2 activation and SMC growth. Taken together, our results reveal a novel function of Vinpocetine in attenuating neointimal hyperplasia and pathological vascular remodeling, at least partially through suppressing ROS production and ERK1/2 activation in SMCs. Given the safety profile of Vinpocetine, this study provides insight into the therapeutic potential of Vinpocetine in proliferative vascular disorders.
Qiu-hua Liang - One of the best experts on this subject based on the ideXlab platform.
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Vinpocetine Attenuates the Osteoblastic Differentiation of Vascular Smooth Muscle Cells.
PloS one, 2016Co-Authors: Lin Sun, Xiu-juan Chen, Na Wang, Min Song, Bo Zhang, Yu-zhong Wang, Qiu-hua LiangAbstract:Vascular calcification is an active process of osteoblastic differentiation of vascular smooth muscle cells; however, its definite mechanism remains unknown. Vinpocetine, a derivative of the alkaloid vincamine, has been demonstrated to inhibit the high glucose-induced proliferation of vascular smooth muscle cells; however, it remains unknown whether Vinpocetine can affect the osteoblastic differentiation of vascular smooth muscle cells. We hereby investigated the effect of Vinpocetine on vascular calcification using a beta-glycerophosphate-induced cell model. Our results showed that Vinpocetine significantly reduced the osteoblast-like phenotypes of vascular smooth muscle cells including ALP activity, osteocalcin, collagen type I, Runx2 and BMP-2 expression as well as the formation of mineralized nodule. Vinpocetine, binding to translocation protein, induced phosphorylation of extracellular signal-related kinase and Akt and thus inhibited the translocation of nuclear factor-kappa B into the nucleus. Silencing of translocator protein significantly attenuated the inhibitory effect of Vinpocetine on osteoblastic differentiation of vascular smooth muscle cells. Taken together, Vinpocetine may be a promising candidate for the clinical therapy of vascular calcification.
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Effect of Vinpocetine on phosphorylation of MAPK and Akt as well as the translocation of NF-кB p65 in β-GP-stimulated VSMCs.
2016Co-Authors: Lin Sun, Xiu-juan Chen, Na Wang, Min Song, Bo Zhang, Yu-zhong Wang, Qiu-hua LiangAbstract:β-GP-stimulated VSMCs were treated with Vinpocetine for the indicated time. After the culture, VSMCs were harvested for the Western blot analysis. As it was shown, 15μM of Vinpocetine induced significant phosphorylation of ERK and Akt as well as the inhibition of NF-кB translocation in VSMCs at 5min after treatment, and the effect of Vinpocetine peaked at 15min after treatment (A-B). Neither p38 nor JNK were phosphorylated by the treatment of Vinpocetine (C). To further confirm the effect of Vinpocetine on phosphorylation of ERK, Akt and translocation of NF-кB in VSMCs, VSMCs with and without β-GP were respectively treated with Vinpocetine for 15 min. As it was shown (D-E), there was no difference in the phosphorylation of ERK and Akt as well as the expression of NF-кB p65 in the nucleus between VSMCs treated with β-GP plus Vinpocetine and those with Vinpocetine only. Representative results from three independent experiments were shown.
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Vinpocetine inhibited the osteoblastic differentiation of VSMCs via TSPO.
2016Co-Authors: Lin Sun, Xiu-juan Chen, Na Wang, Min Song, Bo Zhang, Yu-zhong Wang, Qiu-hua LiangAbstract:As it was shown, VSMCs were treated with or without Vinpocetine under different conditions. After the culture, cells were harvested for the analysis of the mRNA expression of TSPO. Our data showed that Vinpocetine significantly promoted the mRNA expression of TSPO in VSMCs (A). β-GP-stimulated VSMCs were transfected with TSPO siRNA or the scramble siRNA in the presence of 15μM Vinpocetine. The Western blot analysis showed that TSPO siRNA significantly silenced the expression of TSPO in VSMCs (B-C). TSPO siRNA significantly blockaded the effect of Vinpocetine on phosphorylation of ERK and Akt as well as the translocation of NF-кB p65 in β-GP-stimulated VSMCs (D-E). Meanwhile, the inhibitory effect of Vinpocetine on both ALP activity and the mRNA expression of Runx2, BMP-2 and TGF-β1 in β-GP-stimulated VSMCs were significantly blockaded by the TSPO siRNA (F-G). The Alizad S staining showed that TSPO siRNA significantly attenuated the inhibitory effect of Vinpocetine on β-GP-induced matrix mineralization of VSMCs (H-I). Representative results from three independent experiments were shown.
K L Bedi - One of the best experts on this subject based on the ideXlab platform.
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amelioration of intracerebroventricular streptozotocin induced cognitive dysfunction and oxidative stress by Vinpocetine a pde1 inhibitor
European Journal of Pharmacology, 2009Co-Authors: Rahul Deshmukh, Vivek Sharma, Sidharth Mehan, Nidhi Sharma, K L BediAbstract:Enhancing cyclic nucleotides signaling by inhibition of phosphodiesterases (PDEs) is known to be beneficial in disorders associated with cognitive decline. The present study was designed to investigate the effect of Vinpocetine (PDE1 inhibitor) on intracerebroventricular (i.c.v.) streptozotocin induced experimental sporadic dementia of Alzheimer's type. Infusion of streptozotocin impaired learning and memory, increased oxidative-nitritive stress and induced cholinergic hypofunction in rats. Chronic treatment with Vinpocetine (5, 10 and 20 mg/kg i.p.) for 21 days following first i.c.v. streptozotocin infusion significantly improved learning and memory in Morris water maze and passive avoidance paradigms. Further, Vinpocetine significantly reduced the oxidative-nitritive stress, as evidenced by decrease in malondialdehyde (MDA) and nitrite levels, and restored the reduced glutathione (GSH) levels. Significant increase in acetylcholinesterase activity and lactate dehydrogenase levels was observed in the present model indicating cholinergic hypofunction and increase in neuronal cell damage. Chronic treatment with Vinpocetine also reduced significantly the increase in acetylcholinesterase activity and lactate dehydrogenase levels indicating restorative capacity of Vinpocetine with respect to cholinergic functions and preventing the neuronal damage. The observed beneficial effects of Vinpocetine on spatial memory may be due to its ability to favorably modulate cholinergic functions, prevent neuronal cell damage and possibly through its antioxidant mechanism also.
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Amelioration of intracerebroventricular streptozotocin induced cognitive dysfunction and oxidative stress by Vinpocetine — a PDE1 inhibitor
European Journal of Pharmacology, 2009Co-Authors: Rahul Deshmukh, Vivek Sharma, Sidharth Mehan, Nidhi Sharma, K L BediAbstract:Enhancing cyclic nucleotides signaling by inhibition of phosphodiesterases (PDEs) is known to be beneficial in disorders associated with cognitive decline. The present study was designed to investigate the effect of Vinpocetine (PDE1 inhibitor) on intracerebroventricular (i.c.v.) streptozotocin induced experimental sporadic dementia of Alzheimer's type. Infusion of streptozotocin impaired learning and memory, increased oxidative-nitritive stress and induced cholinergic hypofunction in rats. Chronic treatment with Vinpocetine (5, 10 and 20 mg/kg i.p.) for 21 days following first i.c.v. streptozotocin infusion significantly improved learning and memory in Morris water maze and passive avoidance paradigms. Further, Vinpocetine significantly reduced the oxidative-nitritive stress, as evidenced by decrease in malondialdehyde (MDA) and nitrite levels, and restored the reduced glutathione (GSH) levels. Significant increase in acetylcholinesterase activity and lactate dehydrogenase levels was observed in the present model indicating cholinergic hypofunction and increase in neuronal cell damage. Chronic treatment with Vinpocetine also reduced significantly the increase in acetylcholinesterase activity and lactate dehydrogenase levels indicating restorative capacity of Vinpocetine with respect to cholinergic functions and preventing the neuronal damage. The observed beneficial effects of Vinpocetine on spatial memory may be due to its ability to favorably modulate cholinergic functions, prevent neuronal cell damage and possibly through its antioxidant mechanism also.
Vladimir Nekrassov - One of the best experts on this subject based on the ideXlab platform.
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Vinpocetine blockade of sodium channels inhibits the rise in sodium and calcium induced by 4 aminopyridine in synaptosomes
Neurochemistry International, 2005Co-Authors: Maria Sitges, Emilio J Galvan, Vladimir NekrassovAbstract:The objective of this study was to get a more understandable picture of the mechanism underlying the anticonvulsant action of Vinpocetine. The question of how the cerebral excitability is affected was investigated by determining the effect of Vinpocetine on the changes on the internal concentrations of Na(+) (Na(i)) and Ca(2+) (Ca(i)) induced by different concentrations of the convulsing agent 4-aminopyridine (4-AP) in striatal isolated nerve endings. The cytosolic concentrations of Na(i) and Ca(i) were detected fluorimetrically with sodium-binding benzofuran isophthalate (SBFI) and fura-2, respectively. Vinpocetine, like the Na(+) channel blocker, tetrodotoxin, abolished the increase in Na(i) induced by 0.1 mM 4-AP and only inhibited in 30% the rise in Na(i) induced by 1mM 4-AP. In contrast with the different sensitivity of the rise in Na(i) induced by 0.1 and 1mM 4-AP to Vinpocetine and tetrodotoxin, the rise in Ca(i) induced by the two concentrations of 4-AP was markedly inhibited by Vinpocetine (and tetrodotoxin), indicating that only the voltage-sensitive sodium channels (VSSC)-mediated fraction of the rise in Na(i) induced by 4-AP is linked with the activation of pre-synaptic Ca(2+) channels. The elevation of Ca(2+) induced by high K(+) (30 mM) does not require a Na(+) gradient and is Vinpocetine and tetrodotoxin insensitive. In contrast, the elevation of Ca(i) induced by 4-AP, requires a physiological (out/in) Na(+) gradient and is Vinpocetine and tetrodotoxin-sensitive. It is concluded that by blocking the tetrodotoxin-sensitive fraction of the rise in Na(i) induced by 4-AP, Vinpocetine inhibits the concomitant rise in Ca(i) induced by 4-AP. The inhibitory effect of Vinpocetine on pre-synaptic voltage-sensitive sodium channels may underlie the in vivo anticonvulsant action of Vinpocetine.
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Vinpocetine Selectively Inhibits Neurotransmitter Release Triggered by Sodium Channel Activation
Neurochemical research, 1999Co-Authors: Maria Sitges, Vladimir NekrassovAbstract:The effects of Vinpocetine on internal Na+ (Nai), cAMP accumulation, internal Ca2+ (Cai) and excitatory amino acid neurotransmitters release, under resting and under depolarized conditions, was investigated in rat striatum synaptosomes. Veratridine (20 μM) or high K+ (30 mM) were used as depolarizing agents. Results show that Vinpocetine in the low μM range inhibits the elevation of Nai, the elevation of Cai and the release of glutamate and aspartate induced by veratridine depolarization. In contrast, Vinpocetine fails to inhibit the rise of Cai and the neurotransmitter release induced by high K+, which are both TTX insensitive responses. Results also show that the inhibition exerted by Vinpocetine on all the above veratridine-induced responses is not reflected in PDE activity. Our interpretation of these results is that Vinpocetine inhibits neurotransmitter release triggered by veratridine activation of voltage sensitive Na+ channels, but not that triggered by a direct activation of VSCC. Thus, the main mechanism involved in the neuroprotective action of Vinpocetine in the CNS is unlikely to be due to a direct inhibition of Ca2+ channels or PDE enzymes, but rather the inhibition of presynaptic Na+ channel-activation unchained responses.
Yu-zhong Wang - One of the best experts on this subject based on the ideXlab platform.
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Vinpocetine Inhibited the CpG Oligodeoxynucleotide-induced Immune Response in Plasmacytoid Dendritic Cells
Immunological investigations, 2016Co-Authors: Xungang Feng, Yu-zhong Wang, Yanlei Hao, Jun Dai, Zhibo Liang, Yantao Liu, Yan SongAbstract:ABSTRACTPlasmacytoid dendritic cells (pDCs) exert dual roles in immune responses through inducing inflammation and maintaining immune tolerance. A switch of pDC phenotype from pro-inflammation to tolerance has therapeutic promise in the treatment of autoimmune diseases. Vinpocetine, a vasoactive vinca alkaloid extracted from the periwinkle plant, has recently emerged as an immunomodulatory agent. In this study, we evaluated the effect of Vinpocetine on phenotype of pDCs isolated from C57BL/6 mice and explored its possible mechanism. Our data showed that Vinpocetine significantly downregulated the expression of CD40, CD80, and CD86 on pDCs and increased the expression of translocator protein (TSPO), the specific receptor of Vinpocetine, in pDCs. Vinpocetine significantly inhibited the Toll-like receptor 9 signaling pathway and reduced the secretion of related cytokines in pDCs through TSPO. Furthermore, viability of pDCs was significantly promoted by Vinpocetine. These findings imply that Vinpocetine serve...
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Vinpocetine Attenuates the Osteoblastic Differentiation of Vascular Smooth Muscle Cells.
PloS one, 2016Co-Authors: Lin Sun, Xiu-juan Chen, Na Wang, Min Song, Bo Zhang, Yu-zhong Wang, Qiu-hua LiangAbstract:Vascular calcification is an active process of osteoblastic differentiation of vascular smooth muscle cells; however, its definite mechanism remains unknown. Vinpocetine, a derivative of the alkaloid vincamine, has been demonstrated to inhibit the high glucose-induced proliferation of vascular smooth muscle cells; however, it remains unknown whether Vinpocetine can affect the osteoblastic differentiation of vascular smooth muscle cells. We hereby investigated the effect of Vinpocetine on vascular calcification using a beta-glycerophosphate-induced cell model. Our results showed that Vinpocetine significantly reduced the osteoblast-like phenotypes of vascular smooth muscle cells including ALP activity, osteocalcin, collagen type I, Runx2 and BMP-2 expression as well as the formation of mineralized nodule. Vinpocetine, binding to translocation protein, induced phosphorylation of extracellular signal-related kinase and Akt and thus inhibited the translocation of nuclear factor-kappa B into the nucleus. Silencing of translocator protein significantly attenuated the inhibitory effect of Vinpocetine on osteoblastic differentiation of vascular smooth muscle cells. Taken together, Vinpocetine may be a promising candidate for the clinical therapy of vascular calcification.
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Effect of Vinpocetine on phosphorylation of MAPK and Akt as well as the translocation of NF-кB p65 in β-GP-stimulated VSMCs.
2016Co-Authors: Lin Sun, Xiu-juan Chen, Na Wang, Min Song, Bo Zhang, Yu-zhong Wang, Qiu-hua LiangAbstract:β-GP-stimulated VSMCs were treated with Vinpocetine for the indicated time. After the culture, VSMCs were harvested for the Western blot analysis. As it was shown, 15μM of Vinpocetine induced significant phosphorylation of ERK and Akt as well as the inhibition of NF-кB translocation in VSMCs at 5min after treatment, and the effect of Vinpocetine peaked at 15min after treatment (A-B). Neither p38 nor JNK were phosphorylated by the treatment of Vinpocetine (C). To further confirm the effect of Vinpocetine on phosphorylation of ERK, Akt and translocation of NF-кB in VSMCs, VSMCs with and without β-GP were respectively treated with Vinpocetine for 15 min. As it was shown (D-E), there was no difference in the phosphorylation of ERK and Akt as well as the expression of NF-кB p65 in the nucleus between VSMCs treated with β-GP plus Vinpocetine and those with Vinpocetine only. Representative results from three independent experiments were shown.
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Vinpocetine inhibited the osteoblastic differentiation of VSMCs via TSPO.
2016Co-Authors: Lin Sun, Xiu-juan Chen, Na Wang, Min Song, Bo Zhang, Yu-zhong Wang, Qiu-hua LiangAbstract:As it was shown, VSMCs were treated with or without Vinpocetine under different conditions. After the culture, cells were harvested for the analysis of the mRNA expression of TSPO. Our data showed that Vinpocetine significantly promoted the mRNA expression of TSPO in VSMCs (A). β-GP-stimulated VSMCs were transfected with TSPO siRNA or the scramble siRNA in the presence of 15μM Vinpocetine. The Western blot analysis showed that TSPO siRNA significantly silenced the expression of TSPO in VSMCs (B-C). TSPO siRNA significantly blockaded the effect of Vinpocetine on phosphorylation of ERK and Akt as well as the translocation of NF-кB p65 in β-GP-stimulated VSMCs (D-E). Meanwhile, the inhibitory effect of Vinpocetine on both ALP activity and the mRNA expression of Runx2, BMP-2 and TGF-β1 in β-GP-stimulated VSMCs were significantly blockaded by the TSPO siRNA (F-G). The Alizad S staining showed that TSPO siRNA significantly attenuated the inhibitory effect of Vinpocetine on β-GP-induced matrix mineralization of VSMCs (H-I). Representative results from three independent experiments were shown.