PDF(Pubmed)
Abstract：
BACKGROUND: Tocotrienols exhibit antioxidant and anti-inflammatory activities. RhoA, a small GTPase protein, plays a crucial role in regulating contractility in airway smooth muscle (ASM). Previous studies have demonstrated that γ-tocotrienols reduce ASM proliferation and migration by inhibiting the activation of RhoA. In this present study, we investigate the effect of another vitamin E isoform, β-tocotrienols, on human ASM cell proliferation and migration stimulated by platelet-derived growth factor-BB (PDGF-BB).
METHODS: Human ASM cells were pre-treated with β-tocotrienol prior to being stimulated with PDGF-BB to induce ASM cell proliferation and migration. The proliferation and migration of PDGF-BB-induced human ASM cells were assessed using colorimetric and transwell migration assays. The intracellular ROS assay kit was employed to quantify reactive oxygen species (ROS) in human ASM cells. Additionally, we explored the effect of β-tocotrienols on the signaling pathways involved in PDGF-BB-induced ASM proliferation and migration.
RESULTS: β-tocotrienol inhibited PDGF-BB-induced ASM cell proliferation and migration by reducing RhoA activation and ROS production. However, in this present study, β-tocotrienol did not affect the signaling pathways associated with cyclin D1, phosphorylated Akt1, and ERK1/2.
CONCLUSIONS: In conclusion, the inhibition of RhoA activation and ROS production by β-tocotrienol, resulting in the reduction in human ASM proliferation and migration, suggests its potential as a treatment for asthma airway remodeling.
METHODS: Human ASM cells were pre-treated with β-tocotrienol prior to being stimulated with PDGF-BB to induce ASM cell proliferation and migration. The proliferation and migration of PDGF-BB-induced human ASM cells were assessed using colorimetric and transwell migration assays. The intracellular ROS assay kit was employed to quantify reactive oxygen species (ROS) in human ASM cells. Additionally, we explored the effect of β-tocotrienols on the signaling pathways involved in PDGF-BB-induced ASM proliferation and migration.
RESULTS: β-tocotrienol inhibited PDGF-BB-induced ASM cell proliferation and migration by reducing RhoA activation and ROS production. However, in this present study, β-tocotrienol did not affect the signaling pathways associated with cyclin D1, phosphorylated Akt1, and ERK1/2.
CONCLUSIONS: In conclusion, the inhibition of RhoA activation and ROS production by β-tocotrienol, resulting in the reduction in human ASM proliferation and migration, suggests its potential as a treatment for asthma airway remodeling.
摘要：
背景:生育三烯酚表现出抗氧化和抗炎活性。RhoA,一种小的GTPase蛋白，在调节气道平滑肌（ASM）的收缩性中起着至关重要的作用。先前的研究已经证明γ-生育三烯酚通过抑制RhoA的活化来减少ASM增殖和迁移。在本研究中,我们研究了另一种维生素E亚型的作用，β-生育三烯酚，血小板衍生生长因子-BB（PDGF-BB）刺激的人ASM细胞增殖和迁移。
方法:在用PDGF-BB刺激之前,用β-生育三烯酚预处理人ASM细胞以诱导ASM细胞增殖和迁移。使用比色和transwell迁移测定评估PDGF-BB诱导的人ASM细胞的增殖和迁移。细胞内ROS测定试剂盒用于定量人ASM细胞中的活性氧(ROS)。此外,我们探讨了β-生育三烯酚对PDGF-BB诱导的ASM增殖和迁移的信号通路的影响。
结果：β-生育三烯酚通过减少RhoA活化和ROS产生抑制PDGF-BB诱导的ASM细胞增殖和迁移。然而,在本研究中，β-生育三烯酚不影响与细胞周期蛋白D1、磷酸化Akt1和ERK1/2相关的信号通路。
结论：结论：β-生育三烯酚对RhoA活化和ROS产生的抑制作用，导致人类ASM增殖和迁移的减少，提示其作为哮喘气道重塑治疗的潜力。
方法:在用PDGF-BB刺激之前,用β-生育三烯酚预处理人ASM细胞以诱导ASM细胞增殖和迁移。使用比色和transwell迁移测定评估PDGF-BB诱导的人ASM细胞的增殖和迁移。细胞内ROS测定试剂盒用于定量人ASM细胞中的活性氧(ROS)。此外,我们探讨了β-生育三烯酚对PDGF-BB诱导的ASM增殖和迁移的信号通路的影响。
结果：β-生育三烯酚通过减少RhoA活化和ROS产生抑制PDGF-BB诱导的ASM细胞增殖和迁移。然而,在本研究中，β-生育三烯酚不影响与细胞周期蛋白D1、磷酸化Akt1和ERK1/2相关的信号通路。
结论：结论：β-生育三烯酚对RhoA活化和ROS产生的抑制作用，导致人类ASM增殖和迁移的减少，提示其作为哮喘气道重塑治疗的潜力。
