EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #73662_C
RHO/ROCK通路抑制剂；抑制ROCK2
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总览
Fasudil（法舒地尔，又名HA-1077）是Rho相关卷曲螺旋蛋白激酶2（ROCK2；IC₅₀=1.9 µM）的强效抑制剂。此外，它还抑制蛋白激酶C相关激酶2（PRK2）、丝裂原活化和应激活化蛋白激酶（MSK1）以及丝裂原活化蛋白激酶活化的蛋白激酶1b（MAPKAP-K1b），其IC₅₀值分别为4µM、5µM和15µM（Davies et al.）。本产品以该分子的二盐酸盐形式供应。
分化
·抑制增殖和胶原蛋白的产生，同时也增加肝星状细胞的胶原酶活性（Fukushima et al.）。
·抑制内皮细胞在HUVEC中的迁移、活力和管形成（Yin et al.）。
·改善脂肪细胞分化，预防胰岛素抵抗糖尿病大鼠患糖尿病和肾病（Kikuchi et al.）。
疾病建模
·降低大鼠的肺动脉高压（Oka et al.）。
·增强脊髓创伤后的神经功能恢复（Hara et al.）。
·抑制小鼠碱烧伤后的角膜新生血管，促进角膜上皮缺损的愈合（Zeng et al.）。
细胞类型
脂肪细胞，内皮细胞，HUVEC细胞（人脐静脉内皮细胞），神经干/祖细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
分化
研究领域
血管生成细胞研究，疾病建模
CAS 编号
203911-27-7
化学式
C₁₄H₁₇N₃O₂S · 2HCl
纯度
≥98%
通路
RHO/ROCK
靶点
ROCK2
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
相关材料与文献
文献 (7)
Fasudil hydrochloride, a potent ROCK inhibitor, inhibits corneal neovascularization after alkali burns in mice. Molecular vision 2015 JAN
Abstract
PURPOSE To investigate the effects and mechanisms of fasudil hydrochloride (fasudil) on and in alkali burn-induced corneal neovascularization (CNV) in mice. METHODS To observe the effect of fasudil, mice with alkali-burned corneas were treated with either fasudil eye drops or phosphate-buffered saline (PBS) four times per day for 14 consecutive days. After injury, CNV and corneal epithelial defects were measured. The production of reactive oxygen species (ROS) and heme oxygenase-1(HO-1) was measured. The infiltration of polymorphonuclear neutrophils (PMNs) and the mRNA expressions of CNV-related genes were analyzed on day 14. RESULTS The incidence of CNV was significantly lower after treatment with 100 μM and 300 μM fasudil than with PBS, especially with 100 μM fasudil. Meanwhile, the incidences of corneal epithelial defects was lower (n=15, all ptextless0.01). After treatment with 100 μM fasudil, the intensity of DHE fluorescence was reduced in the corneal epithelium and stroma than with PBS treatment (n=5, all ptextless0.01), and the number of filtrated PMNs decreased. There were significant differences between the expressions of VEGF, TNF-a, MMP-8, and MMP-9 in the 100 μM fasudil group and the PBS group (n=8, all ptextless0.05). The production of HO-1 protein in the 100 μM fasudil group was 1.52±0.34 times more than in the PBS group (n=5 sample, ptextless0.05). CONCLUSIONS 100 μM fasudil eye drops administered four times daily can significantly inhibit alkali burn-induced CNV and promote the healing of corneal epithelial defects in mice. These effects are attributed to a decrease in inflammatory cell infiltration, reduction of ROS, and upregulation of HO-1 protein after fasudil treatment.
Fasudil inhibits vascular endothelial growth factor-induced angiogenesis in vitro and in vivo. Molecular cancer therapeutics 2007 MAY
Abstract
Vascular endothelial growth factor (VEGF)-induced endothelial cell migration is an important component of tumor angiogenesis. Rho and Rho-associated kinase (ROCK) are key regulators of focal adhesion, stress fiber formation, and thus cell motility. Inhibitors of this pathway have been shown to inhibit endothelial cell motility and angiogenesis. In this study, we investigated the antiangiogenic effect of fasudil, one of the ROCK inhibitors. Fasudil inhibited VEGF-induced endothelial cell migration, viability, and tube formation in vitro in human umbilical vein endothelial cells. VEGF-induced endothelial cell migration was reduced by fasudil associated with loss of stress fiber formation, focal adhesion assembly, and with the suppression of tyrosine phosphorylation of focal adhesion proteins. Furthermore, fasudil inhibited VEGF-induced phosphorylation of myosin light chain, which is one of the main substrates of ROCK. Therefore, the effect of fasudil was suggested to be ROCK dependent. Fasudil not only inhibited VEGF-induced cell proliferation but also reversed the protective effect of VEGF on apoptosis, which resulted in the decrease of cell viability. Moreover, fasudil inhibited VEGF-induced angiogenesis in a directed in vivo angiogenesis assay. These data are the first demonstration that fasudil has antiangiogenic properties. Therefore, fasudil might be useful for the treatment of angiogenesis-related diseases, especially cancer.
Rho kinase-mediated vasoconstriction is important in severe occlusive pulmonary arterial hypertension in rats. Circulation research 2007 MAR
Abstract
Vascular remodeling, rather than vasoconstriction, is believed to account for high vascular resistance in severe pulmonary arterial hypertension (PAH). We have found previously that acute Rho kinase inhibition nearly normalizes PAH in chronically hypoxic rats that have no occlusive neointimal lesions. Here we examined whether Rho kinase-mediated vasoconstriction was also important in a rat model of severe occlusive PAH. Adult rats were exposed to chronic hypoxia ( approximately 10% O(2)) after subcutaneous injection of the vascular endothelial growth factor receptor inhibitor SUGEN 5416. Hemodynamic measurements were made in anesthetized rats after 2 weeks of hypoxia (early group) and 3 weeks of hypoxia plus 2 weeks of normoxia (late group). Both groups developed PAH, with greater severity in the late group. In the early group, intravenous fasudil was more effective than intravenous bradykinin, inhaled NO, or intravenous iloprost in reducing right ventricular systolic pressure. Despite more occlusive vascular lesions, fasudil also markedly reduced right ventricular systolic pressure in late-stage rats. Blood-perfused lungs from late-stage rats showed spontaneous vasoconstriction, which was reversed partially by the endothelin A receptor blocker BQ123 and completely by fasudil or Y-27632. Phosphorylation of MYPT1, a downstream target of Rho kinase, was increased in lungs from both groups of rats, and fasudil (intravenous) reversed the increased phosphorylation in the late group. Thus, in addition to structural occlusion, Rho kinase-mediated vasoconstriction is an important component of severe PAH in SUGEN 5416/hypoxia-exposed rats, and PAH can be significantly reduced in the setting of a severely remodeled lung circulation if an unconventional vasodilator is used.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 203911-27-7 |
| Chemical Formula | C₁₄H₁₇N₃O₂S · 2HCl |
| 纯度 | ≥ 98% |
| Target | ROCK2 |
| Pathway | RHO/ROCK |
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