Thymosin beta 4 (Thymosin β4)
(Synonyms: 胸腺素beta4) 目录号 : GC32448
胸腺素β4（Thymosin beta 4）是细胞中一种主要的肌动蛋白螯合蛋白，可以与G-肌动蛋白相互作用。
Cas No.:77591-33-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
hCMEC/D3 cell line |
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Preparation Method |
Cells were treated with 200μM PrP (106-126) with or without Thymosin β4 and Thymosin β4 siRNA. Cell viability was determined by MTT assay and LDH assay. |
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Reaction Conditions |
0.01, 0.05, 0.1, and 0.5μg/mL |
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Applications |
Pretreatment of hCMEC/D3 cells with various concentrations of Thymosin β4 on 200μM PrP (106-126)-treated cells resulted in significantly increased viability in a dose-dependent (0.1, 0.5 μg/ml) manner compared to cells incubated with 200μM PrP (106-126) alone. Analysis of LDH activity in the cell culture supernatants revealed that 0.1 and 0.5μg/ml Thymosin β4 significantly inhibited 200μM PrP (106-126)-induced cytotoxicity in hCMEC/D3 cells |
| Animal experiment [2]: | |
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Animal models |
CD1 adult nulliparous female mice, 2-5 months |
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Preparation Method |
Only 6 of 10 were pregnant. At 10:00 a.m. on day E14 and E17 of gestation mice were weighed and treated with an intraperitoneal injection of Thymosin β4. Three pregnant mice received treatment with Thymosin β4 and three mice were used as a control group. To keep the same conditions of stress, the mice of the control group underwent corresponding intraperitoneal injections of vehicle (PBS). On the day E19 of gestation, caesarean sections were performed. |
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Dosage form |
6mg/kg, intraperitoneal injection |
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Applications |
Thymosin β4 is capable of accelerating the development of the entire fetus and fetal organs when administered to pregnant mice in the last week of gestation. Regarding the body length at birth, newborns of Thymosin β4-treated animals showed a length always higher than the neonates of non-treated mice. In multiple organs, including heart, kidney, lungs, gut, notochord and cerebral cortex, the degree of differentiation of stem/precursor cells was accelerated by the maternal administration of Thymosin β4, leading to the appearance of a more mature organ architecture |
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References: [1]. Song K, Han HJ, et al. Thymosin beta 4 attenuates PrP(106-126)-induced human brain endothelial cells dysfunction. Eur J Pharmacol. 2020;869:172891. [2]. Faa G, Piras M, et al. Thymosin beta-4 prenatal administration improves fetal development and halts side effects due to preterm delivery. Eur Rev Med Pharmacol Sci. 2021;25(1):431-437. |
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Thymosin β4 is a major actin sequestering protein in cells and can interact with G-actin[1,2]. Thymosin β4 is found in many vertebrate tissues and cells and is especially concentrated in macrophages, fibroblasts, neutrophils, and platelets, which have large pools of G-actin[3]. The main physiological role of Thymosin β4 is the regulation of actin polymerization. Thymosin β4 is also involved in angiogenesis, cell survival, cell migration and fetal development[4].
Thymosin β4 plays a crucial role in the regulation of tight junction stability and acts in cytoskeleton rearrangement, which are closely related with BBB permeability[2]. Thymosin β4 is a novel regulator for primary cilia formation and it affects ciliogenesis by regulating the expression of NPHP3 in HeLa cervical cancer cells[5]. Thymosin β4 regulates HSC activation by influencing the activity of Smoothened and GLI2, suggesting Thymosin β4 as a novel therapeutic target in liver disease[6]. Synthetic Thymosin β4 peptide increases NK cell cytotoxicity mediated by intercellular adhesion molecule-1 (ICAM-1 ) through the secretion of cytolytic granules to target cells, suggests that Thymosin β4 is a key activator of NK cell cytotoxicity[7].
Thymosin β4 enhanced wound healing in a rat full thickness wound model suggest that Thymosin β4 is a potent wound healing factor with multiple activities[1]. Thymosin β4 administration during gestation may act as a powerful fetal growth promoter, by accelerating the development of newborn organs and tissues[4].Recombinant Human Thymosin β4 significantly increased the survival rate of mice infected with MHV-A59 through inhibiting virus replication, balancing the host’s immune response, alleviating pathological damage, and promoting repair of the liver[8].
References:
[1]. Malinda KM, Sidhu GS, et al. Thymosin beta4 accelerates wound healing. J Invest Dermatol. 1999;113(3):364-368.
[2]. Song K, Han HJ, et al. Thymosin beta 4 attenuates PrP(106-126)-induced human brain endothelial cells dysfunction. Eur J Pharmacol. 2020;869:172891.
[3]. Weber A, Nachmias VT, et al, Safer D. Interaction of thymosin beta 4 with muscle and platelet actin: implications for actin sequestration in resting platelets. Biochemistry. 1992;31(27):6179-6185.
[4]. Faa G, Piras M, et al. Thymosin beta-4 prenatal administration improves fetal development and halts side effects due to preterm delivery. Eur Rev Med Pharmacol Sci. 2021;25(1):431-437.
[5]. Lee JW, Kim HS, et al. Thymosin β-4 is a novel regulator for primary cilium formation by nephronophthisis 3 in HeLa human cervical cancer cells. Sci Rep. 2019;9(1):6849. Published 2019 May 2.
[6]. Kim J, Hyun J, et al. Thymosin beta-4 regulates activation of hepatic stellate cells via hedgehog signaling. Sci Rep. 2017;7(1):3815. Published 2017 Jun 19.
[7]. Lee HR, Yoon SY, et al. Thymosin beta 4 enhances NK cell cytotoxicity mediated by ICAM-1. Immunol Lett. 2009;123(1):72-76.
[8]. Yu R, Mao Y, et al. Recombinant Human Thymosin Beta-4 Protects against Mouse Coronavirus Infection. Mediators Inflamm. 2021;2021:9979032. Published 2021 Apr 21.
胸腺素 β4 是细胞中主要的肌动蛋白螯合蛋白，可与 G-肌动蛋白相互作用[1,2]。胸腺素 β4 存在于许多脊椎动物组织和细胞中，尤其集中在巨噬细胞、成纤维细胞、中性粒细胞和血小板中，这些细胞具有大量 G-肌动蛋白[3]。胸腺素 β4 的主要生理作用是调节肌动蛋白聚合。胸腺肽 β4 还参与血管生成、细胞存活、细胞迁移和胎儿发育[4]。
胸腺素β4在调节紧密连接稳定性和细胞骨架重排中起着至关重要的作用，与血脑屏障通透性密切相关[2]。 Thymosin β4 是一种新的初级纤毛形成调节因子，它通过调节宫颈癌细胞 NPHP3 的表达影响纤毛生成[5]。 Thymosin β4 通过影响 Smoothened 和 GLI2 的活性来调节 HSC 活化，表明 Thymosin β4 可作为肝病治疗的新靶点[6]。合成的 Thymosin β4 肽通过向靶细胞分泌细胞溶解颗粒增加由细胞间粘附分子-1 (ICAM-1 ) 介导的 NK 细胞细胞毒性，表明 Thymosin β4 是一种NK细胞细胞毒性的关键激活剂[7].
Thymosin β4 在大鼠全层伤口模型中促进伤口愈合表明 Thymosin β4 是一种具有多种活性的有效伤口愈合因子[1]。妊娠期间给予胸腺素 β4 可作为强大的胎儿生长促进剂，通过加速新生儿器官和组织的发育[4]。重组人胸腺素 β4 显着提高了感染 MHV-A59 的小鼠的存活率通过抑制病毒复制，平衡宿主免疫反应，减轻病理损伤，促进肝脏修复[8]。
| Cas No. | 77591-33-4 | SDF | |
| 别名 | 胸腺素beta4 | ||
| Canonical SMILES | Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr-Gln-Glu-Lys-Asn-Pro-Leu-Pro-Ser-Lys-Glu-Thr-Ile-Glu-Gln-Glu-Lys-Gln-Ala-Gly-Glu-Ser | ||
| 分子式 | C212H350N56O78S | 分子量 | 4963.44 |
| 溶解度 | Water : 50 mg/mL (10.07 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.2015 mL | 1.0074 mL | 2.0147 mL |
| 5 mM | 0.0403 mL | 0.2015 mL | 0.4029 mL |
| 10 mM | 0.0201 mL | 0.1007 mL | 0.2015 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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1. 首先保证母液是澄清的；
2.
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Thymosin beta 4 alleviates non-alcoholic fatty liver by inhibiting ferroptosis via up-regulation of GPX4
Eur J Pharmacol 2021 Oct 5;908:174351.PMID:34280397DOI:10.1016/j.ejphar.2021.174351.
Thymosin beta 4 (T尾4) can improve the liver fibrosis and reduce inflammation, while the role of T尾4 in non-alcoholic fatty liver disease (NAFLD) whether mediated by ferroptosis remains unclear. A rat model of NAFLD was established on a high-fat diet (HFD), and rats were assigned ferroptosis inducer erastin and inhibitor Ferrostatin 1 (Fer-1). Subsequently, histopathology of the liver and the expression of ferroptosis-related genes in rat liver were detected. The steatosis of LO2 cells was induced by palmitic acid (PA) to reproduce the results of the rat experiment. The small interfering RNA (siRNA) was used to interfere with GPX4 expression to explore the influence on T尾4 function. T尾4 improved the inflammation, biochemical and lipid metabolism indexes, increased the antioxidant level, and inhibited abnormal accumulation of intracellular reactive oxygen species in HFD-induced NAFLD rats. Also, T尾4 improved PA-induced LO2 damage and inhibited apoptosis of PA-induced LO2 cells. Both in vivo and in vitro, T尾4 regulated expression of genes associated with ferroptosis, and Fer-1 treatment exaggerated the above effects of T尾4, while erastin attenuated the protective effect of T尾4. Moreover, siRNA GPX4 attenuated the protective effect of T尾4 on the rat liver and on the mitochondrial membrane integrity of LO2 cells. Interfered expression of GPX4 with siRNA also regulated the expression of Bcl-2, Bax, Caspase-3 and SOD1, which attenuated therapeutic effect of T尾4 on rat liver and LO2 cells. This study revealed that T尾4 protects hepatocytes by inhibiting the GPX4-mediated ferroptosis pathway, which provides a new strategy and target for the treatment of NAFLD.
Thymosin beta 4 regulation of actin in sepsis
Expert Opin Biol Ther 2018 Jul;18(sup1):193-197.PMID:29508629DOI:10.1080/14712598.2018.1448381.
Introduction: Sepsis is the dysregulated host response to an infection resulting in life-threatening organ damage. Thymosin beta 4 is an actin binding protein that inhibits the polymerization of G-actin into F-actin and improves mortality when administered intravenously to septic rats. Thymosin beta 4 decreases inflammatory mediators, lowers reactive oxygen species, up-regulates anti-oxidative enzymes, anti-inflammatory genes, and anti-apoptotic enzymes making it an interesting protein to study in sepsis. Areas covered: The authors summarize the current knowledge of actin and Thymosin beta 4 as it relates to sepsis via a comprehensive literature search. Expert opinion: Sepsis results in measurable levels of F-actin in the circulation as well as a decreased concentration of Thymosin beta 4. It is speculated that F-actinemia contributes to microcirculatory perturbations present in patients with sepsis by disturbing laminar flow. Given that Thymosin beta 4 inhibits the polymerization of F-actin, it is possible that Thymosin beta 4 decreases mortality in sepsis via the regulation of actin as well as its other anti-inflammatory properties and should be further pursued as a clinical trial in humans with sepsis.
Thymosin beta 4 interactions
Vitam Horm 2003;66:297-316.PMID:12852258DOI:10.1016/s0083-6729(03)01008-2.
Thymosin beta 4 is a small, 5-kDa protein with a diverse range of activities, including its function as an actin monomer sequestering protein, an antiinflammatory agent, and an inhibitor of bone marrow stem cell proliferation. Only the effects of Thymosin beta 4 on the actin cytoskeleton have an explanation based on identified molecular interactions. Thymosin beta 4 is largely unfolded or perhaps completely unfolded in solution. Based on the paradigm introduced by Wright and Dyson (1999) that unfolded proteins may have multiple functions based on their ability to recognize numerous ligands, the flexible structure of Thymosin beta 4 may facilitate the recognition of a variety of molecular targets, thus explaining the plethora of functions attributed to Thymosin beta 4. Furthermore, if multiple ligands bind to Thymosin beta 4, then it is possible that Thymosin beta 4 has a unique integrative function that links the actin cytoskeleton to important immune and cell growth-signaling cascades.
Thymosin beta 4 and the eye: the journey from bench to bedside
Expert Opin Biol Ther 2018 Jul;18(sup1):99-104.PMID:30063853DOI:10.1080/14712598.2018.1486818.
Thymosin beta 4 (T尾4) has important applications in ocular repair and Phase 3 clinical trials using T尾4 to treat dry eye and neurotrophic keratopathy are currently ongoing. These exciting clinical possibilities for T尾4 in the eye are the result of seminal basic scientific discoveries and contributions from so many talented investigators. Areas covered: My personal T尾4 journey began at the NIH in 1998 and propelled my career as a clinician scientist. As a tribute to the amazing individuals who have guided and supported me along with my brilliant colleagues and students who have contributed and collaborated with me over the years, this review will tell the cumulative story of how T尾4 became a major potential new therapy for corneal wound healing disorders. The journey has been marked by the thrilling exhilaration from fundamental breakthroughs in the laboratory and clinic, combined with the challenging and often harsh realities of submitting grants and obtaining funding. Expert opinion: The electrifying possibility of T尾4 as a revolutionary novel dry eye therapy is something that could have only been dreamed about just a few years ago. We believe that T尾4 eyedrops will help many patients suffering from several ocular surface related disorders.
Thymosin beta 4 Is a Potential Regulator of Hepatic Stellate Cells
Vitam Horm 2016;102:121-49.PMID:27450733DOI:10.1016/bs.vh.2016.04.011.
Liver fibrosis, a major characteristic of chronic liver disease, is inappropriate tissue remodeling caused by prolonged parenchymal cell injury and inflammation. During liver injury, hepatic stellate cells (HSCs) undergo transdifferentiation from quiescent HSCs into activated HSCs, which promote the deposition of extracellular matrix proteins, leading to liver fibrosis. Thymosin beta 4 (T尾4), a major actin-sequestering protein, is the most abundant member of the highly conserved 尾-thymosin family and controls cell morphogenesis and motility by regulating the dynamics of the actin cytoskeleton. T尾4 is known to be involved in various cellular responses, including antiinflammation, wound healing, angiogenesis, and cancer progression. Emerging evidence suggests that T尾4 is expressed in the liver; however, its biological roles are poorly understood. Herein, we introduce liver fibrogenesis and recent findings regarding the function of T尾4 in various tissues and discuss the potential role of T尾4 in liver fibrosis with a special focus on the effects of exogenous and endogenous T尾4. Recent studies have revealed that activated HSCs express T尾4 in vivo and in vitro. Treatment with the exogenous T尾4 peptide inhibits the proliferation and migration of activated HSCs and reduces liver fibrosis, indicating it has an antifibrotic action. Meanwhile, the endogenously expressed T尾4 in activated HSCs is shown to promote HSCs activation. Although the role of T尾4 has not been elucidated, it is apparent that T尾4 is associated with HSC activation. Therefore, understanding the potential roles and regulatory mechanisms of T尾4 in liver fibrosis may provide a novel treatment for patients.