Phosphocreatine di-tris salt
(Synonyms: N-(亚氨基[膦氨基]甲基)-N-甲基甘氨酸) 目录号 : GF04703Phosphocreatine di-tris salt是一种磷酸化的肌酸分子，作为脊椎动物和一些无脊椎动物肌肉中的高能磷酸盐储存库，为ADP转化为ATP提供磷酸盐。
Cas No.:108321-17-1
Sample solution is provided at 25 µL, 10mM.
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Phosphocreatine di-tris salt is a phosphorylated creatine molecule that serves as a high-energy phosphate reservoir in the muscles of vertebrates and some invertebrates, providing phosphate for the conversion of ADP to ATP[1]. Phosphocreatine di-tris salt can prevent hypoxic and ischemic damage to brain neurons[2], has the potential to regulate cellular energy metabolism[3], can also act as an antioxidant to protect cells from oxidative stress and apoptosis[4]. In addition, Phosphocreatine di-tris salt also has a positive role in the treatment of other diseases, including diabetes-induced liver injury, kidney injury，neurodegenerative diseases and osteoporosis in psotemnopausal women[5-7].
In vitro, pretreatment of Phosphocreatine di-tris salt(0.5mM; 24h) enhanced antioxidant activity to reduce oxidative stress, significantly alleviated apoptotic and necroptotic cell death induced by DOX in H9c2 cells[4]. Phosphocreatine (10, 20 and 40 mM; 24h) alleviated NRK-52E cells damage induced by MGO (Methylglyoxal) and inhibit NRK-52E cells apoptosis[6].
In vivo, Phosphocreatine di-tris salt (25, 50mg/kg for 6 weeks; i.p.) significantly reduced blood glucose and MDA levels, increased body weight, decreased kidney weight index, improved kidney histological structure and regulated the ERK/Nrf2/HO-1 signaling pathway (with decreased p-ERK expression and increased Nrf2 and HO-1 expressions) in STZ-induced diabetic rats[5].
References:
[1] Guimarães-Ferreira L. (2014). Role of the phosphocreatine system on energetic homeostasis in skeletal and cardiac muscles. Einstein (Sao Paulo, Brazil), 12(1), 126–131.
[2] Balestrino, M., Lensman, M., Parodi, M., Perasso, L., Rebaudo, R., Melani, R., Polenov, S., & Cupello, A. (2002). Role of creatine and phosphocreatine in neuronal protection from anoxic and ischemic damage. Amino acids, 23(1-3), 221–229.
[3] Loo, J. M., Scherl, A., Nguyen, A., Man, F. Y., Weinberg, E., Zeng, Z., Saltz, L., Paty, P. B., & Tavazoie, S. F. (2015). Extracellular metabolic energetics can promote cancer progression. Cell, 160(3), 393–406.
[4] Wang, C., Hu, L., Guo, S., Yao, Q., Liu, X., Zhang, B., Meng, X., & Yang, X. (2021). Phosphocreatine attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress and activating TAK1 to promote myocardial survival in vivo and in vitro. Toxicology, 460, 152881.
[5] Shopit, A., Niu, M., Wang, H., Tang, Z., Li, X., Tesfaldet, T., Ai, J., Ahmad, N., Al-Azab, M., & Tang, Z. (2020). Protection of diabetes-induced kidney injury by phosphocreatine via the regulation of ERK/Nrf2/HO-1 signaling pathway. Life sciences, 242, 117248.
[6] Li, H., Tang, Z., Chu, P., Song, Y., Yang, Y., Sun, B., Niu, M., Qaed, E., Shopit, A., Han, G., Ma, X., Peng, J., Hu, M., & Tang, Z. (2018). Neuroprotective effect of phosphocreatine on oxidative stress and mitochondrial dysfunction induced apoptosis in vitro and in vivo: Involvement of dual PI3K/Akt and Nrf2/HO-1 pathways. Free radical biology & medicine, 120, 228–238.
[7] Vnučák, M., Michalová, R., Jr, Graňák, K., Benko, J., & Mokáň, M. (2019). Potenciálne možnosti využitia kreatinfosfátu vo vnútornom lekárstve [Potential possibility of phosphocreatine usage in internal medicine]. Vnitrni lekarstvi, 65(1), 30–36.
Phosphocreatine di-tris salt是一种磷酸化的肌酸分子，作为脊椎动物和一些无脊椎动物肌肉中的高能磷酸盐储存库，为ADP转化为ATP提供磷酸盐[1]。Phosphocreatine di-tris salt可以防止大脑神经元的缺氧和缺血性损伤[2]，具有调节细胞能量代谢的潜力[3]，还可以作为抗氧化剂保护细胞免受氧化应激和凋亡的影响[4]。此外，Phosphocreatine di-tris salt在治疗其他疾病方面也具有积极作用，包括糖尿病引起的肝损伤、肾损伤、神经退行性疾病以及绝经后妇女的骨质疏松症[5-7]。
在体外研究中，预先使用Phosphocreatine di-tris salt（0.5mM；24小时）处理可增强抗氧化活性，减轻氧化应激，显著缓解DOX诱导的H9c2细胞的凋亡和坏死[4]。Phosphocreatine di-tris salt（10、20和40 mM；24小时）可减轻MGO（Methylglyoxal）诱导的NRK-52E细胞损伤，并抑制NRK-52E细胞凋亡[6]。
在体内研究中，Phosphocreatine di-tris salt（25、50mg/kg每日给药6周；腹腔注射）显著降低了STZ诱导的糖尿病大鼠的血糖和MDA水平，增加了体重，降低了肾脏重量指数，改善了肾脏组织结构，并调节了ERK/Nrf2/HO-1信号通路（p-ERK表达降低，Nrf2和HO-1表达增加）[5]。
| Cell experiment [1]: | |
Cell lines | H9c2 cells |
Preparation Method | H9c2 cells were cultured in Dulbecco’s modified Eagle’s medium with 10% fetal bovine serum and 1% Penicillin-Streptomycin Solution. Upon reaching 70%～80% confluence, the cells were pretreated with 0.5mM PCr (Phosphocreatine di-tris salt) or 0.5mM NAC (Nacetyl-L-cysteine) or 5z-7-Ox 1μM (5Z-7-oxozeaenol) for 1h, and then exposed to DOX 1μM for 24h. Subsequently, H9c2 cells were incubated with serm-free medium containing 2,7-Dichlorodi-hydrofluorescein diacetate (DCFH-DA, 10μM) for 30 min, then washed with PBS for two times. Then H9c2 cells was observed by an Olympus fluorescence microscope. Mitochondrial membrane potential of H9c2 cells was detected with JC-1 kit. Cells viability was determined using the CCK-8 assay kit. |
Reaction Conditions | 0.5mM; 24h |
Applications | Phosphocreatine di-tris salt enhanced antioxidant activity to reduce oxidative stress, significantly alleviated apoptotic and necroptotic cell death induced by DOX in H9c2 cells. |
| Animal experiment [2]: | |
Animal models | Sprague-Dawley (SD) rats |
Preparation Method | Forty healthy male Sprague-Dawley (SD) rats weighing 180–220g were were placed in the laboratory for one week before the start of the experiments. They were at regular diet, at room temperature (23 ± 2 °C), under natural light, and with relative humidity of 50–70%. The rats were divided into five groups (each group n = 10): control group, model group (STZ), low dose group (STZ + Phosphocreatine di-tris salt 25mg/kg) and high dose group (STZ + Phosphocreatine di-tris salt 50mg/kg). The model group was injected by 70mg/kg of STZ. Above 16.7mmol/L plasma glucose levels (measured by tail vein), after 72h, in all rats wa's considered as successful criterion for DM model. Fasting glucose concentration, body weight and kidney index were measured. |
Dosage form | 25, 50mg/kg/day for 6 weeks; i.p. |
Applications | Phosphocreatine di-tris salt(25, 50mg/kg/day for 6 weeks; i.p.) significantly reduced blood glucose and MDA levels, increased body weight, decreased kidney weight index, improved kidney histological structure and regulated the ERK/Nrf2/HO-1 signaling pathway (with decreased p-ERK expression and increased Nrf2 and HO-1 expressions) in STZ-induced diabetic rats. |
| Cas No. | 108321-17-1 | SDF | |
| 别名 | N-(亚氨基[膦氨基]甲基)-N-甲基甘氨酸 | ||
| 分子式 | C12H32N5O11P | 分子量 | 453.38 |
| 溶解度 | 储存条件 | -20 °C,sealed storage,away from moisture | |
| 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 | 2.2057 mL | 11.0283 mL | 22.0566 mL |
| 5 mM | 0.4411 mL | 2.2057 mL | 4.4113 mL |
| 10 mM | 0.2206 mL | 1.1028 mL | 2.2057 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
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，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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- Purity: >97.00%
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