2. Metabolic Enzyme/Protease MAPK/ERK Pathway PI3K/Akt/mTOR Stem Cell/Wnt Apoptosis Protein Tyrosine Kinase/RTK
  3. Endogenous Metabolite MAP3K Akt Mitochondrial Metabolism ERK Apoptosis ROS Kinase
  4. Phosphocreatine dipotassium

Phosphocreatine dipotassium  (Synonyms: Creatine phosphate dipotassium; Creatinephosphoric acid dipotassium)

目录号: HY-D0885C
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Phosphocreatine (creatine phosphate) 是一种存在于脊椎动物骨骼肌中的有机化合物。Phosphocreatine 增强抗氧化活性，激活 TAK1 通路以保护心脏。Phosphocreatine 通过 Akt 介导的 Nrf2/HO-1 途径使线粒体功能正常化并减少氧化应激。Phosphocreatine 通过 ERK 介导的 Nrf-2/HO-1 途径抑制细胞凋亡 (Apoptosis) 和 ROS (Reactive Oxygen Species) 的产生，从而保护肾脏。

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Phosphocreatine dipotassium Chemical Structure

Phosphocreatine dipotassium Chemical Structure

CAS No. : 18838-38-5

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Other Forms of Phosphocreatine dipotassium:

Phosphocreatine dipotassium 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Phosphocreatine (creatine phosphate) is an organic compound found in vertebrate skeletal muscles. Phosphocreatine enhances antioxidant activity, and activates the TAK1 pathway to protect the heart. Phosphocreatine normalizing mitochondrial function and reducing oxidative stress via Akt mediated Nrf2/HO-1 pathway. Phosphocreatine provides renal protection by suppressing Apoptosis and ROS (Reactive Oxygen Species) generation through ERK mediated mediated Nrf-2/HO-1 pathway.[1][2][3][4].

IC50 & Target

Human Endogenous Metabolite

 

体外研究
(In Vitro)

Phosphocreatine (0-1 mM, 24 h) 通过靶向 TAK1 揭示了抗氧化、抗凋亡和抗坏死性凋亡的作用，以保护 H9c2 细胞免受 DOX (Doxorubicin) (HY-15142A) 诱导的心肌细胞损伤[2]。
Phosphocreatine (0-1 mM, 24 h) 通过增加抗氧化活性来缓解氧化应激，随后将 TAK1 的表达水平恢复到基线水平，并减少 DOX 诱导的心肌损伤中的细胞凋亡和程序性死亡[2]。
Phosphocreatine (5-20 mM, 24 h) 可减轻 MGO (Methylglyoxal) (HY-106634) 诱导的 PC12 细胞损伤和抑制 PC-12 细胞凋亡[3]。
Phosphocreatine (5-20 mM, 24 h) 可防止MGO (Methylglyoxal) 诱导损伤的PC-12 细胞线粒体膜通透性丧失[3]。
Phosphocreatine (5-20 mM, 2 h) 对 PC-12 细胞的神经保护作用依赖于通过 Akt 介导的 Nrf2/HO- 1途径使线粒体功能正常化和减少氧化应激[3]。
Phosphocreatine (5-40 mM, 24 h) 在不同浓度下可能有助于保护 NRK-52E 细胞免受 MGO 诱导的肾损伤[4]。
Phosphocreatine (10-40 mM, 4 h) 抑制肾脏氧化应激代谢物[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Phosphocreatine dipotassium 相关抗体:

Cell Viability Assay[3][4]

Cell Line: PC-12, NRK-52E cells
Concentration: 0, 5, 10, 20, 40 mM
Incubation Time: 24 h
Result: Was not toxic to PC-12 cells under the treatment conditions.
Significantly increased PC-12 cell viability at the concentrations of 5, 10 and 20 mM compared with MGO (Methylglyoxal) (HY-106634) groups.
Contributed to protection of the NRK-52E cells against MGO-induced kidney injury.

Apoptosis Analysis[3][4]

Cell Line: PC-12, NRK-52E cells
Concentration: 5, 10, 20, 40 mM
Incubation Time: 2 h
Result: Significantly suppressed the enhanced early apoptosis in PC-12 cells in a dose-dependent manner.
Increased the expression of Bcl-2, procaspase-3 and procaspase-9 in NRK-52E cells.
Decreased the expression of Bax and cleaved caspase-3 in NRK-52E cells..
Suppressed karyorrhexis and karyopyknosis in NRK-52E cells..
Decreased the apoptotic rate compared with MGO-treated cells in NRK-52E cells..
Prevented the losing of MMP (mitochondrial membrane potential) in NRK-52E cells.

Western Blot Analysis[3][4]

Cell Line: PC-12, NRK-52E cells
Concentration: 20, 40 mM
Incubation Time: 24 h
Result: Increased the expression levels of Akt, Nrf2 (nuclear factor (erythroid-derived-2)-like 2 (Nrf2)) and HO-1 (Hemeoxygenase-1) in PC12 cells.
Increased the expression of nuclear Nrf2 levels, and decreased Nrf2 level in PC12 cells cytoplasm.
Increased the expression of p-Akt, HO-1 and Nrf2 with compared with pre-treatment for 2 h with LY294002 (a PI3K inhibitor) in PC12 cells.
Significantly increased Bcl-2 and procaspase-9 levels and decreased Bax, cleaved caspase-9 and cleaved caspase-3 C level in NRK-52E cells.
Decreased the expression of p-ERK and increased the Nrf2 and HO-1 expressions in NRK-52E cells.
体内研究
(In Vivo)

Phosphocreatine (200 mg/kg, i.p., 每隔一天一次, 7 周) 不仅减轻了氧化应激和心肌细胞凋亡，而且挽救了 DOX 诱导的大鼠心脏毒性中的心肌坏死[2]。
Phosphocreatine (20-40 mg/kg, i.v., 每天, 6 周) 对 SD (Sprague-Dawley) 大鼠的肾组织具有保护作用，可预防糖尿病肾病[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male Sprague Dawley (SD) rats were divided into three groups, normal control group, DOX group and phosphocreatine group[2].
Dosage: 200 mg/kg
Administration: i.p., once every other day, 7 weeks
Result: Improved the heart function abnormality.
Lowered myocardial apoptosis.
Recovered the expression of Nrf2, SOD, FoxO3a and diminished C-Casp3, Bax/Bcl2 in the myocardial tissue of rats.
Markedly improved myocardial necroptosis, as indicated by decreasing expression of RIP3 and CaMKII.
Increased expression level of TAK1.
Animal Model: Male Sprague Dawley (SD) rats were divided into five groups: control group, model group (STZ(Streptozotocin) (HY-13753)), low dose group (STZ+ phosphocreatine 22 mg/kg) and high dose group (STZ (HY-13753) + phosphocreatine 40 mg/kg). [4].
Dosage: 20, 40 mg/kg
Administration: i.v., daily, 6 weeks
Result: Reduced hyperglycemia compared with STZ (Streptozotocin) (HY-13753) -treated rats.
Increased the weight of rats gradually compared with STZ (Streptozotocin) (HY-13753) group.
Decreased kidney weight index (kidney weight/body weight).
Decreased MDA level and increased of GSH and SOD levels compared with STZ group.
Decreased the apoptotic rate compared with MGO-treated groups.
Clinical Trial
分子量

287.29

Formula

C4H8K2N3O5P
CAS 号
结构分类
初始来源

skeletal muscles of vertebrates
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Phosphocreatine dipotassium 相关分类

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  • Do most proteins show cross-species activity?

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Keywords:

Phosphocreatine dipotassium18838-38-5Creatine phosphate dipotassiumCreatinephosphoric acid dipotassiumEndogenous MetaboliteMAP3KAktMitochondrial MetabolismERKApoptosisROS KinaseMAP kinase kinase kinase, MEKK, MAPKKKPKBProtein kinase BExtracellular signal regulated kinasesATPmuscle contractioncardiotoxicitymitochondrial functionoxidative stressInhibitorinhibitorinhibit

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