NADPH tetrasodium salt is a sodium salt form of reduced nicotinamide adenine dinucleotide phosphate (NADPH), which is an essential cofactor in cells and acts as an electron donor[1]. NADPH is a reduced coenzyme II that participates in many biosynthetic metabolic pathways, such as fatty acid synthesis, cholesterol synthesis, oxalic acid cycle, etc.[1]. NADPH tetrasodium salt is a metabolite produced in Escherichia coli (strain K12, MG 1655)[2].
In vitro, NADPH tetrasodium salt (100µM) treated HUVEC and PIEC cells for 30 minutes, significantly increasing the O2− production of both cells[3]. Adding NADPH tetrasodium salt (100µM) to re-concentrated pulmonary artery homogenate significantly increased the activity of soluble guanylate cyclase (sGC), increasing the basal activity by 2.2±1.0 times[4]. Treatment with NADPH tetrasodium salt (0-300µM) induces rodent β-cells and dose-dependently induces Ca2+-dependent exocytosis[5].
In vivo, intravenous injection of NADPH tetrasodium salt (16 mg/kg) in male SD rats resulted in a significant increase in +dp/dt and a significant decrease in -dp/dt within 60 minutes after administration, which enhanced the cardiac function in rats [2]. Intravenous injection of NADPH tetrasodium salt (2.5 mg/kg) treated rat and mouse stroke models, significantly reducing cerebral infarction volume, improving neurological function, and increasing survival rate [6].
References:
[1]Qian K, Tang J, Ling Y J, et al. Exogenous NADPH exerts a positive inotropic effect and enhances energy metabolism via SIRT3 in pathological cardiac hypertrophy and heart failure[J]. EBioMedicine, 2023, 98.
[2]Chou H H, Marx C J, Sauer U. Transhydrogenase promotes the robustness and evolvability of E. coli deficient in NADPH production[J]. PLoS genetics, 2015, 11(2): e1005007.
[3] Li,J. Differential NADPH-versus NADH-dependent superoxide production by phagocyte-type endothelial cell NADPH oxidase[J].Cardiovascular Research, 2001, 52(3):477.
[4] Gupte S A, Rupawalla T, Phillibert D, et al. NADPH and heme redox modulate pulmonary artery relaxation and guanylate cyclase activation by NO[J]. Am J Physiol, 1999, 277:1124-32.
[5] Ivarsson R, Quintens R, Dejonghe S, et al. Redox control of exocytosis: regulatory role of NADPH, thioredoxin, and glutaredoxin[J]. Diabetes, 2005, 54(7): 2132-2142.
[6]Mei,Li,Zhi-Peng,et al.Reduced Nicotinamide Adenine Dinucleotide Phosphate, a Pentose Phosphate Pathway Product, Might Be a Novel Drug Candidate for Ischemic Stroke.[J].Stroke A Journal of Cerebral Circulation, 2016.
NADPH tetrasodium salt是还原型烟酰胺腺嘌呤二核苷酸磷酸（NADPH）的一种钠盐形式，NADPH是细胞内必需的辅因子，充当电子供体[1]。NADPH是一种还原型辅酶Ⅱ，参与许多生物合成代谢途径，如脂肪酸合成、胆固醇合成、草酸循环等[1]。NADPH tetrasodium salt是大肠杆菌（菌株K12，MG 1655）中产生的代谢产物[2]。
在体外，NADPH tetrasodium salt（100µM）处理HUVEC和PIEC细胞30分钟，显著增加了两种细胞的O2−产量[3]。NADPH tetrasodium salt（100µM）加入到再浓缩肺动脉匀浆中，显著升高了可溶性鸟苷酸环化酶（sGC）的活性，使基础活性增加了2.2±1.0倍[4]。NADPH tetrasodium salt（0-300µM）处理诱导啮齿动物β细胞，剂量依赖性地诱导了Ca2+依赖性胞吐作用[5]。
在体内，NADPH tetrasodium salt（16mg/kg）静脉注射处理雄性SD大鼠，给药后60 min内+dp/dt显著升高，-dp/dt显著降低，增强了大鼠体内心脏功能[2]。NADPH tetrasodium salt（2.5mg/kg）静脉注射治疗大鼠和小鼠中风模型，显著减少了脑梗死体积，改善神经功能，提高存活率[6]。