Lysophosphatidylcholines is an important class of phospholipid molecules, which are the products of phosphatidylcholine hydrolysis by phospholipase A2 [1]. Lysophosphatidylcholines participate in regulating the recruitment and activation of immune cells by activating G protein-coupled receptors and regulating leukocyte chemotaxis [2-3]. Lysophosphatidylcholines are commonly used to treat inflammatory-related diseases [4].
In human fibroblasts, the decreased membrane stability by Lysophosphatidylcholines (6μM, 7μM; 0-6h) leads to increased 14C release, which in turn causes changes in cell morphology [5]. In human umbilical vein endothelial cells, Lysophosphatidylcholines (25-100μM; 0-48h) induces apoptosis in human endothelial cells through a p38-MAPK-dependent pathway [6]. In AR42J cells, Lysophosphatidylcholine (0.1-100μM; 25h) induces cell apoptosis [7].
In sepsis mice models, Lysophosphatidylcholines (5mg/kg; ip; 10d) treatment significantly enhanced the clearance of intraperitoneal bacteria and blocked cecal ligation and puncture-induced neutrophil inactivation [8]. In ICR mice, blood glucose levels in mice decreased in a dose-dependent manner after Lysophosphatidylcholines (15μmol/kg, 30μmol/kg; iv; single injection) administration [9].
References:
[1]. Law S H, Chan M L, Marathe G K, et al. An updated review of lysophosphatidylcholine metabolism in human diseases[J]. International journal of molecular sciences, 2019, 20(5): 1149.
[2]. Yang L V, Radu C G, Wang L, et al. Gi-independent macrophage chemotaxis to lysophosphatidylcholine via the immunoregulatory GPCR G2A[J]. Blood, 2005, 105(3): 1127-1134.
[3]. Kabarowski J H. G2A and LPC: regulatory functions in immunity[J]. Prostaglandins & other lipid mediators, 2009, 89(3-4): 73-81.
[4]. Akram W, Rihan M, Ahmed S, et al. Marine-derived compounds applied in cardiovascular diseases: submerged medicinal industry[J]. Marine drugs, 2023, 21(3): 193.
[5]. Colles S M, Chisolm G M. Lysophosphatidylcholine-induced cellular injury in cultured fibroblasts involves oxidative events[J]. Journal of lipid research, 2000, 41(8): 1188-1198.
[6]. Takahashi M, Okazaki H, Ogata Y, et al. Lysophosphatidylcholine induces apoptosis in human endothelial cells through a p38-mitogen-activated protein kinase-dependent mechanism[J]. Atherosclerosis, 2002, 161(2): 387-394.
[7]. Masamune A, Sakai Y, Satoh A, et al. Lysophosphatidylcholine induces apoptosis in AR42J cells[J]. Pancreas, 2001, 22(1): 75-83.
[8]. Yan J J, Jung J S, Lee J E, et al. Therapeutic effects of lysophosphatidylcholine in experimental sepsis[J]. Nature medicine, 2004, 10(2): 161-167.
[9]. Yea K, Kim J, Yoon J H, et al. Lysophosphatidylcholine activates adipocyte glucose uptake and lowers blood glucose levels in murine models of diabetes[J]. Journal of Biological Chemistry, 2009, 284(49): 33833-33840.
Lysophosphatidylcholines是一类重要的磷脂分子，是磷脂酶A2水解磷脂酰胆碱的产物 [1]。Lysophosphatidylcholines通过激活G蛋白偶联受体和调节白细胞趋化性来参与调节免疫细胞的募集和激活 [2-3]。Lysophosphatidylcholines常用于治疗炎症相关疾病 [4]。
在人成纤维细胞中，Lysophosphatidylcholines（6μM，7μM；0-6h）降低膜稳定性，导致14C释放增加，进而引起细胞形态改变 [5]。在人脐静脉内皮细胞中，Lysophosphatidylcholines（25-100μM；0-48h）通过p38-MAPK依赖性途径诱导人内皮细胞凋亡 [6]。在AR42J细胞中，Lysophosphatidylcholines（0.1-100μM；25h）诱导细胞凋亡 [7]。
在脓毒症小鼠模型中，Lysophosphatidylcholines（5mg/kg；ip；10d）治疗显著增强了腹腔内细菌的清除，并阻断了盲肠结扎和穿刺引起的中性粒细胞失活 [8]。在ICR小鼠中，在给予Lysophosphatidylcholines（15μmol/kg，30μmol/kg；iv；单次注射）后，小鼠血糖水平呈剂量依赖性下降 [9]。