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Phosphatidylcholine induces apoptosis of 3T3-L1 adipocytes
简介
【 文献重点摘要 】
Background
Phosphatidylcholine (PPC) formulation is used for lipolytic injection, even though its mechanism of action is not well understood.
Methods
The viability of 3T3-L1 pre-adipocytes and differentiated 3T3-L1 cells was measured after treatment of PPC alone, its vehicle sodium deoxycholate (SD), and a PPC formulation. Western blot analysis was performed to examine PPC-induced signaling pathways.
Results
PPC, SD, and PPC formulation significantly decreased 3T3-L1 cell viability in a concentration-dependent manner. PPC alone was not cytotoxic to CCD-25Sk human fibroblasts at concentrations <1 mg/ml, whereas SD and PPC formulation were cytotoxic. Western blot analysis demonstrated that PPC alone led to the phosphorylation of the stress signaling proteins, such as p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, and activated caspase-9, -8, -3 as well as cleavage of poly(ADP-ribose) polymerase. However, SD did not activate the apoptotic pathways. Instead, SD and PPC formulation induced cell membrane lysis, which may lead to necrosis of cells.
Conclusions
PPC results in apoptosis of 3T3-L1 cells.
Keywords
adipocytes, apoptosis, caspases, mesotherapy, PPC
背景
磷脂酰胆碱(PPC)制剂用于脂溶性注射，尽管其作用机制尚不清楚。
方法
分别用PPC、其载体脱氧胆酸钠(SD)和PPC制剂处理3T3-L1前脂肪细胞和分化后的3T3-L1细胞。Western blot分析PPC诱导的信号通路。
结果
PPC、SD和PPC制剂以浓度依赖的方式显著降低3T3-L1细胞的存活率。当浓度<1 mg/ml时，PPC单独对人成纤维细胞CCD-25Sk无细胞毒性，而SD和PPC制剂具有细胞毒性。Western blot分析表明，PPC单独诱导胁迫信号蛋白p38丝裂原活化蛋白激酶和c-jun氨基末端激酶磷酸化，并激活caspase-9、-8、-3和裂解聚(ADP-核糖)聚合酶。但SD不能激活凋亡通路。相反，SD和PPC制剂诱导细胞膜溶解，这可能导致细胞坏死。
结论
PPC可诱导3T3-L1细胞凋亡。
关键词
脂肪细胞，凋亡，半胱氨酸天冬氨酸蛋白酶，中胚层疗法，PPC
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