Aramaki Y, Arima H, Hara T, Tsuchiya S
School of Pharmacy, Tokyo University of Pharmacy and Life Science, Japan.
Pharm Res. 1996 Sep;13(9):1389-92. doi: 10.1023/a:1016034303012.
The effects of liposomes on nitric oxide (NO) production from mouse peritoneal macrophages following intraperitoneal injection of liposomes were investigated.
Mouse peritoneal macrophages were collected following intraperitoneal injection of liposomes and cultured with and without lipopolysaccharide (LPS). Peritoneal washing fluid was also collected from the mice injected with liposomes. NO production was evaluated by measuring the concentration of nitrite in the macrophage culture supernatant by Griess reagent.
NO production stimulated by LPS was observed in peritoneal macrophages obtained from the liposome-treated mice, but liposomes did not active macrophages directly to induce NO in response to LPS. NO production was higher in the liposomes composed of phosphatidylcholine than that of negatively charged liposomes composed of phosphatidylserine. Peritoneal washing fluid obtained from mice injected with liposomes has a capacity to induce NO production in the macrophages from naive mice. This capacity was not diminished by heat-treatment at 100 degrees C for 5 min.
Peritoneal macrophages were activated to produce NO in response to LPS following intraperitoneal injection of liposomes. They did not activate macrophages directly, and the induction of heat-stable macrophage priming factor, but not cytokines, is suggested.
研究腹腔注射脂质体后脂质体对小鼠腹腔巨噬细胞一氧化氮(NO)产生的影响。
腹腔注射脂质体后收集小鼠腹腔巨噬细胞,并在有或无脂多糖(LPS)的情况下进行培养。还从注射脂质体的小鼠中收集腹腔冲洗液。通过用格里斯试剂测量巨噬细胞培养上清液中亚硝酸盐的浓度来评估NO的产生。
在从脂质体处理的小鼠获得的腹腔巨噬细胞中观察到LPS刺激的NO产生,但脂质体不会直接激活巨噬细胞以响应LPS诱导NO。由磷脂酰胆碱组成的脂质体中的NO产生高于由磷脂酰丝氨酸组成的带负电荷的脂质体。从注射脂质体的小鼠获得的腹腔冲洗液具有诱导未处理小鼠巨噬细胞中NO产生的能力。这种能力在100℃热处理5分钟后没有减弱。
腹腔注射脂质体后,腹腔巨噬细胞被激活以响应LPS产生NO。它们不会直接激活巨噬细胞,提示诱导了热稳定的巨噬细胞启动因子而非细胞因子。