转化生长因子β参与带负电荷脂质体对脂多糖刺激的巨噬细胞一氧化氮产生的抑制作用。
Involvement of TGF-beta in inhibitory effects of negatively charged liposomes on nitric oxide production by macrophages stimulated with lps.
作者信息
Matsuno R, Aramaki Y, Tsuchiya S
机构信息
Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Tokyo, Hachioji, 192-0392, Japan.
出版信息
Biochem Biophys Res Commun. 2001 Mar 2;281(3):614-20. doi: 10.1006/bbrc.2001.4419.
We examined the role of TGF-beta in the inhibitory effects of negatively charged liposomes composed of phosphatidylserine (PS-liposomes) on nitric oxide (NO) production by macrophages stimulated with LPS. The expression of TGF-beta mRNA increased when mouse peritoneal macrophages were treated with PS-liposomes. The inhibitory effect of PS-liposomes on NO production was restored by treatment with anti-TGF-beta antibody. Furthermore, NO production, iNOS mRNA expression, and iNOS protein induction by LPS were inhibited by treatment of macrophages with TGF-beta as well as PS-liposomes. These results indicated that PS-liposomes down-regulate NO production by macrophages through the induction of TGF-beta and suggested that TGF-beta may suppress NO production upstream of the transcription of iNOS mRNA.
我们研究了转化生长因子β（TGF-β）在由磷脂酰丝氨酸组成的带负电荷脂质体（PS-脂质体）对脂多糖（LPS）刺激的巨噬细胞产生一氧化氮（NO）的抑制作用中所起的作用。当用PS-脂质体处理小鼠腹腔巨噬细胞时，TGF-β mRNA的表达增加。用抗TGF-β抗体处理可恢复PS-脂质体对NO产生的抑制作用。此外，用TGF-β以及PS-脂质体处理巨噬细胞可抑制LPS诱导的NO产生、诱导型一氧化氮合酶（iNOS）mRNA表达和iNOS蛋白诱导。这些结果表明，PS-脂质体通过诱导TGF-β下调巨噬细胞的NO产生，并提示TGF-β可能在iNOS mRNA转录上游抑制NO产生。
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