Department of Pediatrics, Xiangya Hospital, Central South University, Changsha 410008, China.
Nitric Oxide. 2010 Dec 15;23(4):327-31. doi: 10.1016/j.niox.2010.09.004. Epub 2010 Sep 25.
We early show that glutamate (Glu) mediate hyperoxia-induced newborn rat lung injury through N-methyl-D-aspartate receptor (NMDAR). In this study, we search for evidence of NMDAR expression on newborn rat alveolar macrophages (AMs) and the difference between newborn and adult rat AMs, and the possible effect on nitric oxide (NO) production of AMs by exogenous NMDA. The protein of NMDAR was showed by immunocytochemistry, and the mRNA was examined by RT-PCR and real-time PCR. The results show that: (i) both newborn and adult rat AMs express NMDAR1 and the four NMDAR2 subtypes and newborn rat AMs are higher expression. (ii) NMDA administration increase NO production, inducible nitric oxide synthase (iNOS) activity and iNOS mRNA expression of AMs. (iii) NMDAR activation elevates NO secretion of AMs, which suggests that AM may be one of the key cellular origin of the elevated NO secretion in hyperoxia-induced lung injury.
我们早期的研究表明，谷氨酸（Glu）通过 N-甲基-D-天冬氨酸受体（NMDAR）介导高氧诱导的新生大鼠肺损伤。在这项研究中，我们寻找 NMDAR 在新生大鼠肺泡巨噬细胞（AMs）上表达的证据，以及新生大鼠和成年大鼠 AMs 之间的差异，以及外源性 NMDA 对 AMs 一氧化氮（NO）产生的可能影响。通过免疫细胞化学显示 NMDAR 蛋白，并通过 RT-PCR 和实时 PCR 检查其 mRNA。结果表明：（i）新生和成年大鼠 AMs 均表达 NMDAR1 和四个 NMDAR2 亚型，且新生大鼠 AMs 的表达更高。（ii）NMDA 给药增加 AMs 的 NO 产生、诱导型一氧化氮合酶（iNOS）活性和 iNOS mRNA 表达。（iii）NMDAR 激活可增加 AMs 的 NO 分泌，提示 AM 可能是高氧诱导肺损伤中升高的 NO 分泌的关键细胞来源之一。
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