Yang Dan-lei, Xu Yong-jian, Zhang Zhen-xiang, Li Chao-qian
Department of Respiratory Medicine, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2003 Jan;19(1):7-9.
To explore the effect of nitric oxide on NF-kappaB activation in rat alveolar macrophage(AM) induced by cigarette smoke extract(CSE) and the involved mechanism.
AMs were co-cultured with NO precursor L-arginine (L-Arg) or inhibitor of inducible nitric oxide synthase L-N(6)(1-iminoethyl)lysine (L-NIL) and CSE. The expression of NF-kappaB was determined by immunocytochemistrical staining, the content of I-kappaB protein was detected by Western blot, the level of NO in supernatant was assayed by Griess reaction.
CSE could induce NF-kappaB activation and decrease level of I-kappaB. L-Arg augmented CSE-induced NF-kappaB activation and decreased I-kappaB content at low concentration while inhibited CSE-induced NF-kappaB activation at high concentration, but there was not any significant difference of the expression of I-kappaB. The percentage of NF-kappaB nucleus dyeing positive cells was lower and the expression of I-kappaB was higher in response to CSE plus various concentrations of L-NIL as compared with that in response to CSE alone (P<0.01). The changes induced by L-NIL were concentration-dependent.
NO may up-regulate and down-regulate the activation of NF-kappaB induced by CSE according to difference in NO concentration in AMs.