Pizza F X, Hernandez I J, Tidball J G
Department of Physiological Science, University of California, Los Angeles 90095-1527, USA.
J Leukoc Biol. 1998 Oct;64(4):427-33.
The objective of this study was to determine the role of nitric oxide in muscle inflammation, fiber necrosis, and apoptosis of inflammatory cells in vivo. The effects of nitric oxide synthase (NOS) inhibition on the concentrations of neutrophils, ED1+ and ED2+ macrophages, apoptotic inflammatory cells, and necrotic muscle fibers in rats subjected to 10 days of hindlimb unloading and 2 days of reloading were determined. Administration of NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) significantly reduced the concentrations of neutrophils, ED1+ and ED2+ macrophages, and necrotic fibers in soleus muscle relative to water-treated controls. The concentration of apoptotic inflammatory cells was also significantly lower for L-NAME-treated animals compared with water-treated controls. However, the proportion of the inflammatory cell population that was apoptotic did not differ between L-NAME-treated and control animals, suggesting that L-NAME treatment did not decrease inflammatory cell populations by increasing the frequency of apoptosis. Thus, nitric oxide or one of its intermediates promotes muscle inflammation and fiber necrosis during modified muscle use and plays no more than a minor role in the resolution of muscle inflammation by inducing apoptosis of inflammatory cells.
本研究的目的是确定一氧化氮在体内肌肉炎症、纤维坏死及炎症细胞凋亡中的作用。测定了一氧化氮合酶（NOS）抑制对经历10天 hindlimb unloading及2天再负荷的大鼠中性粒细胞、ED1 +和ED2 +巨噬细胞、凋亡性炎症细胞及坏死肌纤维浓度的影响。与水处理对照组相比，给予NOS抑制剂N（ω）-硝基-L-精氨酸甲酯（L-NAME）显著降低了比目鱼肌中中性粒细胞、ED1 +和ED2 +巨噬细胞以及坏死纤维的浓度。与水处理对照组相比，L-NAME处理动物的凋亡性炎症细胞浓度也显著降低。然而，L-NAME处理组和对照组动物中凋亡的炎症细胞群体比例并无差异，这表明L-NAME处理并非通过增加凋亡频率来减少炎症细胞群体。因此，一氧化氮或其一种中间体在改变肌肉使用期间促进肌肉炎症和纤维坏死，并且在通过诱导炎症细胞凋亡来解决肌肉炎症方面所起作用不超过次要作用。
