Xia W, Wang Y, Appleyard R C, Smythe G A, Murrell G A C
Orthopaedic Research Institute, St. George Hospital Campus, University of New South Wales, Kogarah, Sydney, NSW 2217, Australia.
Inflamm Res. 2006 Jan;55(1):40-5. doi: 10.1007/s00011-005-0006-4.
To determine if inducible nitric oxide synthase (iNOS) gene could affect Achilles tendon healing using iNOS gene knockout mice.
21 iNOS knockout (iNOS(-/-)) mice and 8 of the wild type (iNOS(+/+)) mice were utilized in this study. Group 1: iNOS(+/+) mice (n = 8), group 2: iNOS(-/-) mice (n = 11) and group 3: iNOS(-/-) with a NOS inhibitor, (aminoguanidine, 500 mg/kg/day, via an intraperitoneal mini-osmotic pump for 7 days, n = 10). The right Achilles tendon was transected in all mice and harvested on day 7 for cross-sectional area and biomechanical properties. Serum nitrate concentration of the mice was measured by gas chromatography mass spectrometry (GC/MS).
A significant reduction in cross-sectional area of the healing Achilles tendon was observed in group 3 mice compared to group 2 mice (p < 0.01). The serum nitrate concentration in both group 2 and group 3 mice was lower than that in group 1 mice (p < 0.01) iNOS gene deletion and inhibition of NOS did not affect the biomechanical properties of the healing tendons.
iNOS gene is not solely responsible for the beneficial effects of nitric oxide (NO) on tendon healing.
使用诱导型一氧化氮合酶（iNOS）基因敲除小鼠来确定iNOS基因是否会影响跟腱愈合。
本研究使用了21只iNOS基因敲除（iNOS(-/-)）小鼠和8只野生型（iNOS(+/+)）小鼠。第1组：iNOS(+/+)小鼠（n = 8），第2组：iNOS(-/-)小鼠（n = 11），第3组：iNOS(-/-)小鼠并给予一氧化氮合酶抑制剂（氨基胍，500 mg/kg/天，通过腹腔内微型渗透泵给药7天，n = 10）。所有小鼠的右跟腱均被切断，并在第7天取材以检测横截面积和生物力学特性。通过气相色谱 - 质谱联用仪（GC/MS）测量小鼠血清硝酸盐浓度。
与第2组小鼠相比，第3组小鼠愈合跟腱的横截面积显著减小（p < 0.01）。第2组和第3组小鼠的血清硝酸盐浓度均低于第1组小鼠（p < 0.01）。iNOS基因缺失和一氧化氮合酶抑制并未影响愈合肌腱的生物力学特性。
iNOS基因并非一氧化氮（NO）对肌腱愈合产生有益作用的唯一原因。
