Diaz-Ruiz Araceli, Vergara Paula, Perez-Severiano Francisca, Segovia Jose, Guizar-Sahagún Gabriel, Ibarra Antonio, Ríos Camilo
Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía, Ave. Insurgentes Sur No. 3877, D.F., Mexico City 14269, Mexico.
Neurosci Lett. 2004 Feb 26;357(1):49-52. doi: 10.1016/j.neulet.2003.12.042.
Nitric oxide is generated from l-arginine by a family of three distinct nitric oxide synthase (NOS) enzymes playing a crucial role in the physiopathology of spinal cord injury (SCI). Cyclosporin-A (CsA), an immunosupressive agent, may be used to inhibit the activity of iNOS and perhaps to protect against neural tissue destruction. Rats were submitted to SCI by contusion, and killed 4, 24 and 72 h after lesion. Results showed an increase in the activity of iNOS at 72 h after the SCI, inhibited by CsA (2.5 mg/kg) administered 12 h after trauma. iNOS Western blot assay showed an increase in the expression of iNOS after trauma, also antagonized by CsA administration.
一氧化氮由左旋精氨酸通过三种不同的一氧化氮合酶（NOS）家族酶生成，这些酶在脊髓损伤（SCI）的生理病理学中起关键作用。环孢素A（CsA）是一种免疫抑制剂，可用于抑制诱导型一氧化氮合酶（iNOS）的活性，并可能预防神经组织破坏。将大鼠通过挫伤造成脊髓损伤，并在损伤后4小时、24小时和72小时处死。结果显示，脊髓损伤后72小时诱导型一氧化氮合酶（iNOS）活性增加，创伤后12小时给予环孢素A（2.5毫克/千克）可抑制该活性。诱导型一氧化氮合酶（iNOS）的蛋白质免疫印迹分析显示创伤后诱导型一氧化氮合酶（iNOS）的表达增加，给予环孢素A也可对抗这种增加。
