Tannahill C L, Stevenot S A, Campbell-Thompson M, Nick H S, Valentine J F
Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, USA.
Gastroenterology. 1995 Sep;109(3):800-11. doi: 10.1016/0016-5085(95)90387-9.
BACKGROUND & AIMS: Oxygen radicals and reactive oxygen species play an important role in inflammatory episodes in the bowel. Nonetheless, little is known about the regulation of colonic superoxide dismutases and key antioxidant enzymes with cytoprotective and radical detoxifying properties. The aim of this study was to examine the regulation of manganese superoxide dismutase (SOD) in acute acetic acid-induced colitis.
Colitis was induced in adult rats by the rectal administration of 5% acetic acid. Total RNA and protein were isolated from the inflamed colon from 1 to 24 hours after the induction of colitis. MnSOD messenger RNA and protein levels were evaluated by Northern and Western analyses, respectively. MnSOD protein was localized in cross sections of the colon by immunocytochemistry.
MnSOD messenger RNA levels showed a rapid 14-96-fold induction in response to acetic acid administration. Western analysis showed a 22-49-fold induction in MnSOD protein levels. Immunocytochemistry showed induction of MnSOD protein, specifically in smooth muscle cells, epithelial cells at the base of the glands, and myenteric plexus neurons.
MnSOD messenger RNA and protein levels are rapidly induced following the inflammatory insult, implicating a role for MnSOD in the acute phase of colonic inflammation. We suggest that induction of MnSOD in specific cell types may have a cytoprotective function.
氧自由基和活性氧在肠道炎症发作中起重要作用。然而，关于具有细胞保护和自由基解毒特性的结肠超氧化物歧化酶及关键抗氧化酶的调节机制，人们了解甚少。本研究旨在探讨急性乙酸诱导的结肠炎中锰超氧化物歧化酶（SOD）的调节机制。
通过直肠给予5%乙酸诱导成年大鼠发生结肠炎。在诱导结肠炎后1至24小时，从发炎的结肠中分离总RNA和蛋白质。分别通过Northern分析和Western分析评估锰超氧化物歧化酶信使RNA和蛋白质水平。通过免疫细胞化学方法在结肠横断面中定位锰超氧化物歧化酶蛋白。
给予乙酸后，锰超氧化物歧化酶信使RNA水平迅速出现14至96倍的诱导增加。Western分析显示锰超氧化物歧化酶蛋白水平有22至49倍的诱导增加。免疫细胞化学显示锰超氧化物歧化酶蛋白被诱导，特别是在平滑肌细胞、腺底部的上皮细胞和肌间神经丛神经元中。
炎症损伤后，锰超氧化物歧化酶信使RNA和蛋白质水平迅速被诱导，这表明锰超氧化物歧化酶在结肠炎症急性期发挥作用。我们认为在特定细胞类型中诱导锰超氧化物歧化酶可能具有细胞保护功能。
