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目的 :探讨一氧化氮 (NO)在实验化学性肝纤维化中的作用。方法 :选用 Wistar纯系大白鼠 ,通过皮下注射四氯化碳复制肝纤维化动物模型。于注射 12周后将已经发生肝纤维化的大白鼠随机分成两组 ,一组尾静脉注射NO合成酶抑制剂 L- NAME,另一组注射生理盐水作为对照 ,4周后检测血清 NO浓度及肝脏病理改变。结果 :血清NO浓度在肝纤维化过程中呈升高趋势 ,尾静脉注射 L - NAME后 ,血清 NO浓度下降 ,病理检查提示 L - NAME组较生理盐水对照组纤维组织增多 ,纤维间隔增宽。结论 :NO不但参与了化学性肝纤维化过程 ,并在此过程中起到抑制纤维化发展的作用
Objective: To investigate the role of nitric oxide (NO) in experimental chemical liver fibrosis. Methods: Wistar rats were used to replicate liver fibrosis animal model by subcutaneous injection of carbon tetrachloride. After 12 weeks of injection, the rats with hepatic fibrosis were randomly divided into two groups. One group injected L-NAME, an NO synthase inhibitor, into the caudal vein. The other group received normal saline as a control. After 4 weeks, Liver pathology changes. Results: Serum NO concentration increased during liver fibrosis. Serum NO concentration decreased after L - NAME injection into the caudal vein. Pathological examination suggested that the L - NAME group had more fibrous tissue and broadened fiber interval than the saline control group. Conclusion: NO not only participates in chemical liver fibrosis, but also plays a role in inhibiting the development of fibrosis