苦参碱对脂多糖诱导肠组织炎症小鼠血清和组织NO及ADMA代谢通路的影响

目的： 探讨苦参碱对脂多糖（LPS）致肠组织炎症小鼠血清和组织一氧化氮（NO）及非对称性二甲基精氨酸（ADMA）代谢通路的影响。 方法： 雄性昆明小鼠随机分为5组：正常对照组、LPS组、苦参碱高、中、低剂量组（80，40，20 mg·kg^-1·d^-1），灌胃3 d（正常对照和LPS组灌胃等量蒸馏水），末次灌胃1 h后腹腔注射生理盐水或LPS（1 mg·kg^-1），于12 h后取血清及组织，测定NO和ADMA水平，观察肠组织病理变化，采用Western blot方法检测小肠组织中蛋白精氨酸甲基转移酶1（PRMT1）和二甲基二甲胺水解酶2（DDAH2）的蛋白表达。 结果： 与模型组比较苦参碱组（80，40，20 mg·kg^-1）均降低血清和组织中NO含量并升高血清ADMA水平，增加肠组织PRMT1表达，但对DDAH2表达无影响。 结论： 苦参碱可抑制脂多糖诱导的小鼠肠组织炎症。该作用机制与降低血清和组织中NO水平，增加血清ADMA水平和肠组织PRMT1的表达有关。

Effect of matrine on NO and ADMA metabolism pathways in serum and tissues of mice with lipopolysaccharide-induced intestine tissue inflammation

Objective: To discuss the effect of matrine on nitric oxide (NO) and asymmetric methylarginine (ADMA) metabolism pathways in serum and tissues of mice with lipopolysaccharide (LPS)-induced intestine tissue inflammation. Method: Kunming mice were randomly divided into five groups: the normal control group, the LPS group and matrine (80, 40, 20 mg·kg^-1·d^-1) groups. The mice were intragastrically administered with drugs for 3 d (distilled water of the same volume for the normal control group and the LPS group). One hour after the last intragastrical administration, normal saline or LPS (1 mg·kg^-1) were intraperitoneally injected. Twelve hours later, serum and tissues were collected to determine NO and ADMA levels and observe the pathological changes of intestinal tissues. The Western blot method was adopted to detect the protein expressions of arginine methyltransferases 1 (PRMT1) and dimethylarginine dimethylaminohydrolase 2(DDAH2) in intestinal tissues. Result: Compared with the model group, matrine (80, 40, 20 mg·kg^-1·d^-1) groups showed lower NO content in serum and tissues, higher ADMA level in serum and increased PRMT1 expression in intestinal tissues, but without effect on DDAH2 expression. Conclusion: Matrine could inhibit LPS-induced intestine tissue inflammation in mice. Its action mechanism is related to the decreased NO content in serum and tissues and increased ADMA level in serum and PRMT1 expression in intestinal tissues.