Adawi D, Molin G, Jeppsson B
Dept. of Surgery, Lund University, Malmö University Hospital, Sweden.
Scand J Gastroenterol. 1997 Aug;32(8):835-40. doi: 10.3109/00365529708996543.
Arginine possesses numerous unique and advantageous biochemical and pharmacologic properties. We have previously shown that arginine supplementation in an acute liver injury model reduces both the extent of the liver injury and bacterial translocation. We therefore studied the role of nitric oxide on the effects of oral arginine supplementation in acute liver injury, bacterial translocation, ileal and cecal mucosal nucleotides, and RNA and DNA, to investigate pathogenetic mechanisms.
Sprague-Dawley rats were divided into normal, liver injury control, N-nitro-L-arginine methyl ester (L-NAME), arginine, and L-NAME + arginine supplementation groups. Oral supplementation was performed daily through a nasogastric tube for 8 days. Acute liver injury was induced on the 8th day by intraperitoneal injection of D-galactosamine (1.1 g/kg body weight). Twenty-four hours after the liver injury, liver function tests, bacterial translocation, and ileal and cecal mucosal nucleotides, RNA, and DNA were evaluated.
Bilirubin and liver enzymes increased significantly in the L-NAME group compared with the arginine group, whereas the liver enzymes increased significantly compared with the liver injury control group. In the L-NAME group the number of bacteria translocated to the portal and arterial blood increased significantly compared with all groups. In the arginine group the bacteria translocated to the liver and mesenteric lymph nodes decreased significantly compared with the liver injury control and L-NAME groups. The ileal and cecal mucosal nucleotides, RNA, and DNA in the arginine group increased significantly compared with the normal, liver injury, and L-NAME groups.
Nitric oxide plays a role in the beneficial effect of the arginine supplementation in acute liver injury. It significantly improves the liver damage indicated by the increase of liver enzymes when its production was inhibited by L-NAME. Nitric oxide has a role in bacterial translocation since the number of bacteria significantly increased in arterial and portal blood when L-NAME was used to inhibit its production. Furthermore, arginine supplementation improved mucosal nucleotides, RNA, and DNA in ileum and colon.
精氨酸具有众多独特且有益的生化和药理特性。我们之前已经表明，在急性肝损伤模型中补充精氨酸可减轻肝损伤程度并减少细菌移位。因此，我们研究了一氧化氮在口服补充精氨酸对急性肝损伤、细菌移位、回肠和盲肠黏膜核苷酸以及RNA和DNA的影响中的作用，以探究发病机制。
将Sprague-Dawley大鼠分为正常组、肝损伤对照组、N-硝基-L-精氨酸甲酯（L-NAME）组、精氨酸组和L-NAME+精氨酸补充组。通过鼻胃管每日进行口服补充，持续8天。在第8天通过腹腔注射D-半乳糖胺（1.1 g/kg体重）诱导急性肝损伤。肝损伤后24小时，评估肝功能、细菌移位以及回肠和盲肠黏膜核苷酸、RNA和DNA。
与精氨酸组相比，L-NAME组的胆红素和肝酶显著升高，而与肝损伤对照组相比，肝酶也显著升高。与所有组相比，L-NAME组中移位至门静脉和动脉血的细菌数量显著增加。与肝损伤对照组和L-NAME组相比，精氨酸组中移位至肝脏和肠系膜淋巴结的细菌显著减少。与正常组、肝损伤组和L-NAME组相比，精氨酸组的回肠和盲肠黏膜核苷酸、RNA和DNA显著增加。
一氧化氮在急性肝损伤中补充精氨酸的有益作用中发挥作用。当L-NAME抑制其产生时，它会显著改善肝酶升高所表明的肝损伤。一氧化氮在细菌移位中起作用，因为使用L-NAME抑制其产生时，动脉血和门静脉血中的细菌数量显著增加。此外，补充精氨酸可改善回肠和结肠的黏膜核苷酸、RNA和DNA。
