Kono Toru, Kotani Hiromi, Asama Toshiyuki, Mamiya Noriaki, Ohara Kei, Yoneda Masashi, Iwamoto Jun, Kasai Shinichi
Second Department of Surgery, Asahikawa Medical College, Hokkaido, Japan.
Int J Colorectal Dis. 2002 Mar;17(2):98-103. doi: 10.1007/s003840100341.
The effect of low-dose lipopolysaccharide (LPS) induced nitric oxide (NO) on liver damage and survival in rats with acute liver failure caused by a lethal dose of D-galactosamine (D-gal) was studied.
Ninety percent of control animals died within 4 days after D-gal injection, but pretreatment with low-dose LPS significantly decreased mortality to 5%. There was marked elevation in serum aspartate aminotransferase and alanine aminotransferase levels 24 h after D-gal injection. These aminotransferases were significantly improved in low-dose LPS pretreated rats 24 h after the administration of D-gal. NG-Nitro-L-arginine-methyl ester, but not NG-nitro-D-arginine-methyl ester, reversed this cytoprotection.
Pretreatment with low-dose LPS prevents experimental liver failure induced by D-gal through activation of endogenous NO synthesis.
研究低剂量脂多糖(LPS)诱导的一氧化氮(NO)对致死剂量D-半乳糖胺(D-gal)所致急性肝衰竭大鼠肝损伤及存活情况的影响。
D-gal注射后4天内,90%的对照动物死亡,但低剂量LPS预处理显著降低死亡率至5%。D-gal注射24小时后,血清天冬氨酸氨基转移酶和丙氨酸氨基转移酶水平显著升高。在给予D-gal 24小时后,低剂量LPS预处理的大鼠中这些氨基转移酶显著改善。NG-硝基-L-精氨酸甲酯而非NG-硝基-D-精氨酸甲酯可逆转这种细胞保护作用。
低剂量LPS预处理通过激活内源性NO合成预防D-gal诱导的实验性肝衰竭。