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低剂量脂多糖预处理对D-半乳糖胺诱导的急性肝衰竭的保护作用。

Protective effect of pretreatment with low-dose lipopolysaccharide on D-galactosamine-induced acute liver failure.

作者信息

Kono Toru, Kotani Hiromi, Asama Toshiyuki, Mamiya Noriaki, Ohara Kei, Yoneda Masashi, Iwamoto Jun, Kasai Shinichi

机构信息

Second Department of Surgery, Asahikawa Medical College, Hokkaido, Japan.

出版信息

Int J Colorectal Dis. 2002 Mar;17(2):98-103. doi: 10.1007/s003840100341.

Abstract

BACKGROUND AND AIMS

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.

RESULTS

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.

CONCLUSION

Pretreatment with low-dose LPS prevents experimental liver failure induced by D-gal through activation of endogenous NO synthesis.

摘要

背景与目的

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。

结果

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。

结论

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。

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