These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Protective mechanism of L-arginine against liver ischemic-reperfusion injury in rats.
    Author: Li SQ, Liang LJ.
    Journal: Hepatobiliary Pancreat Dis Int; 2003 Nov; 2(4):549-52. PubMed ID: 14627517.
    Abstract:
    OBJECTIVE: To investigate the protective effect of L-arginine (L-arg) against liver ischemic-reperfusion (I/R) injury in rat model and its possible mechanism. METHODS: Male Sprague-Dawley rats were randomized into sham group: hepatoduodenal ligament mobilized, but not clamped; control group: hepatic ischemia only; Arg group: 5 minutes before hepatic ischemia, L-arg (200 mg/kg) injected via the dorsal penis vein; Arg+L group: 10 and 5 minutes before hepatic ischemia, L-NAME (30 mg/kg) and L-arg (200 mg/kg) injected via the dorsal penis vein, respectively; and Fmk group: 5 minutes before hepatic ischemia, ZVAD-fmk (15 mg/kg) injected via the dorsal penis vein. The liver was subjected to ischemia for 40 minutes by Pringle's maneuver, and reperfusion was initiated by removing clamp. The 7-day survival rate, alanine transaminase (ALT) level, caspase-3 activity and apoptotic hepatocyte count were compared among these groups. RESULTS: After 40 minutes of ischemia and 6 hours of reperfusion, the 7-day survival rate of the Arg group was significantly higher than that of the control and Arg+L groups (P<0.05). The ALT level, caspase-3 activity and apoptotic hepatocyte count in the Arg group were decreased significantly than those in the control and Arg+L groups (P<0.01). The caspase-3 activity and apoptotic hepatocyte count in the Arg group were slightly higher than those in the sham and Fmk groups, but there was no statistical significance. CONCLUSIONS: L-arg could ameliorate liver I/R injury and the possible protective mechanism is inhibition of hepatocyte apoptosis via inhibition of caspase-3 activity by nitric oxide synthesis.
    [Abstract] [Full Text] [Related] [New Search]