[Leptin protects sepsis-induced renal injury and research for its mechanism].

Objective: To detect the effect of sepsis on renal function and corresponding enzymes in mice, and to explore the role of leptin in acute inflammation.
Methods: Sepsis was reproduced by cecum ligation and puncture in mice. Serum uric acid (UA) and four enzymes related with synthesis of free radicals in kidney homogenized fluids, myeloperoxidase (MPO), glutathione-S-transferase (GST), xanthine oxidase (XOD) and superoxide dismutase (SOD) were determined with spectrophotometry, and leptin level in kidney was detected by radioimmunoassay. Histopathologic changes in kidney were observed with hematoxylin-eosin staining.
Results: Twelve hours after leptin (0.08 mg/kg, i.p.) and indomethacin (8 mg/kg, i.p.) injection, serum UA was significantly decreased [(295.79+/-80.86) micromol/L and (281.78+/-46.35) micromol/L, respectively, vs. sepsis group (474.03+/-75.22) micromol/L]. At the same time, renal leptin levels in leptin injection group [(196.00+/-134.30) microg/g] 12 hours after sepsis and in indomethacin injection group [(169.30+/-132.00) microg/g] 6 hours after sepsis were also significantly higher than sepsis group [(61.65+/-27.29) microg/g]. Six and 12 hours after leptin and indomethacin injection, renal MPO, GST, XOD and SOD activities were affected to certain extent, as the results were not completely inhibited or enhanced. Nevertheless, leptin and indomethacin could promote scavenge and deactivation of free radicals.
Conclusion: Low dose leptin can ameliorate sepsis-induced renal injury, which may be related with scavenge and deactivation of free radicals in renal cells, and this mechanism is similar with that of indomethacin.