【Abstract】: Objective To explore the effect of lidocaine on septic renal injury and the regulation of HMGB 1 / NF- κ B pathway. Methods 30 healthy clean grade male SD rats with body mass of 220-300 g were selected: sham group, control group (group C), and lidocaine group (group L). Cecal ligation perforation method (CLP) was used to replicate the septic acute kidney injury model. Group L received the loading dose of 10mg / kg, followed by continuous tail vein infusion for 3 hours at a rate of 10mg kg-1 h-1, and Group C replaced it with equal volume of saline. Blood from the main abdominal artery was retained at 24h after surgery. The concentrations of blood creatinine (SCr), urea nitrogen (BUN), cystatin C (Cys-C), neutrophil gelatinase-related lipid delivery protein (NGAL) and the concentrations of inflammatory factor interleukin-6 (interleukin-6, IL-6), tumor necrosis factor- α (tumor necrosis factor- α, TNF- α), high mobility group protein B1 (high mobility group protein B1, HMGB 1) were determined by El ISA. HK-2 cells were cultured in vitro and divided into control group, model group, lidocaine group, and HMGB 1 (high mobility group protein B1) inhibitor group. After the end of cell culture, apoptosis was measured by flow cytology; HMGB 1, TNF- α and IL-6, in the supernatant by ELISA; and expression of TLR 4 / NF- κ B protein by western blot.Results The animal experiment found that the serum concentrations of Cr, BUN, Cyc-s and NGAL were increased in group C rats compared with the S group (P 0.05). Compared with group C, serum Cr, Cyc-s concentration, BUN concentration and NGAL concentration decreased in group L rats (P 0.05). Compared with the S group, the serum concentrations of IL-6, TNF- α, and HMGB 1 were increased in group C, with significant differences (P 0.05). Compared with group C, serum concentrations of IL-6, TNF- α, and HMGB 1 decreased, significant (P 0.05). In vitro experiments showed increased apoptosis, HMGB 1, TNF-a and IL-6 (P 0.01), relative expression of TLR 4 / NF- κ B protein (P 0.01), HMGB 1, TNF-a and IL-6 (P 0.01), and TLR 4 / NF- κ B (P 0.01). Compared with the control group, the HMGB 1 inhibitor group showed the expression of HMGB 1, TNF-a and IL-6 (P 0.01) and the relative expression of TLR 4 / NF- κ B protein was decreased (P 0.01). Compared with the HMGB 1 inhibitor group, although the relative expression of NF- κ B protein was not significantly different in the lidocaine group, the relative expression of TLR 4 protein was significantly increased (P 0.01). Conclusions Lidocaine can reduce kidney injury and improve kidney function in septic kidney injured rats. Through the mechanism of inhibiting HMGB 1 expression, blocking HMGB 1 / NF- κ B pathway and reducing the release of inflammatory factors, and its anti-inflammatory effect was not significantly different from that of HMGB 1 inhibitor.