Protective effect of icariin on brain-death induced kidney injury and its mechanisms in rats

Abstract

Objective To investigate the protective effect of icariin on brain-death induced kidney injury in rats and its mechanisms. Methods Thirty SD rats were randomly divided into three groups, including sham group, control group (brain death) and experiment group (brain death with icariin treatment). Icariin was intraperitoneally given at the dose of 100 mg/kg right after brain death. Sham group were anaesthetized and treated with mechanical ventilation for 6 hours at the condition of normal intracranial pressure. The rats in control group and experiment group were sacrificed 6 hours after brain death and rats in sham group were sacrificed 6 hours after mechanical ventilation, and peripheral blood and kidneys were collected and detected. Measurement data was represented as (±s). One-way analysis of variance was used to compare serum creatinine, urea nitrogen, Paller score, CD68+ macrophage count and transcriptional levels of proinflammatory factors (IL-1β, IL-6, TNF-α) and chemokines (MCP-1, IP-10) among the 3 groups, least significant difference method was used to compare the above indexes between any two groups, difference was statistically significant when P<0.05. Results The levels of serum urine nitrogen and creatinine in experiment group were (10.0±1.5) and (92±12) mmol/L, respectively, which were significantly lower than control group and higher than sham group (P all<0.05). Icariin decreased the paller scores of tubular injury and alleviated mitochondria and endoplasmic reticulum injury. Icariin significantly decreased the mRNA levels of proinflammatory factors (IL-1β, IL-6, TNF-α) and chemokines (MCP-1, IP-10) , infiltration degree of macrophages, and phosphorylation levels of JNK, p38-MAPK and STAT3 in kidney tissues of experiment group. Conclusions Icariin protects renal function by alleviation of brain-death induced kidney injury, which might by inhibition of inflammation and SAPK and JAK-STAT signal pathways. Key words: Brain death; Inflammatory injury; Icariin; Signal pathway