Glycyrrhizin protects mice against renal ischemia-reperfusion injury through inhibition of apoptosis and inflammation by downregulating p38 mitogen-activated protein kinase signaling

• Published in: Experimental and therapeutic medicine 2014-05, Vol.7 (5), p.1247-1252
• Main Authors: YE, SHAOJUN, ZHU, YI, MING, YINGZI, SHE, XINGGUO, LIU, HONG, YE, QIFA
• Format: Article
• Language: English
• Subjects: Abdomen; Abdominal surgery; Apoptosis; Care and treatment; Cytokines; Enzymes; glycyrrhizin; Health aspects; inflammation; Ischemia; ischemia-reperfusion; kidney; Kidney diseases; Kidneys; Kinases; Mitogen-activated protein kinases; Neutrophils; Physiological aspects; Phytochemicals; Proteins; Rodents; Studies; Transplants & implants; Tumor necrosis factor-TNF
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2014.1570

Ischemia-reperfusion (I/R) often leads to acute kidney injury, chronic renal failure and kidney transplantation failure. Glycyrrhizin is extracted from Glycyrrhiza glabra roots and is the predominant active component, which exhibits anti-inflammatory effects. However, to the best of our knowledge, the effect of glycyrrhizin on I/R-induced renal injury has not been investigated. In the present study, glycyrrhizin was demonstrated to attenuate renal I/R injury in mice via administration of glycyrrhizin, which suppressed the serum levels of creatinine and blood urea nitrogen 6 h following reperfusion; furthermore, the superoxide anions as well as the activity of superoxide dismutase within renal tissues was reduced by glycyrrhizin pretreatment. Moreover, the protein level of cleaved caspase-3, as well as its activity in renal tissue, was suppressed as a result of the glycyrrhizin pretreatment, indicating that glycyrrhizin inhibits I/R-induced renal cell apoptosis. In addition, glycyrrhizin pretreatment appeared to ameliorate I/R-induced renal injury via inhibition of inflammatory cell infiltration, as well as the production of pro-inflammatory cytokines, including tumor necrosis factor-α, interferon-γ, interleukin (IL)-1β and IL-6. The underlying molecular mechanism was investigated and it was shown that the activity of p38 mitogen-activated protein kinase signaling was downregulated as a result of glycyrrhizin administration. In conclusion, the present study indicated that glycyrrhizin provided significant protection against I/R-induced renal injury in mice by inhibiting inflammatory responses and renal cell apoptosis. Therefore, glycyrrhizin may be used in abdominal surgery and kidney transplantation for the prevention of renal I/R damage.