Panax notoginseng Alleviates Sepsis-Induced Acute Kidney Injury by Reducing Inflammation in Rats

Background. Sepsis is defined as a host inflammatory response to infection that can result in end-organ dysfunction. One of the most common consequences of sepsis is acute kidney injury (AKI). Panax notoginseng powder (PNP) has been previously reported to protect against overactive inflammation process. However, the potential effect of PNP on septic AKI is poorly described. The current study was conducted to investigate the protective effects of PNP in septic AKI rats. Methods. A model of septic AKI was established on male SD rats by using the cecal ligation and puncture procedure. PNP was administrated by gavage after the cecal ligation and puncture (CLP) procedure, and the mice were sacrificed at 6, 12, and 72 h after induction of sepsis. The serum and kidney samples were collected and assayed for biochemical tests, histopathological staining, inflammation, and apoptosis-related gene/protein expression. In addition, 15 rats in each group were used to calculate the 7-day survival rate. Results. CLP-induced kidney injury was observed by the histopathological score, which markedly was attenuated by PNP treatment. Consistently, PNP intervention significantly alleviated the elevated levels of serum creatinine and blood urea nitrogen in CLP-induced sepsis rats. The CLP procedure also triggered proinflammatory cytokine production and increased the expression of various inflammation-related proteins in the kidneys. However, PNP inhibited the renal expression of IL-18, IL-1 beta, TNF-alpha, and IL-6 to substantially improve inflammatory response. Mechanistically, CLP induced the increase of the NF-kappa B p65 level in the injured kidneys, while PNP notably inhibited the corresponding protein expression. Conclusion. PNP attenuated kidney inflammation to protect against CLP-induced septic AKI in rats via inhibiting the NF-kappa B signaling pathway.

Automated summary

This study found that Panax notoginseng powder (PNP) can protect against septic acute kidney injury (AKI) induced by cecal ligation and puncture (CLP) by inhibiting the NF-kappa B signaling pathway.