Icariin reduces cadmium-induced renal injury in rats
Jiewei Zheng, Xin Yang, Cong Zhang, Weipeng Zhang, Yue Hu, Lihai Zeng, Lili Liu, Guoliang Li
Abstract
Icariin (ICA), an active ingredient found in Epimedium, possesses antioxidant and anti-inflammatory properties and has garnered widespread attention in recent years. This study investigated the protective effects of ICA against cadmium (Cd)-induced kidney injury in rats. Healthy male specific pathogen-free Sprague-Dawley rats were randomly divided into a control group, Cd group, a low-dose ICA group, a middle-dose ICA group, and a high-dose ICA group using a random number table. Tissue and blood samples were analyzed for renal function markers, histopathology, and gene expression. We found that ICA intervention ameliorates Cd-induced nephrotoxicity by enhancing glomerular filtration, mitigating renal tubular epithelial cell damage, reducing cellular degeneration and edema, and decreasing oxidative stress. ICA demonstrated anti-apoptotic activity through the regulation of pro- and anti-apoptotic gene transcription and by inhibiting apoptosis, thus protecting the kidneys. ICA also exhibited anti-inflammatory effects by reducing the transcription of Cd-induced pro-inflammatory genes, inhibiting nucleotide oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3) inflammasome formation, and preventing pyroptosis. ICA potentially regulated the Toll-like receptor 4/P2rx7/nuclear factor kappa B signaling pathway, which modulated the activation of the NLRP3 inflammasome and contributed to its anti-inflammatory action. ICA reduced Cd-induced renal injury in rats, likely through a mechanism involving antioxidant, anti-apoptotic, and anti-inflammatory effects.