Intervention effect of Lycium barbarum polysaccharide on lead-induced kidney injury mice and its mechanism: A study based on the PI3K/Akt/mTOR signaling pathway

Abstract

Ethnopharmacological relevanceThe traditional medicinal application of Lycium barbarum is centered on the improvement of eyesight, as well as the nourishment of liver and kidney functions. Lycium barbarum polysaccharide (LBP), serving as the principal active constituent of Lycium barbarum, has been identified as the main contributor to these beneficial effects. Previous studies have indicated that Lycium barbarum polysaccharide exhibits a renoprotective effect against lead-induced injury, but its mechanism and efficacy remain unclear. Aim of the studyThe objective of this study was to examine the effectiveness of LBP in preventing lead-induced renal injury and investigate both the toxic mechanism of lead-induced renal injury and the efficacy mechanism of LBP against it, with a focus on the PI3K/AKT/mTOR signaling pathway. Materials and methodsThe drug effect and mechanism of LBP on lead-induced kidney injury were investigated by administering positive drugs and LBP to mice with established lead-induced kidney injury. ResultsThe renal function of mice with lead-induced renal injury was significantly restored, renal tissue lesions and renal mitochondrial damage were delayed, a disorder of hematological parameters induced by lead was improved, the increase of lead-induced renal index was reduced, and the body weight of mice with lead-induced renal injury was increased by the LBP intervention, as revealed by the results of pharmacodynamic experiments. Based on PI3K /AKT /mTOR signaling pathway, the toxic mechanism of lead-induced kidney injury and the pharmacodynamic mechanism of LBP against lead-induced kidney injury were studied. The results showed that lead could activate the TLR4 receptor, and then activate PI3K /AKT /mTOR signaling pathway, inhibit autophagy of kidney tissue cells, and enhance apoptosis of kidney tissue cells to induce kidney injury; LBP inhibits the activation of TLR4 receptor, which in turn inhibits the PI3K/AKT/mTOR signaling pathway, enhances the autophagy of kidney tissue cells, reduces the apoptosis of kidney tissues, and delays lead-induced kidney injury.