Abstract：
BACKGROUND: The 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.
OBJECTIVE: The 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.
METHODS: The 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.
RESULTS: The 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.
OBJECTIVE: The 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.
METHODS: The 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.
RESULTS: The 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.
摘要：
背景：枸杞的传统药用以提高视力为中心，以及肝脏和肾脏功能的营养。枸杞多糖(LBP),作为枸杞的主要活性成分，已被确定为这些有益效果的主要贡献者。先前的研究表明，枸杞多糖对铅引起的损伤具有肾脏保护作用，但其机制和疗效尚不清楚。
目的：本研究的目的是研究LBP预防铅肾损伤的有效性，并探讨铅肾损伤的毒性机制和LBP的疗效机制。重点关注PI3K/AKT/mTOR信号通路。
方法：通过对已建立的铅肾损伤小鼠给予阳性药物和LBP，研究LBP对铅肾损伤的作用和机制。
结果：铅致肾损伤小鼠的肾功能显著恢复，肾组织损伤和肾线粒体损伤延迟，铅引起的血液学参数紊乱得到改善，铅诱导肾指数的增加减少，LBP干预可增加铅肾损伤小鼠的体重，正如药效学实验的结果所揭示的那样。基于PI3K/AKT/mTOR信号通路,研究了铅肾损伤的毒性机制和LBP抗铅肾损伤的药效学机制。结果表明，铅可以激活TLR4受体，然后激活PI3K/AKT/mTOR信号通路，抑制肾组织细胞自噬，促进肾组织细胞凋亡,诱导肾损伤;LBP抑制TLR4受体激活,进而抑制PI3K/AKT/mTOR信号通路，增强肾组织细胞的自噬，减少肾组织的凋亡，并延缓铅引起的肾损伤。
目的：本研究的目的是研究LBP预防铅肾损伤的有效性，并探讨铅肾损伤的毒性机制和LBP的疗效机制。重点关注PI3K/AKT/mTOR信号通路。
方法：通过对已建立的铅肾损伤小鼠给予阳性药物和LBP，研究LBP对铅肾损伤的作用和机制。
结果：铅致肾损伤小鼠的肾功能显著恢复，肾组织损伤和肾线粒体损伤延迟，铅引起的血液学参数紊乱得到改善，铅诱导肾指数的增加减少，LBP干预可增加铅肾损伤小鼠的体重，正如药效学实验的结果所揭示的那样。基于PI3K/AKT/mTOR信号通路,研究了铅肾损伤的毒性机制和LBP抗铅肾损伤的药效学机制。结果表明，铅可以激活TLR4受体，然后激活PI3K/AKT/mTOR信号通路，抑制肾组织细胞自噬，促进肾组织细胞凋亡,诱导肾损伤;LBP抑制TLR4受体激活,进而抑制PI3K/AKT/mTOR信号通路，增强肾组织细胞的自噬，减少肾组织的凋亡，并延缓铅引起的肾损伤。
