Institute of Modern Physics, Chinese Academy of Sciences, No. 509 Nanchang Road, Lanzhou 730000, China.
University of Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, China.
Anal Cell Pathol (Amst). 2022 Jan 29;2022:7847135. doi: 10.1155/2022/7847135. eCollection 2022.
polysaccharide (LBP) as one of the main bioactive constituents of the fruit of L. (L.) has many pharmacological activities, but its antihyperglycemic activity is not fully understood yet. This study investigated the hypoglycemic and renal protective effects of LBP on high-fat diet/streptozotocin- (HFD/STZ-) induced diabetic nephropathy (DN) in mice. Blood glucose was assessed before and after 8-week administration of LBP, and the homeostasis model assessment-insulin resistance (HOMA-IR) index was calculated for evaluating the antidiabetic effect of LBP. Additionally, serum creatinine (sCr), blood urea nitrogen (BUN), and urine microalbumin were tested to evaluate the renal function. HE and PAS stainings were performed to evaluate the morphology and injury of the kidney. The results showed that LBP significantly reduces the glucose level and ameliorates the insulin resistance of diabetic mice. Importantly, LBP improves renal function by lowering the levels of sCr, BUN, and microalbumin in diabetic mice and relieves the injury in the renal glomeruli and tubules of the DN mice. Furthermore, LBP attenuates renal inflammation as evidenced by downregulating the mRNA levels of , , , and in the renal cortex, as well as reducing the elevated circulating level and protein depositions of SAA3 in the kidney. In addition, our western blot results showed that NF-B p65 nuclear translocation and the degradation of inhibitory B- (IB) occurred during the progress of inflammation, and such activated signaling was restrained by LBP. In conclusion, our findings suggest that LBP is a potential antidiabetic agent, which ameliorates the inflammation in DN through inhibiting NF-B activation.
多糖(LBP)作为 (L.)果实的主要生物活性成分之一,具有多种药理活性,但它的降血糖活性尚未完全了解。本研究探讨了 LBP 对高脂肪饮食/链脲佐菌素(HFD/STZ-)诱导的糖尿病肾病(DN)小鼠的降血糖和肾脏保护作用。在给予 LBP 前和 8 周后评估血糖,并计算稳态模型评估-胰岛素抵抗(HOMA-IR)指数,以评估 LBP 的抗糖尿病作用。此外,还检测了血清肌酐(sCr)、血尿素氮(BUN)和尿微量白蛋白,以评估肾功能。进行 HE 和 PAS 染色以评估肾脏的形态和损伤。结果表明,LBP 可显著降低糖尿病小鼠的血糖水平并改善胰岛素抵抗。重要的是,LBP 通过降低糖尿病小鼠 sCr、BUN 和微量白蛋白水平改善肾功能,并缓解 DN 小鼠肾小球和肾小管的损伤。此外,LBP 通过下调肾皮质中 、 、 和 的 mRNA 水平以及降低肾脏中 SAA3 的循环水平和蛋白沉积来减轻肾脏炎症。此外,我们的 Western blot 结果表明,在炎症进展过程中,NF-B p65 核易位和抑制 B-(IB)的降解发生,而这种激活的信号被 LBP 抑制。总之,我们的研究结果表明,LBP 是一种潜在的抗糖尿病药物,通过抑制 NF-B 激活改善 DN 中的炎症。