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通过调节丝裂原活化蛋白激酶（MAPK）信号通路，研究负载二甲双胍的硒纳米颗粒与L. flower提取物联合使用对雄性Sprague Dawley大鼠肾脏草酸钙沉积的减轻作用。

Investigating the attenuating effects of metformin-loaded selenium nanoparticles coupled with L. flower extract on CaOx deposition in male Sprague Dawley rat kidneys via regulating MAPK signaling pathway.

作者信息

Kang Jian, Tong Yanqing

机构信息

School of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun 130021, China.

Department of Nephrology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun 130021, China.

出版信息

Regen Ther. 2024 May 17;26:14-26. doi: 10.1016/j.reth.2024.04.006. eCollection 2024 Jun.

DOI:10.1016/j.reth.2024.04.006
PMID:39691916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11652069/
Abstract

Kidney stones are a foremost clinical concern in urology with CaOx crystals accounting for roughly 80% of these renal formations. This research endeavor seeks to ascertain the protective effects of Metformin-encapsulated selenium nanoparticles (M@Se NPs), combined with a 55% hydroethanolic flower extract from () in countering the formation of kidney stones in Male Sprague Dawley rats. The particle's diameter was measured to be 39 nm and 13.8 nm from DLS and HR-TEM analysis. Rat groups administered with the -M@Se NPs (1:1.5:1) exhibited reduced renal stone formation in urine and serum analysis compared to the negative control group. Histological evaluations of kidney samples using H&E, and MTS staining indicated a subdued presence of ECM deposition in contrast to other rat groups. Conclusively, the protective mechanism of -M@Se NPs against CaOx stone damage can be confidently attributed to the obstruction of the MAPK signaling pathway.

摘要

肾结石是泌尿外科的一个首要临床问题，草酸钙晶体约占这些肾脏结石的80%。本研究旨在确定包裹二甲双胍的硒纳米颗粒（M@Se NPs）与来自（此处原文缺失植物名称）的55%氢乙醇花提取物联合使用对雄性Sprague Dawley大鼠肾结石形成的保护作用。通过动态光散射（DLS）和高分辨率透射电子显微镜（HR-TEM）分析测得该颗粒直径为39纳米和13.8纳米。与阴性对照组相比，给予-M@Se NPs（1:1.5:1）的大鼠组在尿液和血清分析中肾结石形成减少。使用苏木精-伊红（H&E）染色和MTS染色对肾脏样本进行组织学评估表明，与其他大鼠组相比，细胞外基质（ECM）沉积减少。总之，-M@Se NPs对草酸钙结石损伤的保护机制可以确切地归因于丝裂原活化蛋白激酶（MAPK）信号通路受阻。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/9aeffcb0d66f/gr10.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/13765454defa/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/ba2ddc572108/gr3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/3ed01746c7f1/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/ce36904fb02f/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/84c824a3849d/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/f5c14ea074df/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/9aeffcb0d66f/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/ba125399ad0d/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/2e8f209a7de6/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/13765454defa/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/ba2ddc572108/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/383eba124fb5/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/d5904ec18d3a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/3ed01746c7f1/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/ce36904fb02f/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/84c824a3849d/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/f5c14ea074df/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7670/11652069/9aeffcb0d66f/gr10.jpg

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