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HydroZitLa 抑制肾结石大鼠的草酸钙结石形成，并延长线虫秀丽隐杆线虫的寿命。

HydroZitLa inhibits calcium oxalate stone formation in nephrolithic rats and promotes longevity in nematode Caenorhabditis elegans.

机构信息

Departments of Biochemistry, Faculty of Medicine, Chulalongkorn University, Rama IV Rd, Bangkok, 10330, Thailand.

Department of Food Technology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand.

出版信息

Sci Rep. 2022 Mar 24;12(1):5102. doi: 10.1038/s41598-022-08316-8.

DOI:10.1038/s41598-022-08316-8
PMID:35332173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8948263/
Abstract

Low fluid intake, low urinary citrate excretion, and high oxidative stress are main causative factors of calcium oxalate (CaOx) nephrolithiasis. HydroZitLa contains citrate and natural antioxidants and is developed to correct these three factors simultaneously. Antioxidants theoretically can prolong the lifespan of organisms. In this study, we preclinically investigated the antilithogenic, lifespan-extending and anti-aging effects of HydroZitLa in HK-2 cells, male Wistar rats, and Caenorhabditis elegans. HydroZitLa significantly inhibited CaOx crystal aggregation in vitro and reduced oxidative stress in HK-2 cells challenged with lithogenic factors. For experimental nephrolithiasis, rats were divided into four groups: ethylene glycol (EG), EG + HydroZitLa, EG + Uralyt-U, and untreated control. CaOx deposits in kidneys of EG + HydroZitLa and EG + Uralyt-U rats were significantly lower than those of EG rats. Intrarenal expression of 4-hydroxynonenal in EG + HydroZitLa rats was significantly lower than that of EG rats. The urinary oxalate levels of EG + HydroZitLa and EG + Uralyt-U rats were significantly lower than those of EG rats. The urinary citrate levels of EG + HydroZitLa and EG + Uralyt-U rats were restored to the level in normal control rats. In C. elegans, HydroZitLa supplementation significantly extended the median lifespan of nematodes up to 34% without altering feeding ability. Lipofuscin accumulation in HydroZitLa-supplemented nematodes was significantly lower than that of non-supplemented control. Additionally, HydroZitLa inhibited telomere shortening, p16 upregulation, and premature senescence in HK-2 cells exposed to lithogenic stressors. Conclusions, HydroZitLa inhibited oxidative stress and CaOx formation both in vitro and in vivo. HydroZitLa extended the lifespan and delayed the onset of aging in C. elegans and human kidney cells. This preclinical evidence suggests that HydroZitLa is beneficial for inhibiting CaOx stone formation, promoting longevity, and slowing down aging.

摘要

低液体摄入、低尿枸橼酸排泄和高氧化应激是草酸钙（CaOx）肾结石形成的主要原因。HydroZitLa 含有枸橼酸和天然抗氧化剂，旨在同时纠正这三个因素。抗氧化剂理论上可以延长生物体的寿命。在这项研究中，我们在 HK-2 细胞、雄性 Wistar 大鼠和秀丽隐杆线虫中对 HydroZitLa 的抗结石、延长寿命和抗衰老作用进行了临床前研究。HydroZitLa 显著抑制了体外 CaOx 晶体聚集，并减轻了致石因子刺激的 HK-2 细胞的氧化应激。对于实验性肾结石，大鼠分为四组：乙二醇（EG）、EG+HydroZitLa、EG+Uralyt-U 和未处理的对照组。EG+HydroZitLa 和 EG+Uralyt-U 大鼠肾脏中的 CaOx 沉积明显低于 EG 大鼠。EG+HydroZitLa 大鼠肾内 4-羟壬烯醛的表达明显低于 EG 大鼠。EG+HydroZitLa 和 EG+Uralyt-U 大鼠的尿草酸盐水平明显低于 EG 大鼠。EG+HydroZitLa 和 EG+Uralyt-U 大鼠的尿枸橼酸盐水平恢复到正常对照组大鼠的水平。在秀丽隐杆线虫中，HydroZitLa 补充剂可显著延长线虫的中位寿命，最长可达 34%，而不影响摄食能力。HydroZitLa 补充剂线虫中的脂褐素积累明显低于未补充的对照组。此外，HydroZitLa 抑制了暴露于致石应激物的 HK-2 细胞中端粒缩短、p16 上调和过早衰老。结论，HydroZitLa 抑制了体外和体内的氧化应激和 CaOx 形成。HydroZitLa 延长了秀丽隐杆线虫和人肾细胞的寿命并延缓了衰老的发生。这些临床前证据表明，HydroZitLa 有利于抑制 CaOx 结石形成、促进长寿和减缓衰老。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/17de8008f03e/41598_2022_8316_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/a41c25843c15/41598_2022_8316_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/33738cc2163e/41598_2022_8316_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/96b492d4c2bf/41598_2022_8316_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/17de8008f03e/41598_2022_8316_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/a41c25843c15/41598_2022_8316_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/33738cc2163e/41598_2022_8316_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/43de83612837/41598_2022_8316_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/1b657a1c0343/41598_2022_8316_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/96b492d4c2bf/41598_2022_8316_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c74c/8948263/17de8008f03e/41598_2022_8316_Fig6_HTML.jpg

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