Corn Silk Polysaccharides Before and After Selenization Reduced Calcium Oxalate Crystal-Induced HK-2 Cells Pyroptosis by Inhibiting the NLRP3-GSDMD Signaling Pathway.

IF 4.2 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2025-03-12 eCollection Date: 2025-01-01 DOI:10.2147/JIR.S506093
Jin Han, Xin-Yi Tong, Yu-Yun Zheng, Jia-Hui Cheng, Jian-Ming Ouyang, Ke Li
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引用次数: 0

Abstract

Objective: Pyroptosis is a new type of programmed cell death associated with many inflammatory diseases. Polysaccharides have anti-inflammatory effects. In this study, we investigated whether corn silk polysaccharides (DCSP) before and after selenization (Se-DCSP) can reduce the renal tubule pyroptosis induced by calcium oxalate crystals.

Methods: HK-2 cells were exposed to calcium oxalate monohydrate with a size of 3 µm (COM-3μm) to establish a pyroptosis model. The degree of cell damage was determined by detecting cell viability, reactive oxygen species (ROS), and lactate dehydrogenase (LDH) content. The proportion of pyroptosis cells was quantitatively detected by Caspase-1/PI double staining. The expression levels of NLRP3, GSDMD, IL-18, and IL-1β were detected by confocal microscopy and Western blot analyses.

Results: DCSP and Se-DCSP can reduce the secretion of inflammatory factors IL-1β/18 related to pyroptosis by reducing cell damage and oxidative stress, as well as down-regulate the expression of Caspase-1, NLRP3, GSDMD, and TNF-α, repair damaged cells, and inhibit pyroptosis in HK-2 cells. The inhibitory effect of selenized polysaccharide was significantly enhanced compared with that before selenification.

Conclusion: Se-DCSP can inhibit pyroptosis through the NLRP3/Caspase-1/GSDMD/IL-1β/IL-18 signaling pathway to reduce the risk of kidney-stone formation.

硒化前后玉米丝多糖通过抑制NLRP3-GSDMD信号通路降低草酸钙晶体诱导的HK-2细胞焦亡
目的:焦亡是一种与多种炎性疾病相关的新型程序性细胞死亡。多糖有抗炎作用。本研究研究了硒化前后玉米丝多糖(Se-DCSP)是否能减轻草酸钙晶体引起的肾小管焦亡。方法:将HK-2细胞暴露于尺寸为3µm (COM-3μm)的一水草酸钙中,建立细胞焦亡模型。通过检测细胞活力、活性氧(ROS)和乳酸脱氢酶(LDH)含量来确定细胞损伤程度。Caspase-1/PI双染色定量检测细胞凋亡比例。用共聚焦显微镜和Western blot检测NLRP3、GSDMD、IL-18和IL-1β的表达水平。结果:DCSP和Se-DCSP可通过减轻细胞损伤和氧化应激,减少与焦亡相关的炎性因子IL-1β/18的分泌,下调Caspase-1、NLRP3、GSDMD、TNF-α的表达,修复受损细胞,抑制HK-2细胞焦亡。与硒化前相比,硒化多糖的抑制作用显著增强。结论:Se-DCSP可通过NLRP3/Caspase-1/GSDMD/IL-1β/IL-18信号通路抑制肾衰,降低肾结石形成风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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