Butyric acid inhibits oxidative stress and inflammation injury in calcium oxalate nephrolithiasis by targeting CYP2C9

Zhou, Zijian; Zhou, Xuan; Zhang, Yu; Yang, Yuanyuan; Wang, Lujia; Wu, Zhenlong

doi:10.1016/j.fct.2023.113925

Cited by 7 publications

(5 citation statements)

References 53 publications

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“…All the initial HK-2 cells were seeded equally in each case after counting with trypan blue. Since the effect of 1 mM oxalate on HK-2 cells for 24h was the most significant, we chose 1 mM concentration to carry out the follow-up experiments [ 18 , 19 ], while a subset of HK-2 cells, designated as the Fer-1 group, received a 2-hour pretreatment with Fer-1 (2 μM). After accurately calculating the number of cells with trypan blue, 3 × 10 3 HK-2 cells from different groups were seeded in a 96-well plate.…”

Section: Methodsmentioning

confidence: 99%

“…The structure of LAMP2 (PDB ID: 2MOF) and MDM4 (PDB ID: 3FDO) was obtained from the Protein Data Bank (PDB, https://www.rcsb.org/ ), while the structure of Fer-1 (PubChem CID: 4068248) was achieved from PubChem database ( https://pubchem.ncbi.nlm.nih.gov/ ). Molecular docking was carried out using AutoDock Vina (version 1.1.2) for all calculations in this project as described in our previous study [ 18 ].…”

Section: Methodsmentioning

confidence: 99%

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Identification and validation of the biomarkers related to ferroptosis in calcium oxalate nephrolithiasis

Hou,

Zhong,

et al. 2024

Aging

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Ferroptosis is a specific type of programmed cell death characterized by iron-dependent lipid peroxidation. Understanding the involvement of ferroptosis in calcium oxalate (CaOx) stone formation may reveal potential targets for this condition. The publicly available dataset GSE73680 was used to identify 61 differentially expressed ferroptosis-related genes (DEFERGs) between normal kidney tissues and Randall's plaques (RPs) from patients with nephrolithiasis through employing weighted gene co-expression network analysis (WGCNA). The findings were validated through in vitro and in vivo experiments using CaOx nephrolithiasis rat models induced by 1% ethylene glycol administration and HK-2 cell models treated with 1 mM oxalate. Through WGCNA and the machine learning algorithm, we identified LAMP2 and MDM4 as the hub DEFERGs. Subsequently, nephrolithiasis samples were classified into cluster 1 and cluster 2 based on the expression of the hub DEFERGs. Validation experiments demonstrated decreased expression of LAMP2 and MDM4 in CaOx nephrolithiasis animal models and cells. Treatment with ferrostatin-1 (Fer-1), a ferroptosis inhibitor, partially reversed oxidative stress and lipid peroxidation in CaOx nephrolithiasis models. Moreover, Fer-1 also reversed the expression changes of LAMP2 and MDM4 in CaOx nephrolithiasis models. Our findings suggest that ferroptosis may be involved in the formation of CaOx kidney stones through the regulation of LAMP2 and MDM4.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Identification and validation of the biomarkers related to ferroptosis in calcium oxalate nephrolithiasis

Hou,

Zhong,

et al. 2024

Aging

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“…Various compounds have been effective in mitigating the inflammatory damage to TECs and kidneys caused by CaOx crystals. [55][56][57][58] For example, sulforaphane reduces CaOx nephrocalcinosis-induced inflammation in TECs by enhancing the nuclear factor erythroid 2-related factor 2-microRNA-93toll-like receptor 4-interferon regulatory factor 1 (Nrf2-miR-93-TLR4/IRF1) pathway, thereby resulting in decreased TECs injury and inflammation both in vitro and in vivo. [59] Sirtuin1 also plays a crucial role by inhibiting TLR4 signaling and M1 macrophage polarization, thereby reducing inflammation and oxidative damage to TECs and diminishing CaOx crystal deposition and renal inflammation.…”

Section: Inhibiting Oxidative Damagementioning

confidence: 99%

“…Several ingredients-such as Compound 42, Vitexin, and Ferrostatin-1 [55,56,[60][61][62] -have been identified as potential inhibitors of stone formation, acting by suppressing apoptosis and autophagy in renal TECs. FK506 binding protein 5 (FKBP5) deficiency has shown efficacy in mitigating kidney injury and stone aggregation in CaOx kidney stones, primarily by reducing cell-crystal adhesion and apoptosis, boosting cell proliferation, and inhibiting M1 macrophage polarization and chemotaxis via the NF-κB signaling pathway.…”

Section: Inhibiting Oxidative Damagementioning

confidence: 99%

Exploring the Interplay between Calcium Oxalate Crystals and Renal Tubular Epithelial Cell Injury: Implications for the Formation and Prevention of Kidney Stones

Zhao,

Yang,

Yang

et al. 2024

Integr Med Nephrol Androl

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Kidney stones are a prevalent and clinically significant disease that affects millions of individuals worldwide, which have emerged as a significant global public health concern. The majority of kidney stones are composed of calcium oxalate (CaOx). The mechanisms of stone formation and development are unclear, involving a complex interplay of physical and biochemical processes. The injury of tubular epithelial cells (TECs) represents a pivotal event in the pathogenesis of this condition, as it initiates oxidative stress and immune-inflammatory reactions. Macrophages play a pivotal role in the inflammatory process, interacting with a multitude of molecules and pathways, thereby influencing the stone formation. Furthermore, apoptosis and autophagy induce TECs injury and contribute to the pathogenesis of CaOx stones. The current treatment strategies mainly focus on the management of crystal-cell interactions and the protection of TECs, in conjunction with the application of antioxidants, anti-inflammatory agents, and inhibitors of apoptosis and autophagy. These strategies have demonstrated promising results. Future research will aim to modulate the immune-inflammatory response, offering hope for the effective prevention of stone recurrence.

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“…Enhancer of zeste homolog 2 (EZH2) inhibition can restore cell viability, inhibit lactate dehydrogenase release and intracellular ROS production via the regulation of the JNK/FOXO3a pathway, and significantly reduce renal CaOx crystal deposition and oxidative and inflammatory damage induced by hyperoxaluria in vivo ( 62 ). Sodium butyrate may partially reverse the oxidative stress, inflammation and apoptosis induced by CaOx crystallization or nephrolithiasis by inhibiting CYP2C9 ( 63 ). FKBP prolyl isomerase 5, regarded as a predictor of kidney damage, promotes cell-crystal adhesion, apoptosis, stone aggregation and kidney injury in cells and mice ( 64 ).…”

Section: The Various Forms Of Cell Death and Urolithiasismentioning

confidence: 99%

Cell death‑related molecules and targets in the progression of urolithiasis (Review)

Wu,

Xue,

et al. 2024

Int J Mol Med

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Urolithiasis is a high-incidence disease caused by calcium oxalate (mainly), uric acid, calcium phosphate, struvite, apatite, cystine and other stones. The development of kidney stones is closely related to renal tubule cell damage and crystal adhesion and aggregation. Cell death, comprising the core steps of cell damage, can be classified into various types (i.e., apoptosis, ferroptosis, necroptosis and pyroptosis). Different crystal types, concentrations, morphologies and sizes cause tubular cell damage via the regulation of different forms of cell death. Oxidative stress caused by high oxalate or crystal concentrations is considered to be a precursor to a variety of types of cell death. In addition, complex crosstalk exists among numerous signaling pathways and their key molecules in various types of cell death. Urolithiasis is considered a metabolic disorder, and tricarboxylic acid cycle-related molecules, such as citrate and succinate, are closely related to cell death and the inhibition of stone development. However, a literature review of the associations between kidney stone development, metabolism and various types of cell death is currently lacking, at least to the best of our knowledge. Thus, the present review summarizes the major advances in the understanding of regulated cell death and urolithiasis progression.

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Butyric acid inhibits oxidative stress and inflammation injury in calcium oxalate nephrolithiasis by targeting CYP2C9

Cited by 7 publications

References 53 publications

Identification and validation of the biomarkers related to ferroptosis in calcium oxalate nephrolithiasis

Identification and validation of the biomarkers related to ferroptosis in calcium oxalate nephrolithiasis

Exploring the Interplay between Calcium Oxalate Crystals and Renal Tubular Epithelial Cell Injury: Implications for the Formation and Prevention of Kidney Stones

Cell death‑related molecules and targets in the progression of urolithiasis (Review)

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