Hederagenin inhibits high glucose‐induced fibrosis in human renal cells by suppression of NLRP3 inflammasome activation through reducing cathepsin B expression

Yang, Guohua; Yang, Wang; Jiang, Hairong; Yi, Qing; Ma, Wei

doi:10.1111/cbdd.14332

Cited by 4 publications

(1 citation statement)

References 64 publications

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“…Using a cell model of diabetic nephropathy induced by high glucose, Yang et al discovered that HG prevented renal cell fibrosis by reducing the elevated levels of fibronectin, collagen IV, plasminogen activator inhibitor 1, and TGF-β1. The anti-renal fibrosis effect of HG was accomplished by suppressing activation of the NLRP3 inflammasome through decreasing cathepsin B expression ( Yang et al, 2023 ).…”

Section: Effects and Mechanisms Of Hg And Its Derivativesmentioning

confidence: 99%

An updated review of the pharmacological effects and potential mechanisms of hederagenin and its derivatives

Zhang,

Li,

Liu

2024

Front. Pharmacol.

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Hederagenin (HG) is a natural pentacyclic triterpenoid that can be isolated from various medicinal herbs. By modifying the structure of HG, multiple derivatives with superior biological activities and safety profiles have been designed and synthesized. Accumulating evidence has demonstrated that HG and its derivatives display multiple pharmacological activities against cancers, inflammatory diseases, infectious diseases, metabolic diseases, fibrotic diseases, cerebrovascular and neurodegenerative diseases, and depression. Previous studies have confirmed that HG and its derivatives combat cancer by exerting cytotoxicity, inhibiting proliferation, inducing apoptosis, modulating autophagy, and reversing chemotherapy resistance in cancer cells, and the action targets involved mainly include STAT3, Aurora B, KIF7, PI3K/AKT, NF-κB, Nrf2/ARE, Drp1, and P-gp. In addition, HG and its derivatives antagonize inflammation through inhibiting the production and release of pro-inflammatory cytokines and inflammatory mediators by regulating inflammation-related pathways and targets, such as NF-κB, MAPK, JAK2/STAT3, Keap1-Nrf2/HO-1, and LncRNA A33/Axin2/β-catenin. Moreover, anti-pathogen, anti-metabolic disorder, anti-fibrosis, neuroprotection, and anti-depression mechanisms of HG and its derivatives have been partially elucidated. The diverse pharmacological properties of HG and its derivatives hold significant implications for future research and development of new drugs derived from HG, which can lead to improved effectiveness and safety profiles.

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Section: Effects and Mechanisms Of Hg And Its Derivativesmentioning

confidence: 99%

An updated review of the pharmacological effects and potential mechanisms of hederagenin and its derivatives

Zhang,

Li,

Liu

2024

Front. Pharmacol.

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Hederagenol improves multiple sclerosis by modulating Th17 cell differentiation

Guan,

Li,

Zhao

et al. 2024

IUBMB Life

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Multiple sclerosis (MS) is a common autoimmune illness that is difficult to treat. The upregulation of Th17 cells is critical in the pathological process of MS. Hederagenol (Hed) has been shown to lower IL‐17 levels, although its role in MS pathophysiology is uncertain. In this study, we explore whether Hed could ameliorate MS by modulating Th17 cell differentiation, with the goal of identifying new treatment targets for MS. The experimental autoimmune encephalomyelitis (EAE) mouse model was conducted and Hed was intraperitoneally injected into mice. The weight was recorded and the clinical symptom grade was assessed. Hematoxylin‐eosin staining was carried out to determine the extent of inflammation in the spinal cord and liver. The luxol Fast Blue staining was performed to detect the pathological changes in the myelin sheath. Nerve damage was detected using NeuN immunofluorescence staining and terminal deoxynucleotidyl transferase dUTP nick‐end labeling staining. Immunohistology approaches were used to study alterations in immune cells in the spinal cord. The proportions of T cell subsets in the spleens were analyzed by flow cytometry. RORγt levels were measured using quantitative real‐time PCR or Western blot. The activity of the RORγt promoter was analyzed by Chromatin immunoprecipitation. Hed administration reduced the clinical symptom grade of EAE mice, as well as the inflammatory infiltration, demyelination, and cell disorder of the spinal cord, while having no discernible effect on the mouse weight. In addition, Hed treatment significantly reduced the number of T cells, particularly Th17 cells in the spinal cord and spleen‐isolated CD4+ T cells. Hed lowered the RORγt levels in spleens and CD4+ T cells and overexpression of RORγt reversed the inhibitory effect of Hed on Th17 differentiation. Hed decreased nerve injury by modulating Th17 differentiation through the RORγt promoter. Hed regulates Th17 differentiation by reducing RORγt promoter activity, which reduces nerve injury and alleviates EAE.

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Curcumin prevents high glucose-induced stimulatory effects of renal cell secretome on fibroblast activation via mitigating intracellular free radicals and TGF-β secretion

Noonin,

Thongboonkerd

2024

Biomedicine & Pharmacotherapy

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Hederagenin inhibits high glucose‐induced fibrosis in human renal cells by suppression of NLRP3 inflammasome activation through reducing cathepsin B expression

Cited by 4 publications

References 64 publications

An updated review of the pharmacological effects and potential mechanisms of hederagenin and its derivatives

An updated review of the pharmacological effects and potential mechanisms of hederagenin and its derivatives

Hederagenol improves multiple sclerosis by modulating Th17 cell differentiation

Curcumin prevents high glucose-induced stimulatory effects of renal cell secretome on fibroblast activation via mitigating intracellular free radicals and TGF-β secretion

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