Astragaloside IV alleviates oxidative stress‑related damage via inhibiting NLRP3 inflammasome in a MAPK signaling dependent pathway in human lens epithelial cells

Xiao, Xili; Zheng, Yanlin; Mo, Ya; Wang, Wanjie; Li, Xiang; Wang, Juan

doi:10.1002/ddr.21929

Cited by 4 publications

(3 citation statements)

References 27 publications

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“…Conversely, Sanguinarine was reported to upregulate JNK and p38 signaling leading to increased lens epithelial cell apoptosis [205]. Recently, two further in vitro studies reported an amelioration of oxidative stress-related damage by MAPK suppression through regulation of the NLRP3 inflammasome [206] or through as of yet unelucidated functions of the flavonoid Diosmetin from chrysanthemum, that is used in traditional Chinese medicine [207]. Another recent study has similarly reported corroborating results, with p38 and ERK phosphorylation downregulation also being associated with decreased apoptosis via another proxy (TRIM22) [208].…”

Section: Mapk In Other Ocular Pathophysiologiesmentioning

confidence: 99%

MAPK Pathways in Ocular Pathophysiology: Potential Therapeutic Drugs and Challenges

Moustardas

Aberdam

Lagali

2023

Cells

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Mitogen-activated protein kinase (MAPK) pathways represent ubiquitous cellular signal transduction pathways that regulate all aspects of life and are frequently altered in disease. Once activated through phosphorylation, these MAPKs in turn phosphorylate and activate transcription factors present either in the cytoplasm or in the nucleus, leading to the expression of target genes and, as a consequence, they elicit various biological responses. The aim of this work is to provide a comprehensive review focusing on the roles of MAPK signaling pathways in ocular pathophysiology and the potential to influence these for the treatment of eye diseases. We summarize the current knowledge of identified MAPK-targeting compounds in the context of ocular diseases such as macular degeneration, cataract, glaucoma and keratopathy, but also in rare ocular diseases where the cell differentiation, proliferation or migration are defective. Potential therapeutic interventions are also discussed. Additionally, we discuss challenges in overcoming the reported eye toxicity of some MAPK inhibitors.

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Section: Mapk In Other Ocular Pathophysiologiesmentioning

confidence: 99%

MAPK Pathways in Ocular Pathophysiology: Potential Therapeutic Drugs and Challenges

Moustardas

Aberdam

Lagali

2023

Cells

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“…Astragaloside IV (AST, Figure 1A), a cycloartane-type triterpene glycoside chemical, is one of the major compounds extracted from Astragalus membranaceus (Zhang et al, 2020). In LECs, AST could ameliorate oxidative stress-induced damage through the inhibition of NLRP3 inflammasomes via regulating MAPK signaling pathway (Xiao et al, 2022). It is revealed that AST alleviates TGF-β-induced cardiac fibrosis, pulmonary fibrosis, hepatic fibrosis and renal fibrosis (Du et al, 2018;Qian et al, 2018;Singh et al, 2021;Wei et al, 2020), indicating the anti-fibrosis effects of AST.…”

Section: Astragaloside IV Inhibits the Growth Of Lens Epithelial Cellsmentioning

confidence: 99%

Astragaloside IV inhibits the proliferation and migration of lens epithelial cells induced by TGF-β through the Jagged-1/Notch pathway

Zhou

Zhong²,

Lv³

2023

Qual. Assur. Saf. Crops Foods

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Aberrant proliferation and migration of residual lens epithelial cells (LECs) is the main cause of posterior capsule opacification (PCO) after cataract surgery. The purpose of this study was to confirm the protective effects of Astragaloside IV (AST) in transforming growth factor beta (TGF-β)-induced proliferation and migration of LECs. Human LECs, SRA01/04, were used in this study. MTT assay and EdU assay were used to perform cell viability and proliferation, respectively. The cell cycle was determined using flow cytometry. Cell invasion and migration were determined using transwell assay and wound healing assay, respectively. Protein expression was examined using western blotting. Type I and IV collagen (Col I and IV) and fibronectin (FN) in cells were also detected using immunofluorescence (IF). Cell viability, proliferation, migration and invasion were suppressed by AST in a concentration-dependent manner in TGF-β-treated LECs. AST stopped the cell cycle at G2 phase in a concentration-dependent manner. Expression of Cyclin B1 and CDK1 was suppressed by AST in TGF-β-treated LECs. Protein expression of FN, Col I, Col IV, α-SMA (α-smooth muscle actin), Snail and Slug was downregulated by AST in a concentration-dependent manner. AST inhibited the protein expression of Jagged-1, Notch1, Notch2, Notch3, Hes-1 and Hey-1. Taken together, data from this study demonstrated that AST inhibited LEC viability, proliferation, migration and invasion, as well as fibroblastic differentiation and epithelial-mesenchymal transition process through inhibition of Jagged-1/Notch pathway, providing a potential supplemental treatment for PCO.

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“…Astragaloside IV (AS-IV) is a saponin derived from a commonly used Chinese herb, Astragalus membranaceus Bge. AS-IV is known to possess a wide range of pharmacological activities, including, cardioprotective [7][8][9], anti-inflammatory [10,11], anti-oxidant [12][13][14], and anti-cancer properties [15][16][17]. Moreover, AS-IV is well established as a promoter of osteogenesis [18][19][20][21], and inhibitor of osteoclastogenesis [22].…”

Section: Introductionmentioning

confidence: 99%

Astragaloside IV attenuates glucocorticoid-induced osteoclastogenesis and bone loss via the MAPK/NF-κB pathway

Guo,

Li,

Yang

et al. 2023

Preprint

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Background Astragaloside IV (AS-IV) is a bioactive saponin extracted from astragalus membranaceus, and it is reported to promote osteoblast differentiation while inhibiting osteoclastogenesis. However, the mechanism of AS-IV in glucocorticoid-induced osteoclastogenesis (GIO) remains undetermined. Herein, we examined the influence of AS-IV on GIO and bone loss. Methods RAW264.7 cells were incubated with dexamethasone (Dex) alone or Dex and receptor activator of nuclear factor-B ligand (RANKL) (Dex and RANKL) for 2 days, and then treated with Dex or Dex and RANKL through AS-IV for the timeframes indicated. Following, mice were intraperitoneally administered with an intermediate-acting glucocorticoid, methylprednisolone (MP), or MP and AS-IV for 6 weeks. Results AS-IV significantly decreased Dex-induced osteoclast nucleus and area, however, it did not impact the number of Dex-induced osteoclasts in RAW264.7 cells. AS-IV also significantly decreased the osteoclastic marker protein expressions in Dex-induced RAW264.7 cells with concentration of dose dependent fashion. Additionally, AS-IV promoted p38 phosphorylation (p-) and p-p65 translocation to the nucleus, while inhibiting phosphorylation of extracellular signal-regulated kinase (ERK) (p-ERK) and inhibitor of Nuclear factor κB (NF-κB) (p-IκB) levels. However, the AS-IV-mediated action on p-MAPK, p-NF-κB, and osteoclastic marker expressions were reversed by MAPK or IκB inhibitor in Dex-induced RAW264.7 cells. Furthermore, our in vivo evaluation revealed that AS-IV also attenuated the MP-mediated bone loss, and suppressed osteoclastogenesis. Conclusions This study demonstrates that AS-IV inhibits GIO and attenuates bone loss via the MAPK/NF-κB pathway. This also suggested that AS-IV could be a potential promising therapeutic agent for glucocorticoid-triggered bone loss.

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Astragaloside IV alleviates oxidative stress‑related damage via inhibiting NLRP3 inflammasome in a MAPK signaling dependent pathway in human lens epithelial cells

Cited by 4 publications

References 27 publications

MAPK Pathways in Ocular Pathophysiology: Potential Therapeutic Drugs and Challenges

MAPK Pathways in Ocular Pathophysiology: Potential Therapeutic Drugs and Challenges

Astragaloside IV inhibits the proliferation and migration of lens epithelial cells induced by TGF-β through the Jagged-1/Notch pathway

Astragaloside IV attenuates glucocorticoid-induced osteoclastogenesis and bone loss via the MAPK/NF-κB pathway

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