Therapeutic effects of traditional Chinese medicine on gouty nephropathy: Based on NF-κB signalingpathways

Liu, Peng; Ma, Guijie; Wang, Yan; Wang, Lifan; Li, Ping

doi:10.1016/j.biopha.2022.114199

Cited by 5 publications

(3 citation statements)

References 153 publications

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“…UAN can induce kidney inflammation, the injury is in a crystal‐dependent manner (Braga et al., 2020). The inflammatory response caused by the destruction of urate crystals plays a leading role in the pathogenesis of UAN (Liu et al., 2023). Uric acid can induce kidney inflammation, which is an important clinicopathologic manifestation of UAN (Mei et al., 2022).…”

Section: Discussionmentioning

confidence: 99%

Study of hispidulin in the treatment of uric acid nephropathy based on NF‐κB signaling pathway

Li,

Gu,

Ren

et al. 2023

Chem Biol Drug Des

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Uric acid nephropathy (UAN) is caused by purine metabolism disorders. UAN rat models were established in SD rats. The modeling rats received different doses of hispidulin (10, 20, 50 mg/mL). Febuxostat was applied as the positive drug. Serum creatinine, uric acid (UA), and cystatin‐C (cys‐C), neutrophil gelatinase‐associated lipocalin (NGAL), IL‐1β, IL‐8, TNF‐α, and IL‐6 in rats were detected. HE staining was done to assess kidney injury. UAN rats possessed prominent levels of serum creatinine, UA, cys‐C, and NGAL, which all reduced after hispidulin treatment in a dose‐dependent manner. HE staining determined the improvement of kidney injury after treatment, which was comparable to the efficacy of febuxostat. Hispidulin inhibited the release of IL‐1β, IL‐8, TNF‐α, and IL‐6 in UAN rats. Hispidulin enhanced autophagy in UAN rats, presenting as ascending LC3II/I ratio and downregulated P62. The increasing trend of inflammasome‐related proteins of NLRP3 and Caspase‐1 was changeovered by hispidulin. The activation of NF‐kB signaling was intercepted by hispidulin in UAN rats. Hispidulin can effectively improve renal function injury caused by UAN in rats. The mechanism may be related to the inhibition of inflammatory response induced by autophagy and activation of NF‐κB pathway.

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Section: Discussionmentioning

confidence: 99%

Study of hispidulin in the treatment of uric acid nephropathy based on NF‐κB signaling pathway

Li,

Gu,

Ren

et al. 2023

Chem Biol Drug Des

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“…Clinical studies have shown that the increase in uric acid levels leads to the saturation of blood uric acid which results in the precipitation and deposition of urate crystals within renal tissue. This process leads to renal tubule injury, glomerulosclerosis, and renal interstitial fibrosis, culminating in gouty nephropathy ( 9 ). Long-term hyperuricemia induces blockage of renal tubules due to the deposition of urate crystals.…”

Section: Overview Of the Pathogenesis Of Gnmentioning

confidence: 99%

“…MyD88 serves as a regulator of the NF-κB signaling pathway. In the presence of abnormal uric acid metabolism, TLRs activate Iκκ by recruiting MyD88, ultimately leading to the phosphorylation of I κB and the release of NF-κB into the nucleus ( 9 ). The activation of NF-κB results in the production of a large number of pro-inflammatory mediators, including cytokines, chemokines, and adhesion factors such as IL-1β, IL-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1), etc.…”

Section: Overview Of the Pathogenesis Of Gnmentioning

confidence: 99%

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

Wang,

Zhang,

Shen

et al. 2024

Front. Med.

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Gouty nephropathy (GN) is a metabolic disease with persistently elevated blood uric acid levels. The main manifestations of GN are crystalline kidney stones, chronic interstitial nephritis, and renal fibrosis. Understanding the mechanism of the occurrence and development of GN is crucial to the development of new drugs for prevention and treatment of GN. Currently, most studies exploring the pathogenesis of GN are primarily based on animal and cell models. Numerous studies have shown that inflammation, oxidative stress, and programmed cell death mediated by uric acid and sodium urate are involved in the pathogenesis of GN. In this article, we first review the mechanisms underlying the abnormal intrinsic immune activation and programmed cell death in GN and then describe the characteristics and methods used to develop animal and cell models of GN caused by elevated uric acid and deposited sodium urate crystals. Finally, we propose potential animal models for GN caused by abnormally high uric acid levels, thereby provide a reference for further investigating the methods and mechanisms of GN and developing better prevention and treatment strategies.

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Mechanism of Cordyceps militaris in gouty nephropathy explored using network pharmacology and molecular docking technology

Zhou,

Feng,

Liang

et al. 2024

Food Bioscience

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Therapeutic effects of traditional Chinese medicine on gouty nephropathy: Based on NF-κB signalingpathways

Cited by 5 publications

References 153 publications

Study of hispidulin in the treatment of uric acid nephropathy based on NF‐κB signaling pathway

Study of hispidulin in the treatment of uric acid nephropathy based on NF‐κB signaling pathway

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

Mechanism of Cordyceps militaris in gouty nephropathy explored using network pharmacology and molecular docking technology

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