ArticleBMC complementary medicine and therapies2022
Simiao pill inhibits epithelial mesenchymal transition in a mouse model of chronic hyperuricemic nephropathy by inhibiting NLRP3 inflammasome activation.
Article in BMC complementary medicine and therapies, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Phytochemical compounds for treating hyperuricemia associated with gout: a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Pooled it
- Therapeutic potential of traditional Chinese medicine for hyperuricemia: mechanistic insights and clinical prospects.Frontiers in pharmacology · 2026Review
- Yipishen Xiezhuo Jiedu Decoction in Ameliorating Kidney Damage Through miR-223/NLRP3/ Caspase-1 PathwayEndocrine, metabolic & immune disorders drug targets · 2026Article
- Mechanisms of NLRP3 inflammasome in chronic kidney disease and the effects of traditional Chinese medicines.Renal failure · 2025Review
- Therapeutic potential and pharmacological mechanisms of Traditional Chinese Medicine in gout treatment.Acta pharmacologica Sinica · 2025Review
- Gut microbiota mediated the therapeutic efficiency of Simiao decoction in the treatment of gout arthritis mice.BMC complementary medicine and therapies · 2023Article
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7 authors at 2 institutions in 1 country.
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Abstract
backgroundSimiao pill module (SMM), a traditional Chinese medicine formula, has been widely used to treat gout and gouty arthritis. The goal of this study was to investigate the effects of SMM on epithelial-mesenchymal transition (EMT) and activation of NLR family pyrin domain containing 3 (NLRP3) inflammasome in a mouse model of potassium oxonate (PO)-induced chronic hyperuricemic nephropathy (HN).
methodsMice were randomly divided into the following four groups: control, HN model (PO), febuxostat (FEB)-treated (PO + FEB), and SMM-treated (PO + SMM) groups. Following 6 weeks of treatment, blood samples were collected and mice were sacrificed to collect kidney samples to study the biochemical parameters associated with renal function and histopathological changes associated with HN, respectively. The samples were analyzed for the expression of markers of EMT (collagen type 3, α-smooth muscle actin [α-SMA], fibronectin, vimentin and E-cadherin) and activation of NLRP3 inflammasome (NLRP3, apoptosis-associated speck-like protein [ASC], caspase-1, interleukin [IL]-1β, and IL-18).
resultsOur results showed that hyperuricemia, impaired kidney function, and renal pathological characteristics induced by PO treatment were improved following treatment with SMM and FEB. Additionally, treatment with SMM and FEB decreased the expression of vimentin, collagen 3, fibronectin, and α-SMA, and increased the expression of E-cadherin. Moreover, NLRP3 inflammasome activation, as assessed by the increased expression of NLRP3, ASC, and caspase-1, and secretion of IL-1β and IL-18, was inhibited by treatment with SMM and FEB.
conclusionThese results suggest that SMM inhibited EMT and NLRP3 inflammasome activation in chronic HN mice, and the beneficial effect of SMM was compared with a standard drug, FEB.
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