ArticlePharmaceutical biology2026
lncRNA MALAT1-mediated regulation of cholesterol-oxidative stress-iron metabolic dysregulation by paeoniflorin in osteoarthritic chondrocytes.
Article in Pharmaceutical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
contextOsteoarthritis is a chronic degenerative disease characterized by metabolic dysregulation, inflammation, and oxidative stress. MALAT1 plays a key role in OA pathogenesis. Pae exhibits anti-inflammatory activity, but its regulatory role in cholesterol-oxidative stress-iron metabolism in chondrocytes remains unclear.
objectiveTo investigate whether Pae can alleviate cholesterol-oxidative stress-iron metabolic dysregulation in OA chondrocytes MATERIALS &
methodsOA was induced in mice using a modified Hulth method, followed by intra-articular injection of MALAT1 overexpression plasmid. Cartilage morphology and the expression of MALAT1 and related genes/proteins were assessed by histology, RT-PCR, and Western blot.
resultsIn vivo In vivo, Pae improved cartilage morphology and restored the expression of key genes and proteins, whereas MALAT1 overexpression attenuated these effects. In IL-1β-treated OA chondrocytes, Pae reversed abnormal mRNA expression of MALAT1 and related genes. FISH analysis showed that Pae reduced MALAT1 fluorescence in chondrocytes. Western blot revealed that Pae significantly restored protein expression in sh-MALAT1 chondrocytes. Furthermore, flow cytometry analysis revealed that Pae intervention significantly reduced the apoptosis rate of IL-1β-induced chondrocytes from 34.57% to 27.74%. sh-MALAT1 resulted in a more pronounced reduction in chondrocyte apoptosis, with the apoptotic rate further decreasing to 13.21%. DISCUSSION AND
conclusionPaeoniflorin ameliorates cholesterol-oxidative stress-iron metabolic dysregulation in OA chondrocytes
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