Rhapontin

Rhapontin (Rhaponiticin) is an orally aactive SIRT1 agonist and AMPK activator with anti-inflammatory and anti-fibrotic activities. Rhapontin inhibits NLRP3 inflammasome activation by activating SIRT1 and inhibits TGF-β/Smad signaling via the AMPK pathway. Rhapontin reduces intestinal and lung inflammation, inhibits fibroblast differentiation and extracellular matrix deposition, and enhances tight junction protein expression to repair epithelial barriers. Rhapontin can be used in the study of inflammatory bowel diseases (such as ulcerative colitis) and pulmonary fibrosis^[1][2][3]. In Vitro:Rhapontin (0.4-20 μM; 24 h) inhibits NLRP3 inflammasome activation, reduces IL-1β secretion, and reverses the activation of NF-κB and MAPK signaling pathways by upregulating SIRT1 expression in LPS-stimulated THP-1 macrophages^[1].
Rhapontin (0.4-10 μM; 24 h) inhibits NLRP3 inflammasome activation, reduces IL-1β secretion, and reverses the activation of NF-κB and MAPK signaling pathways by upregulating SIRT1 expression in LPS-stimulated THP-1 macrophages^[1].
Rhapontin (5-10 μM; 24 h) increases the expression of tight junction proteins ZO-1 and occludin, reduces the Bcl-2/Bax apoptotic protein ratio, and restores epithelial barrier function in NCM460 colon epithelial cells stimulated with TNF-α (10 ng/mL; 6 h)^[1].
In Vivo:Rhapontin (100 mg/kg; gavage; once a day; 8 days) significantly reduces colon pathological damage in the DSS (HY-116282C)-induced acute colitis model in mice, inhibits inflammatory cell infiltration, MPO activity and NLRP3 inflammasome activation, and upregulates tight junction proteins ZO-1 and occludin to repair the epithelial barrier^[1].
Rhapontin (25-100 mg/kg; gavage; once a day; 14 days) significantly reduces lung tissue collagen deposition, inhibits TGF-β/Smad signaling pathway, activates AMPK and downregulates Lox2 and HIF-1α expression, and improves lung function^[2] in the Bleomycin (HY-108345)-induced pulmonary fibrosis model in mice^[1].