Mogroside III-E

Mogroside III-E is a cucurbitane-type triterpenoid glycoside extracted from Siraitia grosvenorii, and it is an orally active TLR4 inhibitor. Mogroside III-E downregulates the expression of TLR4 and MyD88, and blocks the phosphorylation of downstream ERK, JNK and p38 MAPK molecules; meanwhile, it inhibits TGF-β- or LPS-mediated transdifferentiation of primary pulmonary fibroblasts into myofibroblasts, reduces the content of fibrosis markers such as hydroxyproline, suppresses the pro-fibrotic TGF-β/Smad signaling pathway, and downregulates the levels of inflammatory factors MPO and IL-1β. Mogroside III-E alleviates Bleomycin (HY-108345)-induced pulmonary collagen deposition and inflammatory infiltration in mice. Mogroside III-E can be used in studies related to idiopathic pulmonary fibrosis^[1][2]. In Vitro:Mogroside III-E (1% (w/v); 4-7 days) is produced by Saccharomyces cerevisiae las21Δ mutant which completely converts mogroside V to mogroside III-E, resulting in 100% relative abundance of mogroside III-E after 7 days of fermentation^[1].
Mogroside III-E (MGIIIE) (3.125-50 μM; 24 h) potently inhibits LPS-induced NO release in RAW264.7 cells with an IC₅₀ of 10.22 μM, exhibiting stronger anti-inflammatory activity than other tested mogrosides^[2].
Mogroside III-E (10 μM; 48 h) inhibits TGF-β1-induced fibroblast activation, extracellular matrix deposition, and TLR4/MyD88-MAPK signaling in primary mouse lung fibroblasts, with no observed cytotoxicity at concentrations up to 100 μM^[2].
Mogroside III-E (10 μM; 48 h) inhibits LPS-induced fibroblast activation and collagen production in primary mouse lung fibroblasts, likely acting primarily through the TLR4 signaling pathway^[2]. In Vivo:Mogroside III-E (MGIIIE) (1-20 mg/kg; p.o.; daily; 14 days) potently attenuates Bleomycin (HY-108345)-induced pulmonary fibrosis in mice by inhibiting lung inflammation, extracellular matrix deposition, and activation of the TGF-β/Smad2/3 and TLR4/MyD88-MAPK signaling pathways^[2].