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<i>Cutibacterium acnes</i> (formerly <i>Propionibacterium acnes</i>) is one of the major bacterial species responsible for acne vulgaris. Numerous bioactive compounds from <i>Momordica charantia</i> Linn. var. <i>abbreviata</i> Ser. have been isolated and examined for many years. In this study, we evaluated the suppressive effect of two cucurbitane-type triterpenoids, 5β,19-epoxycucurbita-6,23-dien-3β,19,25-triol (Kuguacin R; KR) and 3β,7β,25-trihydroxycucurbita-5,23-dien-19-al (TCD) on live <i>C. acnes</i>-stimulated in vitro and in vivo inflammatory responses. Using human THP-1 monocytes, KR or TCD suppressed <i>C. acnes</i>-induced production of interleukin (IL)-1β, IL-6 and IL-8 at least above 56% or 45%, as well as gene expression of these three pro-inflammatory cytokines. However, a significantly strong inhibitory effect on production and expression of tumor necrosis factor (TNF)-α was not observed. Both cucurbitanes inhibited <i>C. acne</i>s-induced activation of the myeloid differentiation primary response 88 (MyD88) (up to 62%) and mitogen-activated protein kinases (MAPK) (at least 36%). Furthermore, TCD suppressed the expression of pro-caspase-1 and cleaved caspase-1 (p10). In a separate study, KR or TCD decreased <i>C. acne</i>s-stimulated mouse ear edema by ear thickness (20% or 14%), and reduced IL-1β-expressing leukocytes and neutrophils in mouse ears. We demonstrated that KR and TCD are potential anti-inflammatory agents for modulating <i>C. acnes</i>-induced inflammation in vitro and in vivo.