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Phytochemical analysis of the rhizome extract of Curcuma ecalcarata, a hitherto uninvestigated south Western Ghats endemic species, resulted in the isolation and identification of the diaryl heptanoid trans, trans-1,7-diphenyl-5-hydroxy-4,6-heptadiene-3-one (1), steroid β-sitosterol (2), flavanone pinocembrin (4) and monoterpenoids piperitenone (3) and 8-hydroxy piperitone (5). HPTLC estimation of pinocembrin in the rhizome revealed the plant as a rich source of pinocembrin (0.37% dry wt.). The rhizome essential oil was isolated by hydrodistillation and analysed by GC-FID, GC-MS and (13)C NMR. Among the 30 constituents identified in the oil, monoterpenoids predominated (94.2%) followed by sesquiterpenoids (5.8%). The major compound consisting of 65.2% of the oil was isolated and identified as piperitenone (3). The study highlights the plant as a rich source of the flavanone pinocembrin and the volatile aroma compound piperitenone.

Purpose: Deoxyelephantopin (ESD) and isodeoxyelephantopin (ESI) are two sesquiterpene lactones derived from the medicinal plant Elephantopus scaber Linn. (Asteraceae). Although they are used for the treatment of a wide variety of proinflammatory diseases, very little is known about their mechanism of action. Because most genes that control inflammation are regulated by activation of the transcription factor nuclear factor-kappaB (NF-kappaB), we postulated that ESD and ESI mediate their activities through modulation of the NF-kappaB activation pathway., Experimental Design: We investigated the effect of ESI and ESD on NF-kappaB activation by electrophoretic mobility shift assay and NF-kappaB-regulated gene expression by Western blot analysis., Results: We found that ESI suppressed NF-kappaB activation induced by a wide variety of inflammatory agents, including tumor necrosis factor (TNF), interleukin-1beta, phorbol 12-myristate 13-acetate, and lipopolysaccharide. The suppression was not cell type specific, and both inducible and constitutive NF-kappaB activation was blocked. ESI did not interfere with the binding of NF-kappaB to DNA but rather inhibited IkappaBalpha kinase, IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 phosphorylation, and subsequent p65 nuclear translocation. ESI also suppressed the expression of TNF-induced NF-kappaB-regulated, proliferative, antiapoptotic, and metastatic gene products. These effects correlated with enhancement of apoptosis induced by TNF and suppression of TNF-induced invasion and receptor activator of NF-kappaB ligand-induced osteoclastogenesis., Conclusion: Our results indicate that ESI inhibits NF-kappaB activation and NF-kappaB-regulated gene expression, which may explain the ability of ESI to enhance apoptosis and inhibit invasion and osteoclastogenesis.