Description: |
Sclareol possesses anti-cancer, anti-osteoarthritic, immune-regulation and anti-inflammatory activities, it inhibits the MMPs, iNOS and COX-2 expression on mRNA and protein levels, while increases the TIMP-1 expression, and over-production of NO and PGE2 is also suppressed by Sclareol ameliorated cartilage degradation. Sclareol induces plant resistance to root-knot nematode partially through ethylene-dependent enhancement of lignin accumulation. |
In vitro: |
Mol Med Rep. 2015 Jun;11(6):4273-8. | Sclareol, a plant diterpene, exhibits potent antiproliferative effects via the induction of apoptosis and mitochondrial membrane potential loss in osteosarcoma cancer cells.[Pubmed: 25672419] | The objective of the current study was to evaluate the antiproliferative activity of Sclareol against MG63 osteosarcoma cells. A 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay was used to evaluate the cell viability of cells following treatment with Sclareol. METHODS AND RESULTS: The extent of cell death induced by Sclareol was evaluated using a lactate dehydrogenase (LDH) assay. The effect of Sclareol on cell cycle progression and mitochondrial membrane potential (ΛΨm) was evaluated with flow cytometry using the DNA‑binding fluorescent dyes propidium iodide and rhodamine‑123, respectively. Fluorescence microscopy was used to detect the morphological changes in the MG63 osteosarcoma cancer cells and the appearance of apoptotic bodies following Sclareol treatment. The results revealed that Sclareol induced dose‑ and time‑dependent growth inhibition of MG63 cancer cells with an IC50 value of 65.2 µM following a 12‑h incubation. Furthermore, Sclareol induced a significant increase in the release of LDH from MG63 cell cultures, which was much more pronounced at higher doses. Fluorescence microscopy revealed that Sclareol induced characteristic morphological features of apoptosis and the appearance of apoptotic bodies. Flow cytometry revealed that Sclareol induced G1‑phase cell cycle arrest, which showed significant dose‑dependence. Additionally, Sclareol induced a progressive and dose‑dependent reduction in the ΛΨm. CONCLUSIONS: In summary, Sclareol inhibits the growth of osteosarcoma cancer cells via the induction of apoptosis, which is accompanied by G1‑phase cell cycle arrest and loss of ΛΨm. | Mol Plant Microbe Interact. 2015 Apr;28(4):398-407. | Sclareol induces plant resistance to root-knot nematode partially through ethylene-dependent enhancement of lignin accumulation.[Pubmed: 25423264] | The root-knot nematode (RKN) is one of the most devastating parasitic nematodes of plants. Although some secondary metabolites released by the host plant play roles as defense substances against parasitic nematodes, the mechanism underlying the induction of such defense responses is not fully understood. METHODS AND RESULTS: We found that Sclareol, a natural diterpene known as an antimicrobial and defense-related molecule, inhibited RKN penetration of tomato and Arabidopsis roots. Sclareol induced genes related to ethylene (ET) biosynthesis and signaling and phenylpropanoid metabolism in Arabidopsis roots. In roots of ein2-1, an ET-insensitive mutant line, both Sclareol-induced inhibition of RKN penetration and Sclareol-induced enhancement of lignin accumulation were abolished. A mutant defective in lignin accumulation did not exhibit such inhibition. Sclareol also activated MPK3 and MPK6, Arabidopsis mitogen-activated protein kinases whose activation is required for triggering ET biosynthesis. Sclareol-induced inhibition of RKN penetration was exhibited by mutants of neither MPK3 nor MPK6. Treatment with a biosynthetic precursor of ET was insufficient compared with Sclareol treatment to inhibit RKN penetration, suggesting the existence of an ET-independent signaling pathway leading to RKN resistance. CONCLUSIONS: These results suggested that Sclareol induced resistance to RKN penetration partially through ET-dependent accumulation of lignin in roots. |
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