| Description: |
Cedrol shows antifungal activity against the fungus Botrytis cinerea , it has the potential of becoming a new hair growth promoter.
Cedrol has sedative effects, it induces autophagy and apoptotic cell death in A549 non-small cell lung carcinoma cells through the P13K/Akt signaling pathway, the loss of mitochondrial transmembrane potential and the generation of ROS. Cedrol is a potent competitive inhibitor of CYP2B6-mediated bupropion hydroxylase with the inhibition constant (Ki) value of 0.9, μM, it also markedly inhibited CYP3A4-mediated midazolam hydroxylation with a Ki value of 3.4 μM.
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| In vitro: |
| Journal of Molecular Catalysis B Enzymatic, 2001, 11(4-6):329-334. | | Biotransformation of the fungistatic sesquiterpenoids patchoulol, ginsenol, cedrol and globulol by Botrytis cinerea.[Reference: WebLink] |
METHODS AND RESULTS:
The antifungal activity of natural sesquiterpenoids patchoulol, ginsenol, cedrol and globulol against the fungus Botrytis cinerea has been determined. The diminishing of the effect after 3–6 days suggests that a mechanism of detoxification is present.
CONCLUSIONS:
Biotransformation of these fungistatic compounds has been investigated as a method of studying this mechanism. | | International Journal of Molecular Medicine, 2016,38(1): 291-299. | | Cedrol induces autophagy and apoptotic cell death in A549 non-small cell lung carcinoma cells through the P13K/Akt signaling pathway, the loss of mitochondrial transmembrane potential and the generation of ROS.[Reference: WebLink] | The objective of the present study was to determine the anticancer effects of cedrol in A549 human non-small cell lung cancer cells by examining the effects of cedrol on apoptosis induction, the phosphatidylinositol 3'-kinase (PI3K)/Akt signaling pathway, autophagy, reactive oxygen species (ROS) generation and mitochondrial transmembrane potential (MTP).
METHODS AND RESULTS:
The anticancer effects of cedrol were examined using A549 human lung carcinoma cells as an in vitro model. Cell viability was determined using MTT and lactate dehydrogenase (LDH) assays, and an inverted phase contrast microscope was used to examine the morphological changes in these cells. Cedroltriggered autophagy was confirmed by transmission electron microscopy (TEM) analysis of the cells, as well as by western blot analysis of microtubule-associated protein light-chain 3 (LC3)B expression. Intracellular ROS generation was measured by flow cytometry using 5-(6)-carboxy-2',7'-dichlorodihydrofluorescein diacetate (CM-DCFH2-DA) staining and MTP was measured using flow cytometry.
The results demonstrated that cedrol reduced cell viability and induced cell apoptosis in a dose-dependent manner. Mechanistic evaluations indicated that cedrol induced apoptosis by reducing the MTP and by decreasing the levels of phosphorylated (p-)PI3K and p-Akt. Cedrol induced autophagy, which was confirmed by TEM analysis, by increasing intracellular ROS formation in a concentration-dependent manner, which was almost completely reversed by N-acetyl-L-cysteine (NAC) and tocopherol.
CONCLUSIONS:
Taken together, these findings reveal that cedrol inhibits cell proliferation and induces apoptosis in A549 cells through mitochondrial and PI3K/Akt signaling pathways. Our findings also reveal that cedrol induced pro-death autophagy by increasing intracellular ROS production. |
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