Curcuma xanthorrhiza oil

The prinicipal components, DB11672 and xanthorrhizol, mediate the main pharmacological actions of Curcuma xanthorrhiza oil.

Anti-inflammatory and antioxidant actions: Curcumin and xanthorrhizol are natural antioxidant to exert an anti-inflammatory effect by scavenging the reactive oxygen species, such as hydroxyl radical, superoxide anion, and singlet oxygen, or by chemically reducing oxidized compounds. Curcumin inhibits liposomal peroxidation and peroxide-induced DNA damage, and the mechanism of action is thought to involve modulation of cell adhesion molecules (CAMs) and stimulation of ICAM- 1. Based on the findings in vitro, xanthorrhizol may be a potent inhibitor of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) to decrease their expression via NF-kB pathway and subsequently inhibit the production of pro-inflammatory prostaglandin E2 (PGE2) and nitric oxide (NO). In activated primary cultured microglial cells, xanthorrhizol was found to inhibit COX-2, iNOS, proinflammatory cytokine interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α).

Hepatoprotective actions: The hepatoprotective effect of Curcuma xanthorrhiza oil is considered mainly a result of its antioxidant properties, as well as its ability to decrease the levels of pro-inflammatory cytokines. Xanthorrhizol may also attenuate phosphorylation of c-Jun N-terminal kinases (JNKs).

Antibacterial actions: While the mode of antibacterial action of xanthorrhizol is not fully understood, it is thought to involve suppression of nuclear factor kappaB (NF-kB) and mitogen-activated protein kinase (MAPK) induced by microbial infection.

Anticancer actions: The cytotoxic actions of xanthorrhizol against tumour cells is thought to be contributed by its phenol group and may involve its antioxidative and anti-inflammatory activities, induction of apoptosis and cell cycle arrest by reducing cyclin D1 proto-oncogene expression or triggering cyclin-dependent kinase inhibitors (CDKIs). In various cancer cell models, xanthorrhizol was shown to induce apoptosis via activation of p53-dependent mitochondrial pathway. In HeLa cervical cancer cells, xanthorrhizol upregulated p53 and Bax without any effects on Bax/Bcl-2 expression. There is also evidence that xanthorrhizol-induced cell death is mediated by the activation of caspase. Xanthorrhizol increased the expression and promoter activity pro-apoptotic non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1), which is notably inhibited during the development of human colorectal cancer and neoplastic tumors. Other mode of action involves the regulation of MAPK pathway and inhibition of Akt/NF-kB pathway.

Estrogenic and anti-estrogenic actions: In vitro, xanthorrhizol upregulated pS2 and promoted the interaction of ER-estrogen response elements in MCF-7 cells. It acted as a partial estrogen antagonist of hERα in T47D cells. Curcumin also activates gene expression in the breast cancer cell line MCF7, indicating that it may have low estrogenic activity.