- Add into bath water - Use with a base oil, scent free cream or a lotion for body care.
- Apply directly on infected area
– Traditionally has also been taken as a drop in warm water or green tea.
Sandalwood oil comes from the wood and roots of Santalum album, or the East Indian sandalwood tree. Sandalwood oil has many traditional uses. For centuries, East Indian sandalwood oil has been a popular ingredient in natural medicine, the folk medicine of India. It’s also been used in traditional Chinese medicine. Sandalwood has anti-inflammatory, antiviral, antimicrobial, and antifungal properties and comes as a soothing agent for people suffering from itchiness triggered by skin infections such as Eczema and Psoriasis , . It also modulates the immune reaction and mediates efficient wound healing with minimum scarring . Sandalwood has shown anticancer effect in various studies, due to the presence of active compound Alpha Santalol which kills skin cancer cells and breast cancer cells , . This oil is fit to be consumed internally as well to be used to topically for the skin.
Sharma, M., Levenson, C., Browning, J. C., Becker, E. M., Clements, I., Castella, P., & Cox, M. E. (2018). East Indian Sandalwood Oil Is a Phosphodiesterase Inhibitor: A New Therapeutic Option in the Treatment of Inflammatory Skin Disease. Frontiers in Pharmacology, 9, 200. http://doi.org/10.3389/fphar.2018.00200
ABSTARCT- Cyclic adenosine monophosphate phosphodiesterases (PDEs) regulate pro-inflammatory cytokine production. One isoform, PDE4, is overactive in chronic relapsing inflammatory skin diseases: psoriasis and eczema/atopic dermatitis, and in several cancers. East Indian sandalwood oil (EISO) has significant anti-inflammatory properties. Here, we report that 75% of pediatric eczema/atopic dermatitis patients treated with topical EISO formulations achieved a >50% reduction in their Eczema Area and Severity Index score. EISO treatment of a psoriasis model reduced PDE4 expression and reversed histopathology. EISO directly inhibited PDE enzymatic activity in vitro. In lipopolysaccharide-stimulated human dermal fibroblast, BEAS-2B, A549, and THP-1 cells, EISO suppressed total cellular PDE activity, PDE4, and 7 transcript levels, nuclear factor kappa B (NF-κB) activation, and pro-inflammatory cytokines/chemokine production. These results suggest that EISO anti-inflammatory activity is mediated through suppressing PDE activity, thus facilitating cAMP-regulated inhibition of NF-κB and indicate EISO as an attractive natural therapeutic for chronic and acute inflammatory disorders.
Sharma, M., Levenson, C., Clements, I., Castella, P., Gebauer, K., & Cox, M. E. (2017). East Indian Sandalwood Oil (EISO) Alleviates Inflammatory and Proliferative Pathologies of Psoriasis. Frontiers in Pharmacology, 8, 125. http://doi.org/10.3389/fphar.2017.00125
ABSTRACT- Psoriasis, a chronic inflammatory skin disease marked by hyper proliferation and aberrant differentiation of keratinocytes, affects 2–3% of the world’s population. Research into the pathogenesis of psoriasis has been hampered by the lack of models that accurately reflect the biology of the psoriatic phenotype. We have previously reported that East Indian Sandalwood oil (EISO) has significant anti-inflammatory properties in skin models and hypothesized that EISO might provide therapeutic benefit to psoriasis patients due to its anti-inflammatory and anti-proliferative properties. Here we present interim results from an on-going proof-of-concept Phase 2 clinical trial in which topically applied EISO is demonstrating to be well tolerated and helpful in alleviating mild to moderate psoriasis symptoms. This led us to evaluate the ability of EISO to affect the psoriatic phenotype using MatTek Corporation reconstituted organotypic psoriatic and normal human skin models. EISO had no impact on the phenotype of the normal skin tissue model, however, EISO treatment of the psoriasis tissue model reverted psoriatic pathology as demonstrated by histologic characterization and expression of keratinocyte proliferation markers, Ki67 and psoriasin. These phenotypic affects correlated with suppressed production of ENA-78, IL-6, IL-8, MCP-1, GM-CSF, and IL-1β. Demonstration of the ability of EISO to abrogate these psoriasis symptoms in well-characterized in vitro psoriatic tissue models, supports the hypothesis that the clinically observed symptom alleviation is due to suppression of intrinsic tissue inflammation reactions in afflicted lesions. This study presents a systematic approach to further study the underlying mechanisms that cause psoriasis, and presents data supporting the potential of EISO as a new ethnobotanical therapeutic concept to help direct and accelerate the development of more effective therapies.
Dextran based herbal nanobiocomposite membranes for scar free wound healing
ABSTRACT - Dextran based bionanocomposite membranes encapsulating clove oil (CO) and sandalwood oil (SO) that are capable of preventing infection due to their inherent virtue of antibacterial activity and modifying the wound healing cascade for accelerated scar free healing, were developed. A facile solvent casting technique was used to fabricate dextran/nanosoy/glycerol/chitosan (DNG/Ch) nanocomposite membranes followed by subsequent addition of CO and SO to obtain DNG/Ch/CO and DNG/Ch/SO herbal nanodressings. Dressings exhibited >98% antibacterial activity against both Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) at extremely low loadings of 5% and 10% for CO and SO, respectively. This encapsulation strategy allowed controlled diffusion of EO over a period of 72 h which was measured in terms of drug efficacy using bacterial reduction count test and serial plate transfer disk diffusion test (SPTDDT). Swelling behavior and mechanical properties were also examined. Bacterial adherence study was performed to demonstrate the efficiency of dressings for arresting microbial invasion. In vivo wound healing studies were conducted using male swiss albino mice of BALB/c strain and DNG/Ch/CO dressings exhibited complete healing within 14 days with remarkable efficacy in scar prevention. Histological analysis revealed that CO and SO treatment led to deposition of ordered collagen along with fibroblast migration.
Chemopreventive effects of various concentrations of alpha-santalol on skin cancer development in CD-1 mice. Eur J Cancer Prev. 2005 Oct;14(5):473-6
Previous studies from this laboratory have indicated that alpha-santalol (5%) provides chemopreventive effects in 7,12-dimethylbenz[a]anthracene (DMBA)-initiated and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted skin cancer in CD-1 and SENCAR mice. Skin cancer development is associated with increased ornithine decarboxylase (ODC) activity, DNA synthesis and rapid proliferation of epidermal cells. The purpose of this investigation was to determine the effects of various concentrations (1.25% and 2.5%) of alpha-santalol on DMBA-initiated and TPA-promoted skin cancer development, TPA-induced ODC activity, and DNA synthesis in CD-1 mice. alpha-Santalol treatment at both concentrations (1.25% and 2.5%) prevented the skin cancer development. alpha-Santalol treatment (1.25% and 2.5%) resulted in a significant decrease in the TPA-induced ODC activity and incorporation of [3H]thymidine in DNA in the epidermis of CD-1 mice. There was no significant difference in the effects of 1.25% and 2.5% alpha-santalol on tumour incidence, multiplicity, epidermal TPA-induced ODC activity, or DNA synthesis in CD-1 mice.
Santha, S., Bommareddy, A., Rule, B., Guillermo, R., Kaushik, R. S., Young, A., & Dwivedi, C. (2013). Antineoplastic Effects of α-Santalol on Estrogen Receptor-Positive and Estrogen Receptor-Negative Breast Cancer Cells through Cell Cycle Arrest at G2/M Phase and Induction of Apoptosis. PLoS ONE, 8(2), e56982. http://doi.org/10.1371/journal.pone.0056982
Anticancer efficacy and the mechanism of action of α-santalol, a terpenoid isolated from sandalwood oil, were investigated in human breast cancer cells by using p53 wild-type MCF-7 cells as a model for estrogen receptor(ER)-positive and p53 mutated MDA-MB-231 cells as a model for ER-negative breast cancer. α-Santalol inhibited cell viability and proliferation in a concentration and time-dependent manner in both cells regardless of their ER and/or p53 status. However, α-santalol produced relatively less toxic effect on normal breast epithelial cell line, MCF-10A. It induced G2/M cell cycle arrest and apoptosis in both MCF-7 and MDA-MB-231 cells. Cell cycle arrest induced by α-santalol was associated with changes in the protein levels of BRCA1, Chk1, G2/M regulatory cyclins, Cyclin dependent kinases (CDKs), Cell division cycle 25B (Cdc25B), Cdc25C and Ser-216 phosphorylation of Cdc25C. An up-regulated expression of CDK inhibitor p21 along with suppressed expression of mutated p53 was observed in MDA-MB-231 cells treated with α-santalol. On the contrary, α-santalol did not increase the expression of wild-type p53 and p21 in MCF-7 cells. In addition, α-santalol induced extrinsic and intrinsic pathways of apoptosis in both cells with activation of caspase-8 and caspase-9. It led to the activation of the executioner caspase-6 and caspase-7 in α-santalol-treated MCF-7 cells and caspase-3 and caspase-6 in MDA-MB-231 cells along with strong cleavage of poly(ADP-ribose) polymerase (PARP) in both cells. Taken together, this study for the first time identified strong anti-neoplastic effects of α-santalol against both ER-positive and ER-negative breast cancer cells.
100% Sandalwood steam distilled oil