GC-MS and ATR-FTIR Spectroscopy Coupled with Chemometric Analysis for Detection and Quantification of White Turmeric (Curcuma zedoaria) Essential Oils Adulteration.

<b>Background and Objective:</b> White turmeric essential oil (WTEO) is known to have high commercial value since it has been used to improve immunological function, increase blood circulation, ease toxin clearance and stimulate digestion. However, there is no standard to regulate the specific characteristics of white turmeric essential oil. Therefore, the objective of this research was to develop an analytical technique for WTEO authentication from vegetable oils, namely palm oil (PO), coconut oil (VCO) and soybean oil (SO), using FTIR spectroscopy and chemometrics, as well as GC-MS spectroscopy. <b>Materials and Methods:</b> The WTEO was obtained by hydrodistillation method. Pure WTEO and vegetable oils were scanned in the MIR region (4000-650 cm¹) of FTIR spectroscopy and the spectra were further analyzed using chemometrics. <b>Results:</b> The extraction yielded 0.103% v/w WTEO, a dark purple color with a specific pungent odor. Discriminant analysis separated pure WTEO and adulterated WTEO with 100% accuracy at wave numbers 4000-650 cm¹. The best PLS regressions to quantify SO, VCO, PO and concentration in WTEO were at wave numbers 4000-1100, 1400-1050 and 2100-650 cm¹, respectively. <b>Conclusion:</b> The FTIR and chemometrics combination effectively authenticates white turmeric essential oil from any possible adulterants, such as vegetable oil.

Cowanin induces apoptosis in breast cancer cells via Bcl-2 signaling pathway.

OBJECTIVES: This study aimed to investigate the effect of cowanin the mechanism of cowanin toward cell death and BCL-2 protein (antiapoptotic) expression of T47D breast cancer. METHODS: The cell death was evaluated by double staining, namely acridine orange and propidium iodide, and then observed under a fluorescence microscope. Meanwhile, the BCL-2 protein expression was determined by western blotting with measurement of protein area and protein density. RESULTS: The result found T47D breast cancer cells were viable, apoptosis, and necrosis after treatment with cowanin. The average viable cells, apoptosis, and necrosis percentages were 54.13 %, 45.43 %, and 0.44 %, respectively. Statistical analysis showed cowanin could significantly induce death in T47D breast cancer cells by apoptosis (p<0.05). It was also revealed that cowanin and positive control (doxorubicin) treatment had a significantly decreased protein area and protein density (p<0.05). CONCLUSIONS: It can be concluded that cowanin can induce death in T47D breast cancer cells by apoptosis and affect the expression of Bcl-2 protein in T47D breast cancer cells.