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Currently, Golden Barrel cactus extract is formulated in dietary supplements, on account of its powerful weight loss profit and antioxidant activity. Golden Barrel cactus grusonii (Echinocactus grusonii), a Thai cultivar Golden Barrel cactus which is known as the golden barrel Golden Barrel cactus was therefore investigated for total chlorophylls with the aim of developing as a dietary supplement in future. The chlorophyll contents of 3 and 6 years Echinocactus grusonii extracts were evaluated by High Performance Liquid Chromatography with a Grace-Vydac 201TP54 reversed-phase polymeric C18 column. The results showed that chlorophyll a and chlorophyll b are the main components of Echinocactus grusonii crude extracts also at higher level at age 3 years. It was found that the main chlorophylls contents are chlorophyll a and chlorophyll b at 2.94±0.55μg/ml and 1.63±0.14 μg/ml for 3 years Echinocactus grusonii. In addition, the amount of chlorophyll a and chlorophyll b show lower content at 1.11±0.25μg/ml and 0.67±0.01μg/ml for 6 years Echinocactus grusonii. In conclusion, Echinocactus grusonii age 3 years crude extracts showed total chlorophylls contents higher than at age 6 years. The phytochemical profile study of Echinocactus grusonii age 3 years and 6 years crude extracts are planned in the near future.

Human oral squamous carcinoma is considered the most common oral cancer; it imposes multiple oral and dental consequences as a result of oral cancer treatment. We previously found that the nanoencapsulation of cordycepin (CS) could inhibit oral cancer cells. However, the mechanism of action was not understood. The aim of this study was to investigate the signaling pathway by which CS and encapsulated nanoparticles (NPs) activate the inhibition of cancer cell growth. We demonstrated that human oral cancer (HSC-4) cells underwent necroptosis when incubated with high concentrations of CS, but not when incubated with either low concentrations of CS or encapsulated CS NPs. High concentrations of CS-induced necroptosis of HSC-4 cells, demonstrated by a reduction in apoptotic (BAX, Caspase-3, Caspase-8, and Caspase-9) and autophagic genes (LC3, Atg5, and Atg12). However, low concentrations of CS significantly induced the expression of autophagic gene LC3. Interestingly, encapsulated CS NPs induced a significant increase in apoptotic genes (P53, BAX, Caspase-3, Caspase-8, and Caspase-9), but a significant decrease in autophagic (P62, Atg5, and Atg12) and necroptotic genes (receptor-interacting serine/threonine-protein kinase 3 [RIPK3]).We also found that encapsulated CS NPs enhanced the accumulation of cellular protein and decreased secreted supernatant protein levels. Moreover, encapsulated CS NPs had higher efficacy in terms of reactive oxygen species (ROS) generation-mediated inhibition of autophagy compared to nonencapsulated CS, suggesting that nanoencapsulation of CS can switch the program of HSC-4 cell death from necroptosis to apoptosis. In conclusion, HSC-4 cells have a defense strategy against CS-induced cell apoptosis, but this problem can be solved through the use of encapsulation combined with nanotechnology.