Effect of inlet temperature on the physicochemical properties of spray-dried seed-watermelon seed protein powder.

Here, we studied the effects of inlet temperature on the physicochemical properties of the hydrolyzed protein (seed-watermelon seed hydrolyzed protein [SWSP]) powder in seed-watermelon seeds. The inlet temperature of the study was in the range of 150 to 180 °C, and the remaining experimental parameters remained constant, that is, the feed flow rate was 0.2 L/hr, the concentration of maltodextrin was 30%, and the outlet temperature was 80 °C. We studied the water activity and moisture content, bulk density, flowability (Carr index and Hausner ratio), angle of repose, solubility, color, hygroscopicity, powder morphology, particle size, crystallinity, and odor of the sample. Inlet temperature of 170 to 180 °C reduced the moisture content and increased the particle size. It was found that the value of measured water activity was less than 0.5, which helped in maintaining stability of the sample. Powders produced at the temperatures showed smoother particle surfaces, whereas higher inlet temperature showed spherical particles with some shrinkage as analyzed by scanning electron microscope. The inlet temperature affected the color of the sample, thus at high temperature, the sample had a brighter color. The sample was approximately 18% crystalline. At a preparation temperature of 160 °C, the sample showed significant antioxidant activity (P < 0.05).

Acacetin-induced cell apoptosis in head and neck squamous cell carcinoma cells: Evidence for the role of muscarinic M3 receptor.

Aacacetin, a plant flavone has shown antitumor efficacy recently. However, its associated mechanisms are poorly known. We hypothesized that the muscarinic M3 receptor (M3 R), which is highly expressed in some cancer tissue, is related to the antitumor effect of acacetin in head and neck squamous cell carcinoma (HNSCC) cells. Our results showed that 12.5- to 200-µM acacetin inhibited cell viability in dose- and time-dependent manners in HNSCC cells, but a relative higher concentration was needed for oral adenoid cystic carcinoma cells. M3 R expression level was higher in HNSCC cells than that in adenoid cystic carcinoma cells. Flow cytometry and electron microscopy confirmed acacetin-induced cell apoptosis in 22B cells, a HNSCC cell line. Acacetin promoted mitochondrial cytochrome c release and caspase 9, 3 processing. Knocking down of M3 R expression by specific siRNA significantly prevented the acacetin-induced cell viability damage, cell apoptosis, and caspase 3 activation. Besides, M3 R was also involved in acacetin-induced elevation of reactive oxygen species and intracellular calcium ([Ca2+ ]i ). These data indicate that acacetin-induced cell apoptosis in HNSCC cells may through M3 R related calcium signaling and caspase 3 activation. Acacetin is a potent natural antitumor reagent especially for the tumor cells, which highly expressed M3 R.