Metabolomics approach for understanding geographical dependence of soybean leaf metabolome.

The soybean plant (Glycine max) is widely used as an ingredient in various foods, nutraceuticals and cosmetics, due to their diverse bioactive compounds. Their metabolic compositions are likely affected by environmental conditions during growth. To investigate the influence of different environmental conditions on the metabolite composition of soybean leaves, we cultivated soybean (G. max Sinhwa) in the southernmost island and volcanic region of Korea, and in the central section and limestone region of the Korean peninsula. Comprehensive metabolite variations of their leaves were analyzed through 1H NMR-based metabolomics approach. With marked differences in soil compositions and climatic conditions between the two growing areas, differences in accumulations of pinitol and diverse flavonoids were noted between the soybean leaves, reflecting the distinct metabolism of soybean plants for physiological adaptation toward different environmental conditions. Therefore, the current study highlights the geographical dependences of diverse soybean leaf metabolites for developing biofunction-enhanced soybean products.

Activation of transient receptor potential melastatin 8 reduces ultraviolet B-induced prostaglandin E2 production in keratinocytes.

Transient receptor potential melastatin 8 (TRPM8) is a member of the TRP family, and is activated at temperatures below 22°C, or by cooling compounds such as menthol. In this study, it was found that a new role of TRPM8 activation on prostaglandin E2 (PGE2), an inflammatory cytokine and dendritogenesis stimulator of normal human melanocytes. Normal human keratinocytes were pretreated with menthol or incubated at 22°C for TRPM8 activation before ultraviolet (UV)-B irradiation. To examine the specificity between TRPM8 activation and PGE2 release, we inhibited TRPM8 with the antagonist (capsazepine), or introduced TRPM8 siRNA for a gene silencing experiment. UV-B irradiation significantly induced PGE2 release in normal human keratinocytes. Interestingly, activation of TRPM8 at 22°C or with menthol inhibited UV-B-induced PGE2 release. The effect of the TRPM8 agonist was completely blocked by pretreatment with the TRPM8 antagonist, capsazepine. When TRPM8 expression was suppressed by siRNA, UV-B irradiation still upregulated PGE2 in keratinocytes, but pretreatment of menthol or low temperature did not inhibit UV-B-induced PGE2. In conclusion, the activation of TRPM8 inhibits UV-B-induced PGE2 production in keratinocytes, and the activation of TRPM8 may reduce inflammatory responses in skin.