RESUMEN
High mountain tea (HT) is widely acknowledged as an essential resource of high-quality tea due to its adaptation to superior ecological environments. In this study, the sensory (aroma and taste) and safety (heavy metals and pesticide residues) characteristics of HT were characterized through sensory evaluation, gas chromatography-mass spectrometry (GC-MS), liquid chromatography-mass spectrometry (LC-MS), flavor activity value, and risk factor analysis. The results elucidated that the aroma sensory characteristics of HT were tender and green, accompanied by sweet and slight chestnut. A total of 8 aroma compounds were identified as the primary substances contributing to the unique aroma characteristics; the difference in the ratio of "green substances" and "chestnut substances" might be the reason for different aroma characteristics in HT and LT (low mountain tea). The taste sensory characteristics of HT were high in freshness and sweetness but low in bitterness and astringency. The high content of soluble sugar (SS), nonester catechins, sweet free amino acids, and low content of caffeine and tea polyphenols were the primary reasons for its taste characteristics. Low temperature stress might be the most fundamental reason for flavor characteristics formation in HT. Furthermore, the pollution risks of 5 heavy metals and 50 pesticide residues in HT were less than 1. The complex ecosystem and low chemical control level were speculated to be the primary reasons for the high safety quality of HT. Overall, these findings provide a more comprehensive understanding of quality characteristics and their formation mechanisms in HT.
RESUMEN
Geniposide is a bioactive iridoid glucoside derived from Gardenia jasminoides that has proven anti-inflammatory effects against acute lung injury. The aim of this study was to determine whether geniposide could protect pulmonary arterial smooth muscle cells (PASMCs) from lipopolysaccharide (LPS)-induced injury and to explore the participation of α7 nicotinic acetylcholine receptor (α7nAChR), which was previously reported to suppress pro-inflammatory cytokine production in LPS-stimulated macrophages. In the present study, rat PASMCs were isolated and stimulated using LPS. The effect of geniposide on LPS-induced PASMC injury was then explored. Geniposide exerted anti-apoptotic and anti-inflammatory effects on LPS-treated PASMCs, as demonstrated by the downregulation of pro-apoptotic proteins and pro-inflammatory cytokines, respectively. Furthermore, the α7nAChR agonist PNU282987 accentuated the protective effect of geniposide against LPS-induced injury in PASMCs by inhibiting toll-like receptor-4/myeloid differentiation primary response 88 (TLR-4/MyD88) signaling and downregulating nuclear factor (NF)-κB expression. Conversely, methyllycaconitine, an inhibitor of α7nAChR, attenuated the effects of geniposide. These findings collectively suggested that in conjunction with geniposide, the activation of α7nAChR may contribute to further mitigating LPS-induced PASMC apoptosis and inflammation. In addition, the underlying mechanisms critically involve the NF-κB/MyD88 signaling axis. These results may provide novel insights into the treatment and management of lung diseases via geniposide administration.