RESUMEN
Summer green tea (SGT) has a low cost and high annual yield, but its utilization rate is limited due to suboptimal quality. The aim of this study is to enhance the flavor of SGT using fermentation with A. niger RAF106 while examining changes in its metabolites during this process. The results revealed an elevation in the content of alcohol, alkanes, and nitroxides in tea leaves following the process of fermentation. The predominant volatile compounds identified in tea leaves after undergoing a 6-day fermentation period were linalool, (Z)-α, α, 5-trimethyl-5-vinyltetrahydrofuran-2-methanol, (E)-linalool oxide (furan type), linalool oxide (pyran type), and theapyrrole. These compounds exhibited significant increases of 31.48%, 230.43%, 225.12%, 70.71%, and 521.62%, respectively, compared to the non-fermented control group (CK). The content of non-ester catechins, soluble sugars, and total flavonoids reached their peak on the 4th day of fermentation, exhibiting significant increases of 114.8%, 95.59%, and 54.70%, respectively. The content of gallic acid and free amino acids reached their peak on the 6th day of fermentation, exhibiting significant increases of 3775% and 18.18%, respectively. However, the content of ester catechin decreased by 81.23%, while caffeine decreased by 7.46%. The content of lactic acid, acetic acid, and citric acid in tea after fermentation was 421.03%, 203.13%, and 544.39% higher than before fermentation, respectively. The present study offers a fresh approach for the advancement of SGT.
RESUMEN
AIM: Interleukin-1 beta (IL-1beta) has been implicated as an extracellular signal in the initiation of apoptosis in neurons and oligodendrocytes after spinal cord injury (SCI). To further characterize the apoptotic cascade initiated by IL-1beta after SCI, we examined the expression of IL-1beta, p38 mitogen-activated protein kinase (p38 MAPK) and caspase-3 after SCI, and further investigated whether p38 MAPK was involved in neuron apoptosis induced by IL-1beta. METHODS: Adult rats were given contusion SCI at the T-10 vertebrae level with a weight-drop impactor (10 g weight dropped 25.0 mm). The expression levels of IL-1beta, p38 MAPK and caspase-3 after SCI were assessed with Western blots, immunohistochemistry staining, and real time reverse transcription polymerase chain reactions (RT-PCR). Neuron apoptosis was assessed with the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) method. RESULTS: Increased levels of IL-1beta and p38 MAPK were observed soon after injury, with a peak in expression levels within 6 h of injury. By 24 h after injury, caspase-3 expression was markedly increased in the injured spinal cord. TUNEL-positive cells were first observed in the lesioned area 6 h after SCI. The largest number of TUNEL-positive cells was observed at 24 h post-SCI. Intrathecal injection of the IL-1 receptor antagonist IL-1Ra significantly reduced expression of p38 MAPK and caspase-3, and reduced the number of TUNEL-positive cells. Moreover, intrathecal injection of an inhibitor of p38 MAPK, SB203580, also significantly reduced the expression of caspase-3, and reduced the number of TUNEL-positive cells in the injured spinal cord. CONCLUSION: The p38MAPK signaling pathway plays an important role in IL-1beta mediated induction of neuron apoptosis following SCI in rats.