ABSTRACT
Syzygium zeylanicum L. (DC) (SZL) has been used in antidiabetes treatment for ages. However, the scientific evidence of active agents that have antidiabetic activity and response against biological activities is limited. In this study, the active components of SZL trunk-bark extract (SZL extract) were identified using principal component analysis (PCA), and their antidiabetic activities were assessed. The results indicated that the ethyl acetate fraction (EAF) had the highest concentration of phenolic compounds, antioxidants, and antihyperglycemic activities in the postprandial zebrafish model. The major antioxidant contributors were gallic acid, catechin, epicatechin, ellagic acid, quercetin, caffeine, and apigenin, and their concentrated levels reduced α-amylase inhibitory activity, whereas rutin and ethyl gallate influenced the α-glucosidase inhibitory activity. This study showed the bio-functional properties of active phenolic compounds present in the SZL extract, potentially serving as a functional food to control hyperglycemia.
ABSTRACT
Thrombospondin-1 (TSP-1) is an extracellular matrix protein produced by astrocytes, which can promote synaptogenesis. The regulation of astrocytic TSP-1 involves extracellular ATP through the activation of P2Y receptors coupled to various protein kinase signaling pathways. However, not much is known about the mechanisms regulating TSP-1 expression in primary cortical astrocytes after a traumatic brain injury. Using an in-vitro model of central nervous system trauma that stimulates the release of ATP, we found that trauma-induced expression and release of TSP-1 involved purinergic signaling as both expression and release were significantly attenuated by pyridoxalphosphate-6-azophenyl-2'-4'-disulfonic acid, a P2 receptor antagonist. Further antagonist studies with reactive blue 2 point to a role for P2Y4, as reactive blue 2 is a potent antagonist for rat P2Y4 receptors. In addition, the injury-induced expression of TSP-1 was significantly attenuated by the inhibition of extracellular signal-regulated kinase and p38/mitogen-activated protein kinase, whereas injury-induced release of TSP-1 was significantly blocked by the inhibition of extracellular signal-regulated kinase and Akt. Using an in-vivo model of a moderate parasagittal fluid-percussion brain injury, we found that TSP-1 levels were increased when compared with those in sham animals in the cortex, thalamus, and hippocampus. We conclude that TSP-1 expression after injury can be regulated by the activation of P2 receptors coupled with protein kinase signaling pathways and suggest that purinergic signaling, by regulating TSP expression, may play an important role in cell-matrix and cell-cell interactions such as those occurring during central nervous system repair.
