Fructose‐1,6‐diphosphate attenuates prostaglandin E₂ production and cyclo‐oxygenase‐2 expression in UVB‐irradiated HaCaT keratinocytes

Abstract

1 Fructose-1,6-diphosphate (FDP), a glycolytic metabolite, is reported to ameliorate in¯ammation and inhibit the nitric oxide production in murine macrophages stimulated with endotoxin. It is also reported that FDP has cytoprotective eects against hypoxia or ischaemia/reperfusion injury in brain and heart. However, underlying mechanisms of its various biological activities are not completely understood. 2 In this study, we examined the eects of FDP on UVB-induced prostaglandin production in HaCaT keratinocytes. 3 Ultraviolet B (UVB, 280 ± 320 nm) irradiation (30 mJ cm 72 ) increased prostaglandin E 2 (PGE 2 ) production, which was signi®cantly decreased by FDP in a concentration dependent manner. NS-398, a cyclo-oxygenase-2 (COX-2) selective inhibitor completely inhibited UVB-induced PGE 2 production showing that COX-2 activity is responsible for the increase in PGE 2 production under our experimental conditions. 4 UVB irradiation increased total COX activity and COX-2 mRNA in HaCaT keratinocytes, which were signi®cantly blocked by FDP in a concentration dependent manner. 5 N-acetylcysteine (NAC) signi®cantly attenuated UVB-induced PGE 2 production, COX activity and COX-2 mRNA expression indicating oxidative components might contribute to these events. 6 FDP reduced UVB-induced increase in cellular reactive oxygen species (ROS) level although it did not show direct radical scavenging eect in the experiment using 1,1-diphenyl-2picrylhydrazil (DPPH). FDP preserved the cellular antioxidant capacity including catalase activity and GSH content after irradiation. 7 Our data obtained hitherto suggest that FDP may have a protective role in UVB-injured keratinocyte by attenuating PGE 2 production and COX-2 expression, which are possibly through blocking intracellular ROS accumulation.

Neuroprotection by fructose-1,6-bisphosphate involves ROS alterations via p38 MAPK/ERK

“…Additionally, it has been reported that FBP also has the immunomodulatory function [6], although the mechanism for this has not yet been clearly identified. FBP attenuated prostaglandin E 2 production and cyclooxygenase-2 (COX-2) expression in UVB-irradiated HaCaT keratinocytes [1], and inhibited LPS-induced iNOS expression in macrophages with no reduction of NF-kB activity [12]. ROS and reactive nitric oxide species that have neurotoxic properties are formed by the activity of inducible nitric oxide synthase (iNOS), which is also activated via MAPK [14].…”

Role of antioxidants in the skin: Anti-aging effects

“…UVB-induced erythema is attenuated by the NOS inhibitor NG-monomethyl-L-arginine and the cyclooxygenase (COX) inhibitor indomethacin [26]. ROS, including NO, induce skin erythema through prostaglandin E2 synthesis [27]. Expression of COX-2, a pivotal enzyme in prostaglandin E2 synthesis, is upregulated by ROS to stimulate the inflammation process [28].…”

Extract of the bristles of Dirphia sp. increases nitric oxide in a rat pleurisy model

“…Fructose-1,6-bisphosphate is capable of inhibiting pleurisy induced by carrageenan [26]. The sugar is also capable of exercising a protective effect by attenuating the production of prostaglandin E and the expression of COX-2 [27], as well as controlling the secretion of cytokines and the production of nitric oxide [28]. We have shown that this sugar is effective as an anti-inflammatory agent in pleurisy induced by EBD, reducing cellular infiltration and plasma exudation, suggesting that the EBD may provoke an increase in prostaglandin E and of COX-2 activity.…”