Accumulating evidence suggests that resveratrol may have beneficial effects against traumatic brain injury. However, its effect on the regulation of extracellular levels of gliotransmitter and on the activation of p38 MAPK in astrocytes is still unknown. We have examined whether resveratrol regulates extracellular levels of gliotransmitter as well as the activation of p38 MAPK in cultured astrocytes before and after stretch injury. The extracellular levels of glutamate, D-/L-serine and D-serine were apparently reduced by 100 lM resveratrol in control astrocyte cultures. The dramatic increase of glutamate and D-serine release induced by stretch injury was also clearly inhibited by resveratrol. Resveratrol mediates this response by reduction of release through inhibition of extracellular calcium influx and increment of gliotransmitter uptake through enhancement of amino acid transporter expressed in the membrane of astrocyte. In addition, resveratrol definitely reduced the activation of p38 MAPK in cultured astrocytes following stretch injury. AMPA receptor is involved in the activation of p38 following injury. Conversely, the levels of glutamine and glycine were not obviously affected by resveratrol before and after injury. Intracellular levels of glutamate and D-serine are not apparently changed by stretch injury. Collectively, our data suggest that resveratrol might play an important role in protection of the nervous system after injury by decreasing the extracellular levels of gliotransmitter and inhibiting activation of p38 MAPK following injury.
Aldehyde reductase (ALR) plays key roles in the detoxification of toxic aldehyde. In this study, the authors cloned the swamp eel ALR gene using rapid amplification of cDNA ends‐PCR (RACE‐PCR). The recombinant protein (rALR) was expressed in Escherichia coli and purified using a Ni2+‐NTA chelating column. The rALR protein exhibited efficient reductive activity towards several aldehydes, ketones and S‐nitrosoglutathione (GSNO). A spot assay suggested that the recombinant E. coli strain expressing rALR showed better resistance to formaldehyde, sodium nitrite and GSNO stress, suggesting that swamp eel ALR is crucial for redox homeostasis in vivo. Consequently, the authors investigated the effect of rALR on the oxidative parameters of the liver in swamp eels challenged with Aeromonas hydrophila. The hepatic glutathione (GSH) content significantly increased, and the hepatic NO content and levels of reactive oxygen species and reactive nitrogen species significantly decreased when rALR was administered. In addition, the mRNA expression of hepatic Alr, HO1 and Nrf2 was significantly upregulated, whereas the expression levels of NF‐κB, IL‐1β and NOS1 were significantly downregulated in the rALR‐administered group. Collectively, these results suggest that ALR is involved in the response to nitrosative stress by regulating GSH/NO levels in the swamp eel.
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