Format

Send to

Choose Destination
Biochem Biophys Res Commun. 2014 Jul 18;450(1):135-41. doi: 10.1016/j.bbrc.2014.05.069. Epub 2014 May 24.

Involvement of glutamate-cystine/glutamate transporter system in aspirin-induced acute gastric mucosa injury.

Author information

1
Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078, China.
2
Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078, China. Electronic address: yuan_jianli@sina.com.

Abstract

Large-dose or long-term use of aspirin tends to cause gastric mucosa injury, which is recognized as the major side effect of aspirin. It has been demonstrated that glutamate exerts a protective effect on stomach, and the level of glutamate is critically controlled by cystine/glutamate transporter (Xc(-)). In the present study, we investigated the role of glutamate-cystine/glutamate transporter system in aspirin-induced acute gastric mucosa injury in vitro and in vivo. Results showed that in human gastric epithelial cells, aspirin incubation increased the activity of LDH and the number of apoptotic cells, meanwhile down-regulated the mRNA expression of Xc(-) accompanied with decreased glutamate release. Similar results were seen in a rat model. In addition, exogenous l-glutamate attenuated the gastric mucosa injury and cell damage induced by aspirin both in vitro and in vivo. Taken together, our results demonstrated that acute gastric mucosa injury induced by aspirin is related to reduction of glutamate-cystine/glutamate transporter system activity.

KEYWORDS:

Apoptosis; Aspirin; Gastric epithelial cells; Gastric mucosa injury; l-Glutamate

PMID:
24866234
DOI:
10.1016/j.bbrc.2014.05.069
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center