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Proteomic analysis of intestinal ischemia/reperfusion injury and ischemic preconditioning in rats reveals the protective role of aldose reductase
Author(s) -
Liu KeXuan,
Li Cai,
Li YunSheng,
Yuan Baolong,
Xu Miao,
Xia Zhengyuan,
Huang WenQi
Publication year - 2010
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.201000078
Subject(s) - aldose reductase , western blot , proteome , ischemia , intestinal mucosa , reperfusion injury , intestinal ischemia , pharmacology , apoptosis , chemistry , downregulation and upregulation , reactive oxygen species , biology , medicine , biochemistry , enzyme , gene
Intestinal ischemia/reperfusion (I/R) injury is a critical condition associated with high morbidity and mortality. Studies show that ischemic preconditioning (IPC) can protect the intestine from I/R injury. However, the underlying molecular mechanisms of this event have not been fully elucidated. In the present study, 2‐DE combined with MALDI‐MS was employed to analyze intestinal mucosa proteomes of rat subjected to I/R injury in the absence or presence of IPC pretreatment. The protein content of 16 proteins in the intestinal mucosa changed more than 1.5‐fold following intestinal I/R. These proteins were, respectively, involved in the cellular processes of energy metabolism, anti‐oxidation and anti‐apoptosis. One of these proteins, aldose reductase (AR), removes reactive oxygen species. In support of the 2‐DE results, the mRNA and protein expressions of AR were significantly downregulated upon I/R injury and enhanced by IPC as confirmed by RT‐PCR and western blot analysis. Further study showed that AR‐selective inhibitor epalrestat totally turned over the protective effect of IPC, indicating that IPC confers protection against intestinal I/R injury primarily by increasing intestinal AR expression. The finding that AR may play a key in intestinal ischemic protection might offer evidences to foster the development of new therapies against intestinal I/R injury.