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The anti-inflammatory and anti-apoptotic effects of gallic acid against mucosal inflammation- and erosions-induced by gastric ischemia-reperfusion in rats
被引:0
|作者:
Mard, Seyyed Ali
[1
]
Mojadami, Shahnaz
[2
]
Farbood, Yaghoob
[2
]
Naseri, Mohammad Kazem Gharib
[2
]
机构:
[1] Ahvaz Jundishapur Univ Med Sci, Sch Med, Dept Physiol, Res Ctr Infect Dis Digest Syst,PRC, Ahvaz, Iran
[2] Ahvaz Jundishapur Univ Med Sci, Sch Med, Dept Physiol, PRC, Ahvaz, Iran
关键词:
Caspase-3;
Gallic acid;
Inducible nitric oxide synthase;
Ischemia-reperfusion injury;
Rat;
NITRIC-OXIDE;
OXIDATIVE STRESS;
HYDROGEN-PEROXIDE;
PROTECTIVE ROLE;
INJURY;
ANTIOXIDANT;
INVOLVEMENT;
OXYGEN;
DAMAGE;
CELL;
D O I:
暂无
中图分类号:
S85 [动物医学(兽医学)];
学科分类号:
0906 ;
摘要:
The present study aimed to evaluate the protective effect of gallic acid on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rat. Forty male rats were randomly divided into sham, control (I/R injury) and three gallic acid-pretreated groups. To induce I/R lesions, the celiac artery was clamped for 30 min and then the clamp was removed to allow reperfusion for 6 hr. Pretreated rats received gallic acid (15, 30 or 60 mg kg(-1), intraperitoneally) 30 min prior to the induction of I/R injury. Macroscopic and microscopic evaluations of the areas of ulceration were compared. Samples of gastric mucosa were collected to evaluate the protein expression of pro-apoptotic factor, caspase-3, and pro-inflammatory enzyme, inducible nitric oxide synthase (iNOS) using western blot. Pretreatment with gallic acid decreased the total area of gastric lesions. Gallic acid at 30 mg kg(-1) decreased the levels of protein expression of caspase-3 and iNOS induced by I/R injury. Our findings showed the protective effect of gallic acid on gastric mucosa against ischemia-reperfusion injury. This effect of gallic acid was mainly mediated by reducing protein expression of iNOS and caspase-3. (C) 2015 Urmia University. All rights reserved.
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页码:305 / 311
页数:7
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