PMID- 17914952
OWN - NLM
STAT- MEDLINE
DCOM- 20080118
LR  - 20220317
IS  - 0815-9319 (Print)
IS  - 0815-9319 (Linking)
VI  - 22
IP  - 11
DP  - 2007 Nov
TI  - In vivo and in vitro antioxidant activity of ghrelin: Attenuation of gastric 
      ischemic injury in the rat.
PG  - 1791-9
AB  - BACKGROUND AND AIM: Gherlin, an endogenous ligand for the growth hormone 
      secretagogue receptor (GHS-R), is produced by stomach cells. It regulates food 
      intake, gastric secretion and motility. However, its role as a protective agent 
      in gastric ischemia/reperfusion (I/R) injury has not yet been investigated. 
      Therefore, the objectives of the present study were to: (i) test the in vivo 
      effect of peripherally administered ghrelin on gastric I/R-induced lesions in 
      rats; and (ii) investigate in vitro the effect of ghrelin on reactive oxygen 
      species (ROS) production by human polymorphoneuclear (PMN) cells. METHODS: The 
      present study was carried out on three groups of rats (six per group): control 
      (sham-operated), I/R (clamping of celiac artery for 30 min and reperfusion for 1 
      h), and I/R + ghrelin (200 ng/kg i.v., 15 min before ischemia and before 
      reperfusion, respectively). Histological assessment of hematoxylin and eosin 
      stained sections was performed and immunostaining with inducible nitric oxide 
      (iNOS) antibody were performed on a gastric paraffin embedded section. Oxidative 
      stress markers thiobarbituric acid reactive substance (TBARS) and glutathione 
      (GSH) were measured in gastric tissue homogenates. Serum lactic acid 
      dehydrogenase (LDH) was determined. Tumor necrosis factor-alpha (TNF-alpha) was 
      assayed in gastric tissue homogenate. Gastric permeability was assessed 
      calorimetrically using Evans blue dye. In vitro studies were carried out on 
      isolated human PMN cells incubated with ghrelin and tested for ROS generation as 
      measured by chemiluminecence (CL). RESULTS: Peripheral administration of ghrelin 
      attenuated gastric injury by reducing ulceration, tissue congestion, cellular 
      infiltration and vascular permeability. Serum level of LDH and tissue content of 
      TNF-alpha were markedly reduced. A decrement in TBARS and an increment in GSH 
      were observed. Ghrelin treatment attenuated iNOS protein expression which was 
      upregulated by gastric ischemic injury. In vitro studies showed for the first 
      time that ghrelin inhibited ROS generation by human PMN in a dose-dependent 
      manner. CONCLUSIONS: These results provide evidence that peripherally 
      administered ghrelin protects against gastric I/R injury. We also demonstrated 
      that this protection is possibly accomplished through the antioxidant activity of 
      ghrelin observed in vivo and in vitro.
FAU - El Eter, Eman
AU  - El Eter E
AD  - Department of Physiology, Medical College, King Saud University, Riyadh, Saudi 
      Arabia. emaneleter60@hotmail.com
FAU - Al Tuwaijiri, Ali
AU  - Al Tuwaijiri A
FAU - Hagar, Hanan
AU  - Hagar H
FAU - Arafa, Maha
AU  - Arafa M
LA  - eng
PT  - Journal Article
PL  - Australia
TA  - J Gastroenterol Hepatol
JT  - Journal of gastroenterology and hepatology
JID - 8607909
RN  - 0 (Antioxidants)
RN  - 0 (Ghrelin)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, rat)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Antioxidants/administration & dosage/*metabolism
MH  - Capillary Permeability/drug effects
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Gastric Mucosa/metabolism
MH  - Ghrelin/administration & dosage/*metabolism
MH  - Glutathione/metabolism
MH  - Humans
MH  - In Vitro Techniques
MH  - Injections, Intravenous
MH  - L-Lactate Dehydrogenase/blood
MH  - Leukocytes, Mononuclear/drug effects/*metabolism
MH  - Male
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - *Oxidative Stress/drug effects
MH  - Rats
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/metabolism
MH  - Reperfusion Injury/metabolism/pathology/*prevention & control
MH  - Stomach/blood supply/*drug effects/pathology
MH  - Thiobarbituric Acid Reactive Substances/metabolism
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/blood
EDAT- 2007/10/05 09:00
MHDA- 2008/01/19 09:00
CRDT- 2007/10/05 09:00
PHST- 2007/10/05 09:00 [pubmed]
PHST- 2008/01/19 09:00 [medline]
PHST- 2007/10/05 09:00 [entrez]
AID - JGH4696 [pii]
AID - 10.1111/j.1440-1746.2006.04696.x [doi]
PST - ppublish
SO  - J Gastroenterol Hepatol. 2007 Nov;22(11):1791-9. doi: 
      10.1111/j.1440-1746.2006.04696.x.