title: Octreotide Protects the Mouse Retina against Ischemic Reperfusion Injury through Regulation of Antioxidation and Activation of NF-κB.
abstract: Somatostatin (SST), an endogenous peptide, may exert anti-inflammatory and neuroprotective effects on retinal injury induced by ischemia. Retinal ischemic reperfusion (I/R) injury always produces many reactive oxygen species (ROS), which can aggravate the tissue damage. The effects of octreotide (OCT), a SST analogue, on retinal I/R injury and ROS formation, are not very clear. In this study, we observed the effects of OCT on morphological changes, oxidative stress, and cell death, induced by retinal I/R injury. The activation of nuclear factor κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) were further evaluated in I/R retina treated with or without OCT. The retinal layer thickness was increased at 1 day after I/R and decreased at 7 days after I/R (P < 0.05). This effect was associated with increase in MDA and ROS levels (P < 0.05). The Tunel-positive cells increased and the number of ganglion cell layer (GCL) neurons decreased significantly after I/R injury. The expression of p-p65 and ICAM-1 increased significantly in I/R retinas (P < 0.05). Each effect was markedly attenuated by application of OCT. These data indicate that OCT protects the retina against retinal I/R damage, which could be through inhibition of oxidative stress and downregulation of NF-κB and ICAM-1 expression.
authors.affiliation: Medical College of Henan University, Kaifeng 475004, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.affiliation: Medical College of Henan University, Kaifeng 475004, China.
authors.forename: Ziqiang
authors.initials: Z
authors.lastname: Sun
authors.affiliation: Medical College, Henan Polytechnic University, Jiaozuo 454000, China.
authors.forename: Junsheng
authors.initials: J
authors.lastname: Shen
authors.affiliation: Medical College of Henan University, Kaifeng 475004, China.
authors.forename: Dongdong
authors.initials: D
authors.lastname: Wu
authors.affiliation: The First Affiliated Hospital of Henan University, Kaifeng 475001, China.
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.affiliation: The First Affiliated Hospital of Henan University, Kaifeng 475001, China.
authors.forename: Ruisheng
authors.initials: R
authors.lastname: Yang
authors.affiliation: Medical College of Henan University, Kaifeng 475004, China.
authors.forename: Shaoping
authors.initials: S
authors.lastname: Ji
authors.affiliation: Medical College of Henan University, Kaifeng 475004, China.
authors.forename: Ailing
authors.initials: A
authors.lastname: Ji
authors.affiliation: Medical College of Henan University, Kaifeng 475004, China.
authors.forename: Yanzhang
authors.initials: Y
authors.lastname: Li
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D017209:Apoptosis / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004195:Disease Models, Animal; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D015282:Octreotide / Q000494:pharmacology* / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects; D020011:Protective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D012160:Retina / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D012164:Retinal Diseases / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D020011:Protective Agents; D017382:Reactive Oxygen Species; D051996:Transcription Factor RelA; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D015282:Octreotide