Expression of NF-?B and ICAM-1 in rat′s retina injured by ischemia-reperfusion and the effect of pyrrolidine dithiocarbamate on the expression / 中华眼底病杂志
Chinese Journal of Ocular Fundus Diseases
; (6)2001.
Article
in Chinese
| WPRIM (Western Pacific)
| ID: wpr-522552
Responsible library:
WPRO
ABSTRACT
Objective To investigate the expression of nuclear factor(NF)-?B and intercellular adhesion molecule (ICAM)-1 in rat′s retina injured by ischemia-reperfusion, and the effect of pyrrolidine dithiocarbamate (PDTC) on the expression of NF-?B and ICAM-1. Methods The model of retinal ischemia-reperfusion was set up in 60 SD rats, which were divided into two groups with 30 rats in each ischemia-reperfusion group and ischemia-reperfussion with injection of PDTC group. The left cephalic artery of each rat was ligated, and the right side was the control. Every group was subdivided into group 1 hour, 6, 12, 24, 48, and 72 hours after ischemia-reperfusion injury, and with 5 rats in each group. mRNA of NF-?B and ICAM-1 mRNA was measured by in situ hybridization (ISH) method in rat′s retina. Every rat underwent electroretinography (ERG) at the corresponding time before executed by neck breaking. Results In ischemia-reperfusion group, expression of NF-?B and ICAM-1 was detected at the 6th hour after ischemia-reperfusion, reached the highest level at the 24th hour, and weakened gradually later. In ischemia-reperfusion with injection of PDTC group, expression of NF-?B and ICAM-1 was detected at the 12th hour after ischemia-reperfusion, and reached the highest level at the 24th hour but lower than that in ischemia-reperfusion group. No expression of NF-?B and ICAM-1 was found in the control group. The relative recovery rate of ERG a and b wave amplitude in ischemia-reperfusion groups was lower than that in ischemia-reperfusion with injection of PDTC group at every stage(P
Full text:
Available
Database:
WPRIM (Western Pacific)
Type of study:
Prognostic study
Language:
Chinese
Journal:
Chinese Journal of Ocular Fundus Diseases
Year:
2001
Document type:
Article