Diabetes mellitus aggravates cerebral ischemia-reperfusion injury in rats by inflammatory response
10.3760/cma.j.issn.1673-4165.2015.05.005
- VernacularTitle:糖尿病通过炎症反应加重大鼠脑缺血再灌注损伤
- Author:
Chengling LIU
;
Jiangquan HAN
;
Yongtao HU
- Publication Type:Journal Article
- Keywords:
Brain Ischemia;
Diabetes Melitus,Experimental;
Reperfusion Injury;
TumorNecrosis Factor-α;
NF-κB;
Inflammation;
Rats
- From:
International Journal of Cerebrovascular Diseases
2015;(5):349-353
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the roles of tumor necrosisfactor-α(TNF-α) and nuclear factor-κB (NF-κB) in cerebral ischemia-reperfusion injury in rats w ith diabetes mel itus. Methods Thirty-six healthy male Sprague-Daw ley rats w ere divided into a euglycemic sham operation group, a euglycemic isc hemia-reperfusion group, and a diabetes ischemia-reperfusion group (n=12 in each group) according to a random number table. A diabetes model w as induced by intraperitoneal injection of streptozotocin, and then a focal cerebral ischemia-reperfusion model w as induced by the suture method. The neurological deficit score was performed at 24 h after reperfusion. 2,3,5 triphenyl tetrazolium staining was used to measure the cerebral infarction area. Western blotting w as used to detect the expression levels of NF-κB and TNF-αon the ischemic sides. Results The neurological function scores w ere 0.00 ±0.00, 2.50 ±1.08, and 3.20 ± 1.03, respectively in the euglycemic sham operation, euglycemic cerebral ischemia-reperfusion and diabetes cerebral ischemia-reperfusion groups, and there w ere significant differences (F=38.015, P<0.001). The neurological deficit scores of the diabetes cerebral ischemia-reperfusion group w ere significantly aggravated compared with the euglycemic cerebral ischemia-reperfusion group (P<0.05). The infarct areas of the euglycemic sham operation, euglycemic cerebral ischemia-reperfusion and diabetes cerebral ischemia-reperfusion groups w ere 0.00% ±0.00%, 33.09% ±5.17%, and 55.45% ±9.29%, respectively, and there w ere significant differences among the groups (F=206.614, P<0.001), in w hich the infarct area in the diabetes cerebral ischemia-reperfusion group w as enlarged significantly compared w ith the euglycemic cerebral ischemia-reperfusion group ( P< 0.05 ). At 24 h after reperfusion, there w ere no significant differences in the expression levels of the cortical NF-κB (F=29.993, P<0.001) and TNF-α(F=28.722, P<0.001) on the ischemic sides in each group, in w hich the expression levels of NF-κB and TNF-αin the diabetes cerebral ischemia-reperfusion group w ere increased significantly compared w ith the euglycemic cerebral ischemia-reperfusion group (al P<0.05). Conclusions Diabetes may aggravate cerebral ischemia reperfusion injury. The upregulated expression of TNF-αand NF-κB may be one of the mechanisms of diabetes aggravating cerebral ischemia-reperfusion injury.