Na Zhang1, Gen-Yang Cheng2, Xian-Zhi Liu1, Feng-Jiang Zhang1. 1. Department of Neurosurgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. 2. Department of Nephrology, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. Electronic address: chengrooter@163.com.
Abstract
OBJECTIVE: To investigate the effect of acute renal ischemia reperfusion on brain tissue. METHODS: Fourty eight rats were randomly divided into four groups (n=12): sham operation group, 30 min ischemia 60 min reperfusion group, 60 min ischemia 60 min reperfusion group, and 120 min ischemia 60 min reperfusion group. The brain tissues were taken after the experiment. TUNEL assay was used to detect the brain cell apoptosis, and western blot was used to detect the expression of apoptosis-related proteins and inflammatory factors. RESULTS: Renal ischemia-reperfusion induced apoptosis of brain tissues, and the apoptosis increased with prolongation of ischemia time. The detection at the molecular level showed decreased Bcl-2 expression, increased Bax expression, upregulated expression of NF-κB and its downstream factor COX-2/PGE2. CONCLUSIONS: Acute renal ischemia-reperfusion can cause brain tissue damage, manifested as induced brain tissues apoptosis and inflammation activation.
OBJECTIVE: To investigate the effect of acute renal ischemia reperfusion on brain tissue. METHODS: Fourty eight rats were randomly divided into four groups (n=12): sham operation group, 30 min ischemia 60 min reperfusion group, 60 min ischemia 60 min reperfusion group, and 120 min ischemia 60 min reperfusion group. The brain tissues were taken after the experiment. TUNEL assay was used to detect the brain cell apoptosis, and western blot was used to detect the expression of apoptosis-related proteins and inflammatory factors. RESULTS:Renal ischemia-reperfusion induced apoptosis of brain tissues, and the apoptosis increased with prolongation of ischemia time. The detection at the molecular level showed decreased Bcl-2 expression, increased Bax expression, upregulated expression of NF-κB and its downstream factor COX-2/PGE2. CONCLUSIONS:Acute renal ischemia-reperfusion can cause brain tissue damage, manifested as induced brain tissues apoptosis and inflammation activation.