TY - JOUR
T1 - Ischemia-reperfusion injury causes oxidative stress and apoptosis of Schwann cell in acute and chronic experimental diabetic neuropathy
AU - Wang, Yanping
AU - Schmeichel, Ann M.
AU - Iida, Haruyasu
AU - Schmelzer, James D.
AU - Low, Phillip A.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2005/11
Y1 - 2005/11
N2 - Mild ischemia-reperfusion (IR) injury to diabetic peripheral nerve is known to cause severe ischemic fiber degeneration. Little information is available on its effects on Schwann cell (SC). In this study, we evaluated oxidative stress and apoptosis of SC following mild IR, using immunohistochemistry in streptozotocin (STZ)-induced diabetic rats. Twenty-six rats were divided into four groups according to the duration of diabetes: 1-month STZ-induced diabetic group (n = 7) and age-matched control group (n = 7); 4-month STZ-induced diabetic group (n = 6) and age-matched control group (n = 6). Using our established IR model of 3 h of ischemia followed by 7 days of reperfusion, sciatic and tibial nerves were harvested and labeled with 8- hydroxydeoxyguanosine (8-OHdG; oxidative stress marker), caspase-3 (apoptotic executor), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) activity (apoptotic indicator). Marked positive staining with 8-OHdG, caspase-3, and TUNEL were found in diabetic ischemic nerves (right side) following IR in both 1-month and 4-month groups. Only mild positive staining or no staining was seen in the nonischemic side (left side) of diabetic and age-matched control groups. Co-labeling with S-100 confirmed that the cells labeled with 8-OHdG, caspaseS, and TUNEL were SC. SC was susceptible to oxidative injury and apoptosis in experimental diabetic neuropathy when subjected to mild IR injury.
AB - Mild ischemia-reperfusion (IR) injury to diabetic peripheral nerve is known to cause severe ischemic fiber degeneration. Little information is available on its effects on Schwann cell (SC). In this study, we evaluated oxidative stress and apoptosis of SC following mild IR, using immunohistochemistry in streptozotocin (STZ)-induced diabetic rats. Twenty-six rats were divided into four groups according to the duration of diabetes: 1-month STZ-induced diabetic group (n = 7) and age-matched control group (n = 7); 4-month STZ-induced diabetic group (n = 6) and age-matched control group (n = 6). Using our established IR model of 3 h of ischemia followed by 7 days of reperfusion, sciatic and tibial nerves were harvested and labeled with 8- hydroxydeoxyguanosine (8-OHdG; oxidative stress marker), caspase-3 (apoptotic executor), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) activity (apoptotic indicator). Marked positive staining with 8-OHdG, caspase-3, and TUNEL were found in diabetic ischemic nerves (right side) following IR in both 1-month and 4-month groups. Only mild positive staining or no staining was seen in the nonischemic side (left side) of diabetic and age-matched control groups. Co-labeling with S-100 confirmed that the cells labeled with 8-OHdG, caspaseS, and TUNEL were SC. SC was susceptible to oxidative injury and apoptosis in experimental diabetic neuropathy when subjected to mild IR injury.
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U2 - 10.1089/ars.2005.7.1513
DO - 10.1089/ars.2005.7.1513
M3 - Article
C2 - 16356115
AN - SCOPUS:28844459978
SN - 1523-0864
VL - 7
SP - 1513
EP - 1520
JO - Antioxidants and Redox Signaling
JF - Antioxidants and Redox Signaling
IS - 11-12
ER -