PubMed:21435143 JSONTXT

{"project":"Allie","denotations":[{"id":"SS1_21435143_2_0","span":{"begin":149,"end":163},"obj":"expanded"},{"id":"SS2_21435143_2_0","span":{"begin":165,"end":168},"obj":"abbr"},{"id":"SS1_21435143_2_1","span":{"begin":189,"end":202},"obj":"expanded"},{"id":"SS2_21435143_2_1","span":{"begin":204,"end":208},"obj":"abbr"}],"relations":[{"id":"AE1_21435143_2_0","pred":"abbreviatedTo","subj":"SS1_21435143_2_0","obj":"SS2_21435143_2_0"},{"id":"AE1_21435143_2_1","pred":"abbreviatedTo","subj":"SS1_21435143_2_1","obj":"SS2_21435143_2_1"}],"text":"α-Lipoic acid normalizes nociceptive neuronal activity at the spinal cord of diabetic rats.\nAIM: To evaluate the effects of antioxidant treatment of streptozotocin (STZ)-diabetic rats with α-lipoic acid (α-LA) in neuronal and microglial activation at the spinal cord, an important relay station of nociceptive transmission. Because of the role of the potassium chloride co-transporter 2 (KCC2) in neuronal activation at the spinal cord and the influence of microglia in KCC2 expression, we also evaluated the effects of α-LA in KCC2 expression at the spinal cord.\nMETHODS: Four weeks after STZ injection, the rats received daily intraperitoneal injections of α-LA (100 mg/kg), during 2 weeks. Mechanical nociception was evaluated before and after α-LA treatment. Spinal cords were immunoreacted against 8-OH-dG (marker of oxidative stress damage), Fos (marker of neuronal activation) and CD11b (marker of microglia). KCC2 expression was evaluated by immunohistochemistry and western blotting.\nRESULTS: Treatment with α-LA decreased the 8-OH-dG and Fos expressions to controls' levels, but did not affect CD11b. Treatment with α-LA alleviated mechanical hyperalgesia and partially corrected KCC2 expression.\nCONCLUSIONS: This study shows that neuronal hyperactivity at the spinal cord of STZ-diabetic rats can be corrected by α-LA, which may account for alleviation of mechanical hyperalgesia. These effects are probably partially mediated by KCC2, but are independent from microglia."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":533,"end":562},"obj":"HP_0006333"}],"text":"α-Lipoic acid normalizes nociceptive neuronal activity at the spinal cord of diabetic rats.\nAIM: To evaluate the effects of antioxidant treatment of streptozotocin (STZ)-diabetic rats with α-lipoic acid (α-LA) in neuronal and microglial activation at the spinal cord, an important relay station of nociceptive transmission. Because of the role of the potassium chloride co-transporter 2 (KCC2) in neuronal activation at the spinal cord and the influence of microglia in KCC2 expression, we also evaluated the effects of α-LA in KCC2 expression at the spinal cord.\nMETHODS: Four weeks after STZ injection, the rats received daily intraperitoneal injections of α-LA (100 mg/kg), during 2 weeks. Mechanical nociception was evaluated before and after α-LA treatment. Spinal cords were immunoreacted against 8-OH-dG (marker of oxidative stress damage), Fos (marker of neuronal activation) and CD11b (marker of microglia). KCC2 expression was evaluated by immunohistochemistry and western blotting.\nRESULTS: Treatment with α-LA decreased the 8-OH-dG and Fos expressions to controls' levels, but did not affect CD11b. Treatment with α-LA alleviated mechanical hyperalgesia and partially corrected KCC2 expression.\nCONCLUSIONS: This study shows that neuronal hyperactivity at the spinal cord of STZ-diabetic rats can be corrected by α-LA, which may account for alleviation of mechanical hyperalgesia. These effects are probably partially mediated by KCC2, but are independent from microglia."}