Role of hippocampal AMPK signaling pathway in reduction of postoperative cognitive dysfunction by stellate ganglion block in aged rats
Bin Wang, Gaofeng Zhang, Zeng Yin, Huailong Chen, Lixin Sun, Fei Shi, Mingshan Wang
Abstract
Bin Wang, Gaofeng Zhang, Zeng Yin, Huailong Chen, Lixin Sun, Fei Shi, Mingshan Wang
Abstract
Objective To evaluate the role of hippocampal AMP-activated protein kinase(AMPK)signaling pathway in reduction of postoperative cognitive dysfunction(POCD)by stellate ganglion block(SGB)in aged rats. Methods One hundred and twenty male Sprague-Dawley rats, aged 18-22 months, weighing 450-550 g, were randomly divided into 5 groups(n=24 each)using a random number table: sham operation group(group S); group POCD; group SGB; SGB + AMPK inhibitor group(group SI); AMPK inhibitor group(group AI). SGB was performed with 0.25% bupivacaine 0.15 ml in POCD, SGB and SI groups.Operation was performed at 15 min after the end of administration.Compound C(AMPK inhibitor)20 mg/kg was injected intraperitoneally at the end of surgery in groups SI and AI.Morris water maze test was performed at 1 day before operation and on 1, 3 and 5 days after operation.The escape latency and swimming distance were recorded.The rats were then sacrificed, and the brains were removed for determination of the expression of AMPK and phosphorylated AMPK(p-AMPK)by Western blot. Results Compared with group S, the escape latency and swimming distance were significantly prolonged, and the expression of AMPK and p-AMPK was down-regulated in POCD, SI and AI groups.Compared with group POCD, the escape latency and swimming distance were significantly shortened, and the expression of AMPK and p-AMPK was up-regulated in group SGB.Compared with group SGB, the escape latency and swimming distance were significantly prolonged, and the expression of AMPK and p-AMPK was down-regulated in SI and AI groups. Conclusion Activation of hippocampal AMPK signaling pathway is involved in SGB-induced reduction of POCD in aged rats. Key words: Protein-serine-threonine kinases; Stellate ganglion; Nerve block; Aged; Cognition disorders; Postoperative complications
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Objective To evaluate the role of hippocampal AMP-activated protein kinase(AMPK)signaling pathway in reduction of postoperative cognitive dysfunction(POCD)by stellate ganglion block(SGB)in aged rats. Methods One hundred and twenty male Sprague-Dawley rats, aged 18-22 months, weighing 450-550 g, were randomly divided into 5 groups(n=24 each)using a random number table: sham operation group(group S); group POCD; group SGB; SGB + AMPK inhibitor group(group SI); AMPK inhibitor group(group AI). SGB was performed with 0.25% bupivacaine 0.15 ml in POCD, SGB and SI groups.Operation was performed at 15 min after the end of administration.Compound C(AMPK inhibitor)20 mg/kg was injected intraperitoneally at the end of surgery in groups SI and AI.Morris water maze test was performed at 1 day before operation and on 1, 3 and 5 days after operation.The escape latency and swimming distance were recorded.The rats were then sacrificed, and the brains were removed for determination of the expression of AMPK and phosphorylated AMPK(p-AMPK)by Western blot. Results Compared with group S, the escape latency and swimming distance were significantly prolonged, and the expression of AMPK and p-AMPK was down-regulated in POCD, SI and AI groups.Compared with group POCD, the escape latency and swimming distance were significantly shortened, and the expression of AMPK and p-AMPK was up-regulated in group SGB.Compared with group SGB, the escape latency and swimming distance were significantly prolonged, and the expression of AMPK and p-AMPK was down-regulated in SI and AI groups. Conclusion Activation of hippocampal AMPK signaling pathway is involved in SGB-induced reduction of POCD in aged rats. Key words: Protein-serine-threonine kinases; Stellate ganglion; Nerve block; Aged; Cognition disorders; Postoperative complications
Key concepts: AMPK, Western blot, Protein kinase A, Medicine, Postoperative cognitive dysfunction, Hippocampal formation, Internal medicine, Endocrinology