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C1q/tumor necrosis factor (TNF)-associated protein 6 (CTRP6) ameliorates the cognitive dysfunction induced by sevoflurane by activating AMPK/SIRT1 pathway in rats
Abstract
Purpose: To evaluate the possible effects of C1q/tumor necrosis factor (TNF)-associated protein 6 (CTRP6) on postoperative cognitive dysfunction (POCD), including the potentially-related signaling pathway.
Methods: Behavioral analysis and cognitive impairment were assessed in each group. Immunoblots were used to determine the level of CTRP6 following sevoflurane-induced nerve injury. Hippocampal neurons were identified using Nissl staining, while inflammatory response following neuronal injury was monitored by enzyme-linked immunosorbent assay (ELISA) and quantitative polymerase chain reaction (qPCR). The involvement of adenosine monophosphate-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) pathway was determined using immunoblot.
Results: CTRP6 alleviated sevoflurane-induced cognitive dysfunction in rats (p < 0.001). Moreover, CTRP6 reduced sevoflurane-induced nerve injury and inflammation in rats (p < 0.05).
Conclusion: CTRP6 ameliorates sevoflurane-induced cognitive dysfunction by activating AMPK/SIRT1 pathway, thus offering a novel target for POCD treatment.