Dexmedetomidine protects aged rats from postoperative cognitive dysfunction by alleviating hippocampal inflammation
Nianping Chen, Xiufang Chen, Jianping Xie, Chenglong Wu, Jiang X. Qian
Abstract
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Nianping Chen, Xiufang Chen, Jianping Xie, Chenglong Wu, Jiang X. Qian
Abstract
Open-access reader
The present study investigated the effect of dexmedetomidine on hippocampal inflammation and cognitive function in rats with postoperative cognitive dysfunction (POCD). A total of 80 healthy male Sprague Dawley rats were used, 72 of which developed POCD. The rats were randomly divided into four groups: The control, model, low‑dose and high‑dose dexmedetomidine anesthesia groups. A POCD model was established and dexmedetomidine was administered. Cognitive function tests were performed and expression levels of interleukin 1β (IL‑1β), tumor necrosis factor‑α (TNF‑α) and NF‑κB biomarkers were evaluated on the first, third and seventh day following modeling. The cognitive function of rats was measured using a Y‑maze test. The expression levels of IL‑1β and TNF‑α in the hippocampus were determined by ELISA. The protein expression levels of NF‑κB p65 in the hippocampus were determined by western blotting. It was revealed that at 1, 3 and 7 days after surgery, there were no alterations in the exercise ability of rats in the different groups, as reflected by the number of rats passing the alternative arms in the Y‑maze. On the first and third day after surgery, the cognitive dysfunction reflected by the alteration scores of the low‑dose and high‑dose dexmedetomidine anesthesia groups were significantly higher than those of the model group, and the increase in the high‑dose group was more pronounced. Additionally, on the first day after surgery, the expression levels of IL‑1β, TNF‑α and NF‑κB in the hippocampi of rats in the low‑ and high‑dose dexmedetomidine anesthesia groups were significantly lower than those in the model group, and the decrease was more pronounced in the high‑dose group. At 7 days after surgery, the differences in expression levels of IL‑1β, TNF‑α and NF‑κB in the hippocampus among groups were not identified to be statistically significantly different. Taken together, the results of the present study indicated that dexmedetomidine may inhibit hippocampal inflammation induced by surgical trauma, and that dexmedetomidine may effectively improve postoperative cognitive function in rats.
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The present study investigated the effect of dexmedetomidine on hippocampal inflammation and cognitive function in rats with postoperative cognitive dysfunction (POCD). A total of 80 healthy male Sprague Dawley rats were used, 72 of which developed POCD. The rats were randomly divided into four groups: The control, model, low‑dose and high‑dose dexmedetomidine anesthesia groups. A POCD model was established and dexmedetomidine was administered. Cognitive function tests were performed and expression levels of interleukin 1β (IL‑1β), tumor necrosis factor‑α (TNF‑α) and NF‑κB biomarkers were evaluated on the first, third and seventh day following modeling. The cognitive function of rats was measured using a Y‑maze test. The expression levels of IL‑1β and TNF‑α in the hippocampus were determined by ELISA. The protein expression levels of NF‑κB p65 in the hippocampus were determined by western blotting. It was revealed that at 1, 3 and 7 days after surgery, there were no alterations in the exercise ability of rats in the different groups, as reflected by the number of rats passing the alternative arms in the Y‑maze. On the first and third day after surgery, the cognitive dysfunction reflected by the alteration scores of the low‑dose and high‑dose dexmedetomidine anesthesia groups were significantly higher than those of the model group, and the increase in the high‑dose group was more pronounced. Additionally, on the first day after surgery, the expression levels of IL‑1β, TNF‑α and NF‑κB in the hippocampi of rats in the low‑ and high‑dose dexmedetomidine anesthesia groups were significantly lower than those in the model group, and the decrease was more pronounced in the high‑dose group. At 7 days after surgery, the differences in expression levels of IL‑1β, TNF‑α and NF‑κB in the hippocampus among groups were not identified to be statistically significantly different. Taken together, the results of the present study indicated that dexmedetomidine may inhibit hippocampal inflammation induced by surgical trauma, and that dexmedetomidine may effectively improve postoperative cognitive function in rats.
Key concepts: Dexmedetomidine, Postoperative cognitive dysfunction, Hippocampus, Anesthesia, Hippocampal formation, Medicine, Morris water navigation task, Tumor necrosis factor alpha