Experimental study on the effects of dexmedetomidine via the mTOR signaling pathway on cognitive function in POCD rats after partial hepatectomy.

BACKGROUND

Postoperative cognitive dysfunction (POCD) frequently occurs after liver resection and is potentially mediated by the mTOR signaling pathway. Although dexmedetomidine, an α2 receptor agonist, exhibits neuroprotective effects, it remains unknown whether it improves post-resection cognitive function by modulating the mTOR pathway.

OBJECTIVES

To discuss the influence of dexmedetomidine on the mTOR signaling pathway in the hippocampus of POCD rats after partial hepatectomy.

METHODS

Thirty Wistar rats were randomly divided into three equal groups: normal, model and treatment. The treatment group received dexmedetomidine, whereas the other two groups received saline. Histopathology, cognitive function and related gene/protein expression were compared among groups received saline.

RESULTS

The treatment group showed improved hippocampal neuronal structure and arrangement compared to the model group, though still below normal levels; neural apoptosis was significantly reduced (P<0.05), and spatial learning and memory were enhanced; Akt expression was partially restored, while mTOR, NF-κB and TNF-α expression (protein/mRNA) remained higher than normal but significantly lower than in the model group (P<0.05).

CONCLUSION

Dexmedetomidine ameliorates postoperative cognitive dysfunction in rats after liver resection by inhibiting the hippocampal mTOR pathway, reducing neuronal damage and inflammation.