Postoperative cognitive dysfunction (POCD) is a serious central nervous system complication characterized by impaired memory, reduced information processing ability, and anxiety. Recently, the role of FGF19 in neurological diseases has been reported. However, the effect and mechanisms of FGF19 in improving symptoms of POCD remain unknown. This study aimed to identify the role and exploring the underlying mechanisms of FGF19 in POCD. Here, rats were separated into four different groups, including control, sevoflurane (sev), sev + AAV-empty, and sev + AAV-FGF19 group. Then, the Morris water maze (MWM) test was applied to identify the effect of FGF19 on POCD rats. The result proved that FGF19 improved sevoflurane induced cognitive dysfunction in rats. Subsequently, the expressions of TNF-α, IL-6, IL-1β, and IL-10 were detected to verify the anti-neuroinflammatory effects of FGF19 in POCD rats. Furthermore, DHE fluorescent staining assay showed that FGF19 could inhibit sevoflurane-induced oxidative stress in POCD rats. Besides, NISSL staining and TUNEL assay were applied to reveal that FGF19 could alleviate hippocampal neuron injury induced by sevoflurane in rats. Moreover, mechanistic studies confirmed that FGF19 improved symptoms of POCD by mediated PGC-1α/BDNF/FNDC5 pathway. Together, these results suggested that FGF19 improves sevoflurane-induced POCD in rats through the PGC-1α/BDNF/FNDC5 pathway.
Keywords: BDNF; FGF19; FNDC5; PGC-1α; POCD.
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