Neuroscience letters · 2025
Dexmedetomidine improves postoperative cognitive dysfunction via regulating Adrb2/Pkg: Dexmedetomidine against postoperative cognitive dysfunction.
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Chen Cuirong, Han Hong, Li Hongzhe, Zhang Zitan, Lv Yingbing
Аннотация
BACKGROUND: Postoperative cognitive dysfunction (POCD) refers to postoperative neurological complications in patients, thus affecting patients' normal daily life.
PURPOSE: Our study aimed to confirm whether Adrb2/Pkg are involved in the protective effect of Dexmedetomidine (Dex) against POCD in rats.
METHODS: The targets for Dex against POCD were screened by online databases. An POCD rat model was constructed, and the Morris water maze tests were conducted to evaluate the cognitive function of POCD rats. The inflammatory markers (IL-6, TNF-α, and IL-13) were recorded, and the levels of Adrb2 and Pkg in hippocampus tissue were detected using RT-qPCR. The key targets Adrb2/Pkg were verified through the LPS-induced inflammatory BV-2 cell model.
RESULTS: Network pharmacology analysis predicted that Adrb2 and Pkg were the key genes of Dex against POCD. Dex treatment improved learning and memory skills of POCD rats. In vitro and in vivo experiments showed that Dex treatment alleviated inflammation, and upregulated Adrb2 and Pkg mRNA levels of POCD rats and inflammatory BV-2 cell line. Silencing Adrb2/Pkg reversed the apoptosis suppression in LPS-induced inflammatory BV-2 cells caused by Dex.
CONCLUSION: The Adrb2/Pkg could potentially be the mechanism by which Dex protects POCD rats from cognitive impairment.
PURPOSE: Our study aimed to confirm whether Adrb2/Pkg are involved in the protective effect of Dexmedetomidine (Dex) against POCD in rats.
METHODS: The targets for Dex against POCD were screened by online databases. An POCD rat model was constructed, and the Morris water maze tests were conducted to evaluate the cognitive function of POCD rats. The inflammatory markers (IL-6, TNF-α, and IL-13) were recorded, and the levels of Adrb2 and Pkg in hippocampus tissue were detected using RT-qPCR. The key targets Adrb2/Pkg were verified through the LPS-induced inflammatory BV-2 cell model.
RESULTS: Network pharmacology analysis predicted that Adrb2 and Pkg were the key genes of Dex against POCD. Dex treatment improved learning and memory skills of POCD rats. In vitro and in vivo experiments showed that Dex treatment alleviated inflammation, and upregulated Adrb2 and Pkg mRNA levels of POCD rats and inflammatory BV-2 cell line. Silencing Adrb2/Pkg reversed the apoptosis suppression in LPS-induced inflammatory BV-2 cells caused by Dex.
CONCLUSION: The Adrb2/Pkg could potentially be the mechanism by which Dex protects POCD rats from cognitive impairment.