Dexmedetomidine facilitates the expression of nNOS in the hippocampus to alleviate surgery‑induced neuroinflammation and cognitive dysfunction in aged rats
- Liangyuan Suo
- Mingyu Wang
Affiliations: Department of Anesthesiology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital, Shenyang, Liaoning 110042, P.R. China
- Published online on: July 20, 2021 https://doi.org/10.3892/etm.2021.10470
Copyright: © Suo
et al. This is an open access article distributed under the
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Postoperative cognitive dysfunction (POCD) is a common complication in the postoperative nervous system of elderly patients. Surgery‑induced hippocampal neuroinflammation is closely associated with POCD. Dexmedetomidine (DEX) is an effective α2‑adrenergic receptor agonist, which can reduce inflammation and has neuroprotective effects, thereby improving postoperative cognitive dysfunction. However, the mechanism by which DEX improves POCD is currently unclear. The purpose of the present study was therefore to identify how DEX acted on POCD. Male Sprague Dawley rats with exposed carotid arteries were used to mimic POCD. Locomotor activity was accessed by the open field test and the Morris water maze was performed to estimate spatial learning, memory and cognitive flexibility. Following animal sacrifice, the hippocampus was collected and cell apoptosis was determined by terminal dexynucleotidyl transferase (TdT)‑mediated dUTP nick end labeling staining. Subsequently, the expression of apoptosis‑related proteins Bax, Bcl‑2, cleaved caspase‑3 and cleaved caspase‑9 was determined by western blotting and the concentrations of TNF‑α, IL‑6, IL‑1β and IL‑10 were measured in serum using ELISA. Nitric oxide synthase and neuronal nitric oxide synthase activities in the hippocampus were also measured. The T lymphocyte subsets were analyzed by flow cytometry to evaluate the immune function in each group. Compared with the surgery group, DEX ameliorated POCD by improving cognitive dysfunctions and immune function loss, and attenuated neuroinflammation and neuronal apoptosis.