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Dexmedetomidine Combined with Low-Dose Propofol Declines Learning and Memory Impairment and Neural Cell Injury in
Xiaoxu Yin1, Peng Jiang1, Jing Li2
1Department of Anesthesiology, Huizhou Central People's Hospital, Huizhou, Guangdong 516001, China.
Insights
Dexmedetomidine combined with low-dose propofol improved learning and memory in developing rats. This combination reduced neuroinflammation, oxidative stress, and neuronal apoptosis, offering a safer anesthesia option.
Area of Science:
- Neuroscience
- Anesthesiology
- Developmental Biology
Background:
- General anesthesia in early childhood can impair neurodevelopment, leading to learning and behavioral deficits.
- Existing anesthetics pose risks, necessitating the development of safer alternatives or comprehensive anesthesia strategies.
- Dexmedetomidine (Dex) and propofol (PRO) are commonly used anesthetics, but their impact on developing brains requires further investigation.
Purpose of the Study:
- To investigate the effects of dexmedetomidine (Dex) combined with low-dose propofol (L-PRO) on learning and memory in developing rats.
- To assess the impact of this anesthetic combination on neural cell integrity and function in the hippocampus.
- To explore the underlying mechanisms, including inflammation, oxidative stress, and apoptosis, associated with Dex + L-PRO anesthesia.
Main Methods:
- Eighty Sprague-Dawley rats were divided into Sham, Lipid, L-PRO, and Dex + L-PRO groups.
- Spatial learning and memory were evaluated using the water maze and passive avoidance tests.
- Hippocampal tissue damage, apoptosis, inflammation, oxidative stress, and protein expression (MAPK pathway, neurotrophic factors) were assessed via Nissl staining, TUNEL, ELISA, biochemical assays, qRT-PCR, and Western Blot.
Main Results:
- The Dex + L-PRO group demonstrated significantly improved spatial learning and memory compared to the L-PRO group.
- Dex + L-PRO administration reduced hippocampal neural cell damage, decreased pro-inflammatory cytokines (IL-6, IL-1β, TNF-α), and lowered oxidative stress markers (ROS, MDA).
- This combination upregulated anti-inflammatory cytokine IL-10, antioxidant enzymes (SOD), and neurotrophic factors (BDNF, TrkB, NT-3), while inhibiting the MAPK signaling pathway.
Conclusions:
- Dexmedetomidine combined with low-dose propofol effectively mitigates learning and memory impairments in developing rats.
- This anesthetic regimen significantly reduces neuroinflammation, oxidative stress, and neuronal apoptosis in the hippocampus.
- The findings suggest Dex + L-PRO is a promising anesthesia strategy to protect the developing brain from anesthetic-induced damage.
Background:
General anesthesia in early childhood may affect all aspects of neurodevelopment, resulting in learning and behavior defects. Therefore, there is an urgent need to find safe anesthetics or put forward more comprehensive anesthesia schemes to solve the negative effects caused by existing anesthetics. The objective of this study is to explore the impact of dexmedetomidine (Dex) incorporated with low-dose propofol (PRO) on learning and memory ability and neural cells in developing rats.
Methods:
Eighty SD rats were randomly divided into 4 groups including the Sham group, Lipid group, L-PRO group, and Dex + L-PRO group. After treatment, the spatial learning and memory ability of rats in each group were assessed by the water maze test and the passive avoidance test. The damage of hippocampal tissues was assessed by Nissl staining; the apoptosis, the levels of inflammatory factors, and the level of oxidative stress were measured by Tunel staining, ELISA, and biochemical assays, respectively. Besides, qRT-PCR and Western Blot determined the expression of apoptosis-related proteins, neurotrophic factors, and MAPK signaling pathway-related proteins in the hippocampus.
Results:
Compared with the L-PRO group, the Dex + L-PRO group had better spatial learning and memory ability. Administration of Dex and L-PRO greatly alleviated neural cell damage in the hippocampus and decreased the levels of IL-6, IL-1β, and TNF-α. Besides, it significantly decreased the content of ROS and malondialdehyde (MDA), glutathione (GSH), when up-regulating the levels of IL-10, antioxidant superoxide dismutase (SOD) and BDNF, receptor tyrosine kinase B (TrkB), and neurotrophin-3 (NT-3) related to hearing function and significantly lower activity of MAPK signaling pathway.
Conclusion:
Dex combined with low-dose PRO can significantly inhibit inflammation, oxidative stress response, neuronal apoptosis, MAPK signaling pathway activity and promote the secretion of neurokines in hippocampus to reduce neural cell damage and avoid the learning and memory impairment caused by anesthetics in developing rats.
