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Apamin, an SK2 Inhibitor, Attenuated Neonatal Sevoflurane Exposures Caused Cognitive Deficits in Mice through the
Heying Zhong1, Xiaojuan Ran2, Bin Chen3
1Department of Anesthesiology, Affiliated Huadu Hospital, Southern Medical University (People's Hospital of Huadu District), Guangzhou 510000, Guangdong, China.
Insights
Apamin treatment can protect infant mice from anesthesia-induced cognitive deficits and neuronal injury. This study shows Apamin regulates neuroinflammation in the hippocampus, offering a potential therapeutic strategy for anesthesia-related cognitive issues.
Area of Science:
- Neuroscience
- Anesthesiology
- Pharmacology
Background:
- Infant anesthesia can cause cognitive dysfunction, a significant clinical concern with unclear mechanisms and treatments.
- Neonatal exposure to anesthetics like sevoflurane poses risks to cognitive development.
- Neuroinflammation in the hippocampus is implicated in anesthesia-induced cognitive deficits.
Purpose of the Study:
- To investigate the protective effects of Apamin against sevoflurane-induced cognitive impairment in neonatal mice.
- To explore the underlying mechanisms of Apamin's action, focusing on hippocampal neuroinflammation and microglial polarization.
Main Methods:
- Neonatal C57BL/6 mice were exposed to sevoflurane, with some receiving hippocampal injections of Apamin.
- Cognitive function was assessed using behavioral tests such as object location memory and novel object recognition.
- Hippocampal tissue was analyzed using qRT-PCR, ELISA, and Western blotting to evaluate protein levels and microglial activation (M1/M2 polarization).
Main Results:
- Apamin administration significantly mitigated sevoflurane-induced cognitive impairment and neuronal injury in mice.
- Apamin reduced sevoflurane-induced microglial activation in the hippocampus.
- Apamin inhibited M1-type and promoted M2-type microglial polarization following neonatal sevoflurane exposure.
Conclusions:
- Apamin attenuates cognitive deficits caused by neonatal sevoflurane exposure in mice.
- Apamin exerts its protective effects by modulating hippocampal neuroinflammation and microglial polarization.
- Apamin represents a potential therapeutic agent for preventing anesthesia-induced cognitive impairment in infants.
Abstract:
Cognitive dysfunction induced by anesthesia in the infant is a crucial clinical issue that is still being debated and the focus of concern for the parents. However, the mechanism of cognitive decline caused by anesthesia and the corresponding treatment methods remain unclear. Postnatal day 7 (PND7) C57BL/6 mice included in the study were randomly divided into a control group (Control), a group with repeated exposure to sevoflurane (Sevo), and an Apamin intervention group (Sevo + Apamin). Apamin (0.5 μL at the concentration of 100 nmol/L) was injected into the bilateral hippocampus of mice. qRT-PCR, enzyme-linked immunosorbent assay (ELISA), and western blotting assay were used to evaluate the protein levels in the hippocampus. Object location memory (OLM) and novel object recognition (NOR) tasks, as well as elevated plus maze and contextual and cued fear conditioning tasks were used to evaluate the cognitive function of mice. Apamin mitigated sevoflurane-induced cognitive impairment of mice, sevoflurane-induced neuronal injury, and sevoflurane-induced activation of microglial in the hippocampus of the mice. Apamin inhibited M1-type polarization but promoted M2-type polarization of microglia after neonatal sevoflurane exposures in the hippocampus. In conclusion, Apamin attenuates neonatal sevoflurane exposures that cause cognitive deficits in mice through regulating hippocampal neuroinflammation.
