ArticleJournal of anesthesia and translational medicine2024
Activation of ACE2/Ang-(1-7)/Mas axis improves cognitive dysfunction induced by isoflurane in mice via inhibiting oxidative stress.
Article in Journal of anesthesia and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Neonatal Sevoflurane Exposure Induces Long-Term Cognitive Impairment via Epigenetically Mediated MMP9 Activation and Perineuronal Net Disruption in the Hippocampal CA2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic Reprogramming and Immunometabolic Dysregulation in Diabetic Kidney Disease: From Pathogenesis to Precision Multi-target Therapies.Research (Washington, D.C.) · 2026Review
- Inhibition of Hippocampal Neuronal Ferroptosis by Liproxstatin-1 Improves Learning and Memory Function in Aged Mice with Perioperative Neurocognitive Dysfunction.Journal of inflammation research · 2025Article
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7 authors.
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Abstract
Background: Long-term inhalation anesthesia is known to be associated with postoperative cognitive dysfunction. Our previous studies have confirmed that oxidative stress damage contributes to its mechanistic connection. Angiotensin-converting enzyme 2 (ACE2)/Angiotensin-(1-7)/Mas axis plays a crucial role in balancing the classic Renin-Angiotensin System (RAS) and regulating oxidative stress. This research aims to investigate the involvement of the ACE2/Angiotensin-(1-7)/Mas axis in the development of cognitive impairment induced by long-term isoflurane anesthesia. Methods: 3-month-old male C57BL/6 mice were randomly assigned to four groups: Control + Vehicle (C + Veh), Anesthesia + Vehicle (A + Veh), Control + Diminazene aceturate (C + DIZE), and Anesthesia + Diminazene aceturate (A + DIZE). Long-term isoflurane exposure was utilized to induce cognitive impairment. DIZE was administered intraperitoneally to mice 10 days prior to anesthesia to intervene ACE2. Cognitive function was administered using Y-maze and fear conditioning test. Flow Cytometry was used to measure the levels of ROS. Western blot was used to determine the expression levels of ACE2 and Mas, as well as the cognitive proteins such as phosphorylated N-methyl-D-aspartate receptor subtype 2B (p-NR2B) and Brain-Derived Neurotrophic Factor (BDNF). Results: We successfully constructed a long-term isoflurane anesthesia-mediated cognitive dysfunction model. Following long-term isoflurane anesthesia, there was a decrease in the levels of ACE2 and Mas in the hippocampus, accompanied by increased oxidative stress and significant cognitive impairment. Treatment with the ACE2 activator DIZE effectively restored the levels of ACE2 and Mas and decreased the content of ROS. Notably, DIZE treatment ameliorated cognitive dysfunction induced by long-term isoflurane exposure. Conclusions: The findings suggest that the activation of the ACE2/Ang-(1-7)/Mas axis could reduce oxidative stress and improve cognitive impairment. ACE2/Ang-(1-7)/Mas axis may play a prophylactic role in mitigating isoflurane-induced cognitive decline and other cognitive impairments related to oxidative stress.
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