Tian Yue1, Guo Shanbin2, Ma Ling1, Wang Yuan1, Xu Ying1, Zhao Ping3. 1. Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang 110004, China. 2. Department of Pharmacy, Shengjing Hospital of China Medical University, Shenyang 110004, China. 3. Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang 110004, China. Electronic address: zhaop@sj-hospital.org.
Abstract
AIMS: To investigate the effects of sevoflurane inhalation on β-amyloid (Aβ)-induced cognitive disorders and hippocampal oxidative stress in rat models. MATERIALS AND METHODS: Cognitive dysfunction is induced by hippocampal injection of Aβ1-40 (10μg in 2μl) for 22days. To explore the effect of sevoflurane inhalation on Aβ1-40 induced cognitive disorder, two doses of sevoflurane inhalation are used: 1.3% (Aβ+S1) and 2.6% (Aβ+S2). Sham operation (Sham, for operation control), saline injection (Control, for injection control) and 30% oxygen inhalation after Aβ1-40 injection (Aβ+O2, for inhalation control) were used as controls. All rats were further tested in electrical Y-maze and Morris water maze. Serum S100β levels, hippocampal superoxide dismutase (SOD) activity, S100β expression and malonyldialdehyde (MDA) concentrations were further quantified. KEY FINDINGS: Rats in Aβ+O2, Aβ+S1 and Aβ+S2 groups had lower number of correct actions in the electrical Y maze task, longer escape latencies, less time exploring the original platform, elevated serum S100β levels, depressed hippocampal SOD activity, S100β expression and higher MDA concentrations compared to control group (p<0.05). Such difference was not significant between Aβ+S1 and Aβ+O2 rats. Rats in Aβ+S2 group, however, showed significantly impaired performances compared to those in Aβ+S1 group (p<0.05). SIGNIFICANCE: Sevoflurane (2.6%) can aggravate the Aβ-induced cognitive dysfunction, possibly via the intracerebral oxidative stress response.
AIMS: To investigate the effects of sevoflurane inhalation on β-amyloid (Aβ)-induced cognitive disorders and hippocampal oxidative stress in rat models. MATERIALS AND METHODS:Cognitive dysfunction is induced by hippocampal injection of Aβ1-40 (10μg in 2μl) for 22days. To explore the effect of sevoflurane inhalation on Aβ1-40 induced cognitive disorder, two doses of sevoflurane inhalation are used: 1.3% (Aβ+S1) and 2.6% (Aβ+S2). Sham operation (Sham, for operation control), saline injection (Control, for injection control) and 30% oxygen inhalation after Aβ1-40 injection (Aβ+O2, for inhalation control) were used as controls. All rats were further tested in electrical Y-maze and Morris water maze. Serum S100β levels, hippocampal superoxide dismutase (SOD) activity, S100β expression and malonyldialdehyde (MDA) concentrations were further quantified. KEY FINDINGS:Rats in Aβ+O2, Aβ+S1 and Aβ+S2 groups had lower number of correct actions in the electrical Y maze task, longer escape latencies, less time exploring the original platform, elevated serum S100β levels, depressed hippocampal SOD activity, S100β expression and higher MDA concentrations compared to control group (p<0.05). Such difference was not significant between Aβ+S1 and Aβ+O2rats. Rats in Aβ+S2 group, however, showed significantly impaired performances compared to those in Aβ+S1 group (p<0.05). SIGNIFICANCE: Sevoflurane (2.6%) can aggravate the Aβ-induced cognitive dysfunction, possibly via the intracerebral oxidative stress response.
Authors: Yongping Zhang; Guangling Jiao; Cai Song; Shelly Gu; Richard E Brown; Junzeng Zhang; Pingcheng Zhang; Jacques Gagnon; Steven Locke; Roumiana Stefanova; Claude Pelletier; Yi Zhang; Hongyu Lu Journal: Mar Drugs Date: 2017-03-22 Impact factor: 5.118