Abstract
Isoflurane/surgery (I/S) may induce neurocognitive disorders, but detailed mechanisms and appropriate treatment remain largely unknown. This experiment was designed to determine whether ginsenoside Rg1 could attenuate I/S-induced neurocognitive disorders and Sirtuin3 (Sirt3) dysfunction. C57BL/6J male mice received 1.4% isoflurane plus abdominal surgery for 2 h. Ginsenoside Rg1 10 mg/kg was intraperitoneally given for 8 days before surgery. Neurocognitive function was assessed by the Barnes Maze test. Levels of reactive oxygen species (ROS), oxygen consumption rate (OCR), mitochondrial membrane potential (MMP), expression and deacetylation activity of Sirt3 in the hippocampus tissues were measured. Results showed that I/S induced hippocampus-dependent learning and memory impairments, with increased ROS levels, and reduced OCR, MMP, and expression and deacetylation activity of Sirt3 in hippocampus tissues. Ginsenoside Rg1 treatment before I/S intervention significantly ameliorated learning and memory performance, reduced ROS levels and improved the OCR, MMP, expression and deacetylation activity of Sirt3. In conclusion, this experiment demonstrates that ginsenoside Rg1 treatment can attenuate I/S-induced neurocognitive disorders and Sirt3 dysfunction.
Highlights
Perioperative neurocognitive disorders (PNDs) are the common complications of surgical patients, with deterioration in memory, attention and speed of information processing [1]
There were no significant differences in the escape latency and number of errors between control+Rg1 and control+normal saline (NS) groups
There were no significant differences in the escape speed during training and probe days among groups (Figure 2C,F,I)
Summary
Perioperative neurocognitive disorders (PNDs) are the common complications of surgical patients, with deterioration in memory, attention and speed of information processing [1]. It has become apparent that neurodegenerative diseases are associated with mitochondrial dysfunction [3]. The studies have indicated the role of mitochondrial pathway in the neurocognitive disorders induced by surgery and volatile anesthetics [4,5,6,7]. Declined mitochondrial membrane potential (MMP) may cause the opening of mitochondrial permeability transition pore (mPTP), aggravating the generation of ROS [7]. The MMP decline may be due to the dysfunction of Sirtuin (Sirt3), a key compound to regulate mitochondrial energy metabolism and oxidative stress. The available evidence indicates that Sirt is involved in cognition decline of Alzheimer’s disease [8]. Deficiency of Sirt may increase the acetylated-cyclophilin D and ROS levels to exacerbate the mitochondrial dysfunction [9]
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