Sirtuin 3 protects against anesthesia/surgery-induced cognitive decline in aged mice by suppressing hippocampal neuroinflammation

J Neuroinflammation. 2021 Feb 4;18(1):41. doi: 10.1186/s12974-021-02089-z.

Abstract

Background: Postoperative cognitive dysfunction (POCD) is a very common complication that might increase the morbidity and mortality of elderly patients after surgery. However, the mechanism of POCD remains largely unknown. The NAD-dependent deacetylase protein Sirtuin 3 (SIRT3) is located in the mitochondria and regulates mitochondrial function. SIRT3 is the only sirtuin that specifically plays a role in extending lifespan in humans and is associated with neurodegenerative diseases. Therefore, the aim of this study was to evaluate the effect of SIRT3 on anesthesia/surgery-induced cognitive impairment in aged mice.

Methods: SIRT3 expression levels were decreased after surgery. For the interventional study, an adeno-associated virus (AAV)-SIRT3 vector or an empty vector was microinjected into hippocampal CA1 region before anesthesia/surgery. Western blotting, immunofluorescence staining, and enzyme-linked immune-sorbent assay (ELISA) were used to measure the oxidative stress response and downstream microglial activation and proinflammatory cytokines, and Golgi staining and long-term potentiation (LTP) recording were applied to evaluate synaptic plasticity.

Results: Overexpression of SIRT3 in the CA1 region attenuated anesthesia/surgery-induced learning and memory dysfunction as well as synaptic plasticity dysfunction and the oxidative stress response (superoxide dismutase [SOD] and malondialdehyde [MDA]) in aged mice with POCD. In addition, microglia activation (ionized calcium binding adapter molecule 1 [Iba1]) and neuroinflammatory cytokine levels (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-1β and IL-6) were regulated after anesthesia/surgery in a SIRT3-dependent manner.

Conclusion: The results of the current study demonstrate that SIRT3 has a critical effect in the mechanism of POCD in aged mice by suppressing hippocampal neuroinflammation and reveal that SIRT3 may be a promising therapeutic and diagnostic target for POCD.

Keywords: Microglia; Mitochondrial oxidative stress; Neuroinflammation; Postoperative cognitive dysfunction; SIRT3; Synaptic plasticity.

MeSH terms

  • Aging / drug effects
  • Aging / metabolism*
  • Aging / pathology
  • Anesthetics, Inhalation / toxicity*
  • Animals
  • Hippocampus / drug effects
  • Hippocampus / metabolism*
  • Hippocampus / pathology
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / metabolism*
  • Isoflurane / toxicity
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neuroprotection / drug effects
  • Neuroprotection / physiology
  • Postoperative Cognitive Complications / chemically induced
  • Postoperative Cognitive Complications / etiology
  • Postoperative Cognitive Complications / metabolism*
  • Postoperative Cognitive Complications / prevention & control
  • Sirtuin 3 / biosynthesis*
  • Tibial Fractures / surgery

Substances

  • Anesthetics, Inhalation
  • Inflammation Mediators
  • Sirt3 protein, mouse
  • Isoflurane
  • Sirtuin 3