Vagus Nerve Stimulation Attenuates Hepatic IschemiaReperfusion Injury via the Nrf2HO-1 Pathway

الملخص EN

It has been demonstrated that vagus nerve stimulation (VNS) plays a protective role in ischemia/reperfusion (I/R) injury of various organs.

The present study investigates the protective effect of VNS on hepatic I/R injury and the potential mechanisms.

Male Sprague-Dawley rats were randomly allocated into three groups: the sham operation group (Sham; n=6, sham surgery with sham VNS); the I/R group (n=6, hepatic I/R surgery with sham VNS); and the VNS group (n=6, hepatic I/R surgery plus VNS).

The I/R model was established by 1 hour of 70% hepatic ischemia.

Tissue samples and blood samples were collected after 6 hours of reperfusion.

The left cervical vagus nerve was separated and stimulated throughout the whole I/R process.

The stimulus intensity was standardized to the voltage level that slowed the sinus rate by 10%.

VNS significantly reduced the necrotic area and cell death in I/R tissues.

Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) were also decreased by VNS.

In addition, VNS suppressed inflammation, oxidative stress, and apoptosis in I/R tissues.

VNS significantly increased the protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) in the liver.

These data indicated that VNS may attenuate hepatic I/R injury by inhibiting inflammation, oxidative stress, and apoptosis possibly via the Nrf2/HO-1 pathway.