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Vagus nerve stimulation attenuates acute kidney injury induced by hepatic ischemia/reperfusion injury in rats.

ABSTRACT: Hepatic ischemia/reperfusion (I/R) injury, caused by limited blood supply and subsequent blood supply, is a causative factor resulting in morbidity and mortality during liver transplantation and liver resection. Hepatic I/R injury frequently contributes to remote organ injury, such as kidney, lung, and heart. It has been demonstrated that vagus nerve stimulation (VNS) is effective in remote organ injury after I/R injury. Here, our aim is to investigate the potential action of VNS on hepatic I/R injury-induced acute kidney injury (AKI) and explore its underlying mechanisms. To test this hypothesis, male Sprague-Dawley rats were randomly assigned into three experimental groups: Sham group (sham operation, n = 6); I/R group (hepatic I/R with sham VNS, n = 6); and VNS group (hepatic I/R with VNS, n = 6). VNS was performed during the entire hepatic I/R process. Our results showed that throughout the hepatic I/R process, VNS significantly regulated the expression levels of various iconic factors and greatly enhanced the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) in the kidneys. These findings suggested that VNS may ameliorate hepatic I/R injury-induced AKI by suppressing inflammation, oxidative stress, and apoptosis probably through activating the Nrf2/HO-1 signaling pathway.

SUBMITTER: Deng S

PROVIDER: S-EPMC9755310 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature

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Vagus nerve stimulation attenuates acute kidney injury induced by hepatic ischemia/reperfusion injury in rats.

Deng Simin S Zhang Yifeng Y Xin Ying Y Hu Xinqun X

Scientific reports 20221215 1

Hepatic ischemia/reperfusion (I/R) injury, caused by limited blood supply and subsequent blood supply, is a causative factor resulting in morbidity and mortality during liver transplantation and liver resection. Hepatic I/R injury frequently contributes to remote organ injury, such as kidney, lung, and heart. It has been demonstrated that vagus nerve stimulation (VNS) is effective in remote organ injury after I/R injury. Here, our aim is to investigate the potential action of VNS on hepatic I/R ...[more]

PMID: 36522408

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Project description:BackgroundVagus nerve stimulation (VNS) exhibits protective effects against remote organ injury following ischemia-reperfusion (I/R). However, its effects on acute myocardial injury induced by hepatic I/R in rats, and the underlying mechanisms, remain unclear.MethodsThirty male rats were randomly assigned to five groups: Sham, I/R, VNS, VNS + Erastin, and VNS + DMSO. A hepatic I/R injury model was established by occluding the arterial and portal veins of the left and middle lobes of the liver for 1 h followed by 6 h of reperfusion. VNS was performed throughout the hepatic I/R process. Erastin was administered intraperitoneally 60 min before hepatic ischemia. Blood samples were collected from the left common carotid artery post-reperfusion to measure liver injury markers (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and the myocardial injury marker (cardiac troponin I [cTnI]). Left ventricular myocardial tissue was also collected for ultrastructural analysis via transmission electron microscopy, reactive oxygen species (ROS) detection using dihydroethidium staining, and measurements of Fe2⁺ levels, malondialdehyde (MDA) concentration, glutathione (GSH) levels, and superoxide dismutase (SOD) activity. Western blotting assessed the expression of ferroptosis-related proteins SLC7A11 and GPX4 in the myocardial tissue.ResultsVNS significantly reduced serum levels of ALT, AST, and cTnI, while also mitigating mitochondrial damage in cardiomyocytes. Additionally, VNS decreased ROS levels, alleviated iron overload, and reduced lipid peroxidation in myocardial tissue. These protective effects were associated with the activation of the SLC7A11/GPX4 axis, as evidenced by increased expression of these proteins in the VNS group. However, the cardioprotective effects of VNS were negated by the ferroptosis activator erastin, indicating that ferroptosis is involved in VNS-mediated cardioprotection.ConclusionVNS protects against myocardial injury from hepatic ischemia-reperfusion, likely by inhibiting oxidative stress and ferroptosis through activation of the SLC7A11/GPX4 axis.

Project description:Intestinal ischemia-reperfusion (I/R) injury is a devastating complication when the blood supply is reflowed in ischemic organs. Gastrin has critical function in regulating acid secretion, proliferation, and differentiation in the gastric mucosa. We aimed to determine whether gastrin has an effect on intestinal I/R damage. Intestinal I/R injury was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion, and the rats were induced to be hypergastrinemic by pretreated with omeprazole or directly injected with gastrin. Some hypergastrinemic rats were injected with cholecystokinin-2 (CCK-2) receptor antagonist prior to I/R operation. After the animal surgery, the intestine was collected for histological analysis. Isolated intestinal epithelial cells or crypts were harvested for RNA and protein analysis. CCK-2 receptor expression, intestinal mucosal damage, cell apoptosis, and apoptotic protein caspase-3 activity were measured. We found that high gastrin in serum significantly reduced intestinal hemorrhage, alleviated extensive epithelial disruption, decreased disintegration of lamina propria, downregulated myeloperoxidase activity, tumor necrosis factor-α, and caspase-3 activity, and lead to low mortality in response to I/R injury. On the contrary, CCK-2 receptor antagonist L365260 could markedly impair intestinal protection by gastrin on intestinal I/R. Severe edema of mucosal villi with severe intestinal crypt injury and numerous intestinal villi disintegrated were observed again in the hypergastrinemic rats with L365260. The survival in the hypergastrinemic rats after intestinal I/R injury was shortened by L365260. Finally, gastrin could remarkably upregulated intestinal CCK-2 receptor expression. Our data suggest that gastrin by omeprazole remarkably attenuated I/R induced intestinal injury by enhancing CCK-2 receptor expression and gastrin could be a potential mitigator for intestinal I/R damage in the clinical setting.

Dataset Information

Vagus nerve stimulation attenuates acute kidney injury induced by hepatic ischemia/reperfusion injury in rats.

Publications

Vagus nerve stimulation attenuates acute kidney injury induced by hepatic ischemia/reperfusion injury in rats.

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