Sympathetic Nervous System Control of Carbon Tetrachloride‐Induced Oxidative Stress in Liver through <i>α</i>‐Adrenergic Signaling

Lin, Jung‐Chun; Peng, Yi‐Jen; Wang, Shih-Yu; Lai, Mei-Ju; Young, Ton-Ho; Salter, Donald; Lee, Herng‐Sheng

doi:10.1155/2016/3190617

Cited by 12 publications

(6 citation statements)

References 55 publications

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“…It has been proven that the sympathetic nervous system participates in raising oxidative stress in the liver. Lin et al [19] have reported that hepatic oxidative stress induced by carbon tetrachloride injection was relieved in sympathectomized mice. Oben et al [20] have also reported that 6-hydroxydopamine, an agent used to induce chemical sympathectomy, significantly improved liver injury in mice with antioxidant-depleted diets.…”

Section: Discussionmentioning

confidence: 99%

Vagus Nerve Stimulation Attenuates Hepatic Ischemia/Reperfusion Injury via the Nrf2/HO-1 Pathway

Zhang

Lai

Deng

et al. 2019

Oxidative Medicine and Cellular Longevity

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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.

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Section: Discussionmentioning

confidence: 99%

Vagus Nerve Stimulation Attenuates Hepatic Ischemia/Reperfusion Injury via the Nrf2/HO-1 Pathway

Zhang

Lai

Deng

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…The use of β-AR blockers has been indicated to reduce oxidative stress in cardiac failure [ 31 , 32 ]. Chemical sympathectomy or α-AR antagonist treatment has profound inhibitory effects on CCl4-induced hepatic oxidative injury, which has important implications for understanding how the response to liver injury may be controlled [ 34 ]. Moreover, our results showed that the group infected with E. histolytica and treated with phentolamine increased HO-1 expression.…”

Section: Discussionmentioning

confidence: 99%

Adrenergic regulation during acute hepatic infection withEntamoeba histolyticain the hamster: involvement of oxidative stress, Nrf2 and NF-KappaB

et al. 2017

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Oxidative stress and transcriptional pathways of nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa-B (NF-κB) are critically involved in the etiopathology of amebic liver abscess (ALA). In this work, we studied the relationship between the adrenergic nervous system and ALA in the hamster. ALA was visible at 12 h of infection. While 6-hydroxidopamine (6-OHDA) decreased infection, propranolol (β-adrenergic blocker) treatment was associated with less extensive liver damage, and phentolamine treatment (α-adrenergic blocker) significantly reduced ALA compared to 6-OHDA and propranolol. Serum enzymatic activities of alanine aminotransferase (ALT) and γ-glutamyl transpeptidase (γ-GTP) were increased at 12 h post-infection. Chemical denervation and α and β-adrenergic blockers decreased ALT to normal levels, while 6-OHDA and propranolol showed a trend to decrease γ-GTP but phentolamine significantly reduced γ-GTP. Amebic infection increased oxidized glutathione (GSSG) and decreased both reduced glutathione (GSH) and the GSH/GSSG ratio. Propranolol and 6-OHDA showed a tendency to decrease GSSG. However, GSH, GSSG and GSH/GSSG returned to normal levels with phentolamine. Furthermore, amebic infection increased pNF-κB and interleukin-1β (IL-1β), and showed a tendency to decrease hemoxigenase-1 (HO-1), but not Nrf2. Chemical denervation showed a trend to decrease pNF-κB and IL-1β, and neither Nrf2 nor HO-1 increased significantly. In addition, NF-κB and IL-1β were attenuated by propranolol and phentolamine treatments, although phentolamine showed significant overexpression of Nrf2 and HO-1. This suggests that the adrenergic system may be involved in oxidative stress and in modulation of the Nrf2 and NF-κB pathways during ALA development.

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“…Oxidative stress is critical during the pathogenesis of CCl 4 -induced acute liver injury [27]. CCl 4 challenge produces highly reactive species and increases cellular production of ROS and MDA, leading to oxidative stress in tissues, especially the liver where it is primarily metabolized [6].…”

Section: Discussionmentioning

confidence: 99%

Endogenous n‐3 Fatty Acids Alleviate Carbon‐Tetrachloride‐Induced Acute Liver Injury in Fat-1 Transgenic Mice

Feng

Wang

Yan

et al. 2016

Oxidative Medicine and Cellular Longevity

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n-3 polyunsaturated fatty acids (PUFAs) are beneficial for numerous models of liver diseases. The probable protective effects of n-3 PUFA against carbon-tetrachloride- (CCl4-) induced acute liver injury were evaluated in a fat-1 transgenic mouse that synthesizes endogenous n-3 from n-6 PUFA. Fat-1 mice and their WT littermates were fed a modified AIN93 diet containing 10% corn oil and were injected intraperitoneally with a single dose of CCl4 or vehicle. CCl4 challenge caused severe liver injury in WT mice, as indicated by serum parameters and histopathological changes, which were remarkably ameliorated in fat-1 mice. Endogenous n-3 PUFA decreased the elevation of oxidative stress induced by CCl4 challenge, which might be attributed to the activation of Nrf2/keap1 pathway. Additionally, endogenous n-3 PUFA reduces hepatocyte apoptosis via suppressing MAPK pathway. These findings indicate that n-3 PUFA has potent protective effects against acute liver injury induced by CCl4 in mice, suggesting that n-3 PUFA can be used for the prevention and treatment of liver injury.

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Sympathetic Nervous System Control of Carbon Tetrachloride‐Induced Oxidative Stress in Liver through α‐Adrenergic Signaling

Cited by 12 publications

References 55 publications

Vagus Nerve Stimulation Attenuates Hepatic Ischemia/Reperfusion Injury via the Nrf2/HO-1 Pathway

Vagus Nerve Stimulation Attenuates Hepatic Ischemia/Reperfusion Injury via the Nrf2/HO-1 Pathway

Adrenergic regulation during acute hepatic infection withEntamoeba histolyticain the hamster: involvement of oxidative stress, Nrf2 and NF-KappaB

Endogenous n‐3 Fatty Acids Alleviate Carbon‐Tetrachloride‐Induced Acute Liver Injury in Fat-1 Transgenic Mice

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