Chemotherapeutic doses of arsenic trioxide delays hepatic regeneration by oxidative stress and hepatocyte apoptosis in partial hepatectomy rat

Nithyananthan, Subramaniyam; Thirunavukkarasu, Chinnasamy

doi:10.1016/j.taap.2019.114760

Cited by 10 publications

(3 citation statements)

References 45 publications

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“…Nithyananthan et al showed that the toxicity of ATO to a normal liver causes not only massive histological changes but also severe oxidative stress. 27 were consistent with previous studies, indicating that ATO could cause severe oxidative stress in hepatocytes by producing excessive ROS production.…”

Section: Discussionsupporting

confidence: 93%

“…Nithyananthan et al showed that the toxicity of ATO to a normal liver causes not only massive histological changes but also severe oxidative stress. 27 Therefore, we examined ROS fluorescence and four serum indicators associated with oxidative stress, including three antioxidant enzymes and an oxidative intermediate. The results in this study were consistent with previous studies, indicating that ATO could cause severe oxidative stress in hepatocytes by producing excessive ROS production.…”

Section: Discussionmentioning

confidence: 99%

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Protective effect of baicalin against arsenic trioxide-induced acute hepatic injury in mice through JAK2/STAT3 signaling pathway

Sun

Chu

et al. 2022

Int J Immunopathol Pharmacol

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Baicalin (BA) is a kind of flavonoid that is isolated from Scutellaria baicalensis Georgi, which has been verified to have hepatoprotective effects in some diseases. However, the role of BA in acute hepatic injury induced by arsenic trioxide (ATO) remains unclear. The aim of this study was to investigate the protective action of BA on acute hepatic injury induced by ATO and to probe its possible mechanism. Mice were pretreated with BA (50, 100 mg/kg) by gavage. After 7 h, ATO (7.5 mg/kg) was injected intraperitoneally to induce liver injury. After 7 days of treatment, serum and hepatic specimens were collected and assayed to evaluate the hepatoprotective effect of BA. Pathological sections and the liver function index indicated that ATO caused significant liver injury. The fluorescence of reactive oxygen species and oxidative stress indicators showed that ATO also increased oxidative stress. The inflammatory markers in ATO-induced mice also increased significantly. Staining of the terminal deoxynucleotidyl transferase dUTP nick end labeling and apoptotic factor assay showed that apoptosis increased. However, with BA pretreatment, these changes were significantly weakened. In addition, BA treatment promoted the expression of proteins related to the JAK2/STAT3 signaling pathway. The results suggest that BA can ameliorate acute ATO-induced hepatic injury in mice, which is related to the inhibition of oxidative stress, thereby reducing inflammation and apoptosis. The mechanism of this protection is potentially related to the JAK2/STAT3 signaling pathway.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Protective effect of baicalin against arsenic trioxide-induced acute hepatic injury in mice through JAK2/STAT3 signaling pathway

Sun

Chu

et al. 2022

Int J Immunopathol Pharmacol

View full text Add to dashboard Cite

show abstract

“…Sahay et al ( 2 ) established an acute liver failure model in rats by performing 70% partial hepatectomy (PHx) and consequently evaluated the therapeutic potential of cells in bridging the gap between acute liver failure and liver transplantation. The PHx rat model has been widely used since then to study the involvement of regeneration in the recovery mechanism from acute liver injury ( 3 ). Hepatic resection is characterized by a catabolic state, in which the body’s metabolism as reflected in serum and urine is significantly altered ( 4 ).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of Metabolic Response to Hepatectomy by Integrated Analysis of Gut Microbiota, Metabolomics, and Proteomics

Gao

et al. 2023

Microbiol Spectr

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Hepatotoxic Effects of Atrazine on Clarias gariepinus (Burchell, 1822): Biochemical and Histopathological Studies

Opute

Oboh

2021

Arch Environ Contam Toxicol

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Chemotherapeutic doses of arsenic trioxide delays hepatic regeneration by oxidative stress and hepatocyte apoptosis in partial hepatectomy rat

Cited by 10 publications

References 45 publications

Protective effect of baicalin against arsenic trioxide-induced acute hepatic injury in mice through JAK2/STAT3 signaling pathway

Protective effect of baicalin against arsenic trioxide-induced acute hepatic injury in mice through JAK2/STAT3 signaling pathway

Mechanism of Metabolic Response to Hepatectomy by Integrated Analysis of Gut Microbiota, Metabolomics, and Proteomics

Hepatotoxic Effects of Atrazine on Clarias gariepinus (Burchell, 1822): Biochemical and Histopathological Studies

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