Role of Reduced Nitric Oxide in Liver Cell Apoptosis Inhibition During Liver Damage

Wang, Yingyi; Chen, Mengting; Hong, Huimin; Wang, Ying; Li, Qian; Liu, Hui; Yang, Mei-wen; Hong, Fashui; Yang, Shu‐Long

doi:10.1016/j.arcmed.2018.09.001

Cited by 16 publications

(8 citation statements)

References 39 publications

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“…22 Apoptosis is an autonomous and orderly cell death controlled by multitudinous genes and proteins to maintain the homeostasis of the internal environment. 23 It is regulated by pro-apoptotic and anti-apoptotic families, such as the Bcl-2 family and Caspase family. 24 The Bcl-2 family triggers cytochrome C (Cyt C) release from the mitochondria, and then initiates Caspase activation.…”

Section: Introductionmentioning

confidence: 99%

Cadmium and molybdenum co-induce pyroptosis and apoptosis via the PTEN/PI3K/AKT axis in the livers of Shaoxing ducks (Anas platyrhynchos)

et al. 2022

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Section: Introductionmentioning

confidence: 99%

Cadmium and molybdenum co-induce pyroptosis and apoptosis via the PTEN/PI3K/AKT axis in the livers of Shaoxing ducks (Anas platyrhynchos)

et al. 2022

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“…It is also a second messenger that acts in several pathways and plays a crucial role in regulating blood pressure by relaxing the endothelium, attacking tumor cells, and stimulating the brain ( Gupta et al, 2011b ; Korde Choudhari et al, 2013 ; Picon-Pages et al, 2019 ). Although NO has multiple and complex roles, it has been suggested that it affects the pathogenesis and progression of liver diseases ( Iwakiri and Kim, 2015 ; Ekhlasi et al, 2017 ; Wang et al, 2018 ). On the other hand, LDH (a non-specific tissue damage biomarker) was elevated in vancomycin-treated animals.…”

Section: Discussionmentioning

confidence: 99%

Protective role of resveratrol against VCM-induced hepatotoxicity in male wistar rats

Alshehri

Alorfi²

2023

Front. Pharmacol.

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Background: Vancomycin is a glycopeptide antibiotic with a high risk of acute liver injury. Resveratrol is believed to protect the liver against toxicity.Aim: To investigate the ability of resveratrol to attenuate vancomycin-induced liver toxicity in rats injected with vancomycin.Method: Twenty-four adult male Wistar rats were distributed into three groups. The control group received only a vehicle, while the treated group received either vancomycin 200 (mg/kg, i. p.) only or vancomycin (200 mg/kg, i. p.) with resveratrol (20 mg/kg, oral gavage). All groups received their dose once daily for 7 days. Hepatic damage was assessed by measuring biochemical parameter levels in serum, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH). Also, antioxidants and inflammation biomarkers such as Interleukin-6 (IL-6), malondialdehyde (MDA), nitric oxide (NO), and glutathione (GSH) were measured. Furthermore, the vancomycin-induced pathological changes in the liver were evaluated by histopathological studies.Results: In the vancomycin-treated group, hepatic serum biomarkers such as AST, ALT, ALP, IL-6, and MDA were elevated, while NO and GSH were depleted. However, resveratrol co-treatment with vancomycin prevented the elevation of AST, ALT, ALP, IL-6, and MDA and it protected the liver from NO and GSH depletion. Also, regarding vancomycin-induced degeneration of hepatocytes, resveratrol co-treatment with vancomycin prevented such degeneration and improved mononuclear cells in the liver.Conclusion: The results showed that oral administration of resveratrol has a significant hepatoprotective effect against vancomycin-induced hepatotoxicity.

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“…Previously published studies on the regulatory mechanism of cyt c release during apoptosis are not fully understood. However, it has been established that Bcl-2, Bcl2-like 1(Bcl-xL), and Bax protein are major regulators of VDAC which may exert certain effects in regulating the release of cyt c [96]. To the start, stimulation of proapoptotic factors resulted in the decreased capability of Bcl-2 in maintaining the integrity of the mitochondrial membrane and enforced Bax translocation outside the mitochondrial membrane.…”

Section: The Release Of Apoptosis-related Proteinsmentioning

confidence: 99%

Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury

Zhang

Rao

Yang

et al. 2022

IJMS

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Hepatic ischemia-reperfusion injury is a major cause of post-operative hepatic dysfunction and liver failure after transplantation. Mitochondrial pathways can be either beneficial or detrimental to hepatic cell apoptosis during hepatic ischemia/reperfusion injury, depending on multiple factors. Hepatic ischemia/reperfusion injury may be induced by opened mitochondrial permeability transition pore, released apoptosis-related proteins, up-regulated B-cell lymphoma-2 gene family proteins, unbalanced mitochondrial dynamics, and endoplasmic reticulum stress, which are integral parts of mitochondrial pathways. In this review, we discuss the role of mitochondrial pathways in apoptosis that account for the most deleterious effect of hepatic ischemia/reperfusion injury.

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Role of Reduced Nitric Oxide in Liver Cell Apoptosis Inhibition During Liver Damage

Cited by 16 publications

References 39 publications

Cadmium and molybdenum co-induce pyroptosis and apoptosis via the PTEN/PI3K/AKT axis in the livers of Shaoxing ducks (Anas platyrhynchos)

Cadmium and molybdenum co-induce pyroptosis and apoptosis via the PTEN/PI3K/AKT axis in the livers of Shaoxing ducks (Anas platyrhynchos)

Protective role of resveratrol against VCM-induced hepatotoxicity in male wistar rats

Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury

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