Piceatannol attenuates D-GalN/LPS-induced hepatoxicity in mice: Involvement of ER stress, inflammation and oxidative stress

Wen, Jingjing; Lin, Hongfa; Zhao, Mengyuan; Tao, Liang; Yang, Yuxuan; Xu, Xi; Jia, Ai‐Qun; Zhang, Jianfa; Weng, Dan

doi:10.1016/j.intimp.2018.08.037

Cited by 39 publications

(37 citation statements)

References 38 publications

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“…24,25 In the principle of LPS/D-GalN-induced acute hepatitis, the production of TNF-a plays central roles in the induction of hepatocyte apoptosis. 26 TNF-a initiates the death receptor-dependent apoptotic pathway via its receptor, which leads to the activation of caspase cascade. 27 Finally, the activated executive caspase-3 cleaves functional proteins such as PARP, which is a crucial molecular event for the induction of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Luzindole attenuates LPS/d-galactosamine-induced acute hepatitis in mice

et al. 2019

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Melatonin is a well-documented hormone that plays central roles in the regulation of sleep–wake cycles. There is cumulative evidence to suggest that melatonin is also a pleiotropic regulator of inflammation, and luzindole has been widely used as a melatonin receptor antagonist. This study investigated the potential effects of luzindole on LPS/d-galactosamine (d-GalN)-induced acute hepatitis. The results indicated that treatment with luzindole alleviated histological damage in the liver, reduced the level of transaminases in plasma and improved the survival of LPS/d-GalN-exposed mice. Treatment with luzindole also suppressed the production of the pro-inflammatory cytokines TNF-α and IL-6 in LPS/d-GalN-exposed mice. In addition, treatment with luzindole inhibited the activation of caspase-3, -8 and -9, and suppressed the cleavage of caspase-3 and poly(ADP-ribose) polymerase. Therefore, treatment with luzindole attenuates LPS/d-GalN-induced acute liver injury, suggesting that luzindole might have potential value for the intervention of inflammation-based hepatic disorders.

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Section: Discussionmentioning

confidence: 99%

Luzindole attenuates LPS/d-galactosamine-induced acute hepatitis in mice

et al. 2019

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“…PIC has been proved to possess anti-inflammatory, antioxidative, anti-proliferative activities (Kalariya et al, 2013). Moreover, it has been used to treat many diseases including liver injury (Wen et al, 2018), cardiac injury (Wang et al, 2019), cancer (Lucas et al, 2018) and skin disease (Maruki-Uchida et al, 2018). Evidence indicated that treatment of PIC visibly repressed the secretion of pro-inflammatory cytokines and nitric oxide (NO) in RAW264.7 cells during LPS stimulation (Yamamoto et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Piceatannol Against Acute Lung Injury Through Protecting the Integrity of Air-Blood Barrier and Modulating the TLR4/NF-κB Signaling Pathway Activation

et al. 2020

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Acute lung injury (ALI) is a common and complex inflammatory lung syndrome with higher morbidity and mortality rate. Piceatannol (PIC) has anti-inflammation and anti-oxidant properties. The study was designed to explore the effect and the action mechanisms of PIC on lipopolysaccharide (LPS)-induced ALI. Twenty-four hours after LPS challenge, mice from different treatment groups were euthanized, and the bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected. Then the degree of pulmonary edema, lung pathological changes, myeloperoxidase (MPO) activity, and the production of pro-inflammatory cytokines were detected. Additionally, the messenger RNA (mRNA) expressions associated with cell adhesion molecules and tight junction were analyzed through quantitative real-time (qRT)-PCR, and the TLR4/NF-kB activation was examined by western blot. The results showed that PIC significantly inhibited LPS-induced lung edema, histopathological damage, MPO activity, cell infiltration, and pro-inflammatory cytokines production. Moreover, PIC notably suppressed mRNA expressions associated with inflammation and cell adhesion molecules. Furthermore, PIC also alleviated LPSinduced damage of air-blood barrier through reducing the levels of total proteins in BALF and recovering the expression of occludin and ZO-1 in the lung tissues. We also found that PIC remarkably restrained the LPS-induced TLR4/NF-kB pathway activation in lung tissues. In conclusion, PIC may be potential to treat LPS-induced acute lung injury (ALI) via regulating air-blood barrier and TLR4/NF-kB signaling pathway activation.

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“…D-GaLN is a commonly used experimental drug that causes hepatotoxicity, and its mechanism involves GSH depletion and affecting RNA synthesis (Gehrke et al, 2018). Studies have also confirmed that D-GaLN alone leads to the potent intracellular generation of ROS in HepG2 cells (Bak et al, 2018) which can induce oxidative stress in the accumulation of ROS in hepatocytes in vitro and in vivo (Gonzalez et al, 2009;Wen et al, 2018). By inducing caspase-3 activation and DNA fragmentation in hepatocytes, D-GalN causes hepatocyte apoptosis (Lin et al, 2009).…”

Section: Discussionmentioning

confidence: 96%

Quercetin Attenuates d-GaLN-Induced L02 Cell Damage by Suppressing Oxidative Stress and Mitochondrial Apoptosis via Inhibition of HMGB1

et al. 2020

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High mobility group box-1 (HMGB1) plays an important role in various liver injuries. In the case of acute liver injury, it leads to aseptic inflammation and other reactions, and also regulates specific cell death responses in chronic liver injury. HMGB1 has been demonstrated to be a good therapeutic target for treating liver failure. Quercetin (Que), as an antioxidant, is a potential phytochemical with hepatocyte protection and is also considered to be an inhibitor of HMGB1. However, the mechanism of its hepatoprotective effects remains to be characterized. The present study explored whether the hepatoprotective effect of Que antagonizes HMGB1, and subsequent molecular signaling events. Our results indicated that Que protects L02 cells from Dgalactosamine (D-GaLN)-induced cellular damage by reducing intracellular reactive oxygen species (ROS) production and apoptotic responses in the mitochondrial pathway. Immunofluorescence and Western blot assays showed that HMGB1 was involved in D-GaLN-induced L02 cell damage. Further research showed that after transfection with HMGB1 short hairpin RNA (shRNA), cell viability was improved, and intracellular ROS production and apoptosis were suppressed. When co-treated with Que, the expression of HMGB1 was decreased significantly, the expression of proteins in the corresponding signal pathway were further reduced, and the production of ROS and apoptosis were further suppressed. Molecular docking also indicated the binding of Que and HMGB1. Taken together, these results indicate that Que significantly improves D-GaLN-induced cellular damage by inhibiting oxidative stress and mitochondrial apoptosis via inhibiting HMGB1.

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Piceatannol attenuates D-GalN/LPS-induced hepatoxicity in mice: Involvement of ER stress, inflammation and oxidative stress

Cited by 39 publications

References 38 publications

Luzindole attenuates LPS/d-galactosamine-induced acute hepatitis in mice

Luzindole attenuates LPS/d-galactosamine-induced acute hepatitis in mice

Protective Effect of Piceatannol Against Acute Lung Injury Through Protecting the Integrity of Air-Blood Barrier and Modulating the TLR4/NF-κB Signaling Pathway Activation

Quercetin Attenuates d-GaLN-Induced L02 Cell Damage by Suppressing Oxidative Stress and Mitochondrial Apoptosis via Inhibition of HMGB1

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