Hepatoprotective effect of chiisanoside from <i>Acanthopanax sessiliflorus</i> against LPS/D‐GalN‐induced acute liver injury by inhibiting NF‐<i>κ</i>B and activating Nrf2/HO‐1 signaling pathways

Bian, Xingbo; Liu, Xiaofeng; Liu, Jinping; Zhao, Yan; Li, Haijun; Zhang, Lianxue; Li, Pingya; Gao, Yugang

doi:10.1002/jsfa.9541

Cited by 26 publications

(21 citation statements)

References 34 publications

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“…[54,55] Past research studies have documented that following a challenge of LPS/D-Gal, antioxidant defense capacity deteriorates and level of oxidative stress biomarkers such as MDA and ROS increases in liver tissue. [56,57] We showed that SAC administration (100 mg/kg) is able to effectively ameliorate hepatic oxidative stress following LPS/D-Gal challenge as shown by lower levels of MDA and ROS and improvement of SOD activity and TAC and in this way has protected liver tissue against damaging effects of LPS/D-Gal combination. Consistent with this finding, it has shown that SAC is capable to attenuate H 2 O 2 -induced oxidative stress and apoptosis through suppressing production of ROS and lipid peroxidation products and upregulating heme oxygenase-1 and nuclear factor erythroid 2-related factor 2 in HepG2 cells.…”

Section: Discussionmentioning

confidence: 93%

S‐allyl cysteine, an active ingredient of garlic, attenuates acute liver dysfunction induced by lipopolysaccharide/d‐galactosamine in mouse: Underlying mechanisms

Rousta

Mirahmadi

Shahmohammadi

et al. 2020

J Biochem & Molecular Tox

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In the present study, beneficial effect of S‐allyl cysteine (SAC) was evaluated in the lipopolysaccharide/d‐galactosamine (LPS/d‐Gal) model of acute liver injury (ALI). To mimic ALI, LPS and d‐Gal (50 μg/kg and 400 mg/kg, respectively) were intraperitoneally administered and animals received SAC per os (25 or 100 mg/kg/d) for 3 days till 1 hour before LPS/d‐Gal injection. Pretreatment of LPS/d‐Gal group with SAC‐lowered activities of alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase and partially reversed inappropriate alterations of hepatic oxidative stress‐ and inflammation‐related biomarkers including liver reactive oxygen species, malondialdehyde, and hepatic activity of the defensive enzyme superoxide dismutase, ferric reducing antioxidant power (FRAP), toll‐like receptor‐4 (TLR4), cyclooxygenase 2, NLR family pyrin domain containing 3 (NLRP3), caspase 1, nuclear factor κB (NF‐κB), interleukin 1β (IL‐1β), IL‐6, tumor necrosis factor‐α, and myeloperoxidase activity. Additionally, SAC was capable to ameliorate apoptotic biomarkers including caspase 3 and DNA fragmentation. In summary, SAC can protect liver against LPS/d‐Gal by attenuation of neutrophil infiltration, oxidative stress, inflammation, apoptosis, and pyroptosis which is partly linked to its suppression of TLR4/NF‐κB/NLRP3 signaling.

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Section: Discussionmentioning

confidence: 93%

S‐allyl cysteine, an active ingredient of garlic, attenuates acute liver dysfunction induced by lipopolysaccharide/d‐galactosamine in mouse: Underlying mechanisms

Rousta

Mirahmadi

Shahmohammadi

et al. 2020

J Biochem & Molecular Tox

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“…The transcriptional factor NF- κ B controls the transcription of genes for a family of proteins involved in the response of oxidative stress and toxicity; an increase in the transcription levels of this factor is indicative of cell damage and activation of proinflammatory cytokines. On the other hand, when the transcription factor Nrf-2 is translocated to the nucleus triggers the expression of enzymes and antioxidant compounds, high levels of this factor indicate a protection of liver parenchyma [7, 20]. Therefore, in the present work, Nrf-2 and NF- κ B mRNA expressions were examined (Figure 7).…”

Section: Resultsmentioning

confidence: 99%

Curcumin and α/β-Adrenergic Antagonists Cotreatment Reverse Liver Cirrhosis in Hamsters: Participation of Nrf-2 and NF-κB

Macías‐Pérez

Vázquez-López

Muñoz‐Ortega

et al. 2019

Journal of Immunology Research

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Liver cirrhosis is the result of an uncontrolled fibrogenetic process, due to the activation and subsequent differentiation into myofibroblasts of the hepatic stellate cells (HSC). It is known that HSC express adrenoreceptors (AR), and the use of AR antagonists protects experimental animals from cirrhosis. However, several studies suggest that the toxicity generated by metabolism of these antagonists would hinder its use in cirrhotic patients. In addition, liver fibrosis may be associated with a decrease of the antioxidant response of the nuclear factor erythroid 2-related factor 2 (Nrf-2) and the overregulation of the proinflammatory pathway of nuclear factor kappa B (NF-κB). Therefore, in the present work, the capacity of doxazosin (α1 antagonist), carvedilol (nonselective beta-adrenoceptor blocker with alpha 1-blocking properties), and curcumin (antioxidant and anti-inflammatory compound) to reverse liver cirrhosis and studying the possible modulation of Nrf-2 and NF-κB were evaluated. Hamsters received CCl4 for 20 weeks, and then treatments were immediately administered for 4 weeks more. The individual administration of doxazosin or carvedilol showed less ability to reverse cirrhosis in relation to concomitantly curcumin administration. However, the best effect was the combined effect of doxazosin, carvedilol, and curcumin, reversing liver fibrosis and decreasing the amount of collagen I (Sirius red stain) without affecting the morphology of hepatocytes (hematoxylin and eosin stain), showing normal hepatic function (glucose, albumin, AST, ALT, total bilirubin, and total proteins). In addition, carvedilol treatment and the combination of doxazosin with curcumin increased Nrf-2/NF-κB mRNA ratio and its protein expression in the inflammatory cells in the livers, possibly as another mechanism of hepatoprotection. Therefore, these results suggest for the first time that α/β adrenergic blockers with curcumin completely reverse hepatic damage, possibly as a result of adrenergic antagonism on HSC and conceivably by the increase of Nrf-2/NF-κB mRNA ratio.

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“…1 attenuates CCl 4 -induced liver injury in mice and may be related to their antioxidant properties. Furthermore, the antioxidant enzymes including SOD and GSH-Px are mainly regulated by the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, which is an important regulator of the antioxidant defense system [36,37]. However, more studies are needed to reveal whether Nrf2 pathway played a key role in liver protective activities of the AEMA and Comp.…”

Section: Discussionmentioning

confidence: 99%

Anthraquinones Extract from Morinda angustifolia Roxb. Root Alleviates Hepatic Injury Induced by Carbon Tetrachloride through Inhibition of Hepatic Oxidative Stress

Chen

Liu

Chen

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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In Southwestern China, the root of Morinda angustifolia Roxb. has been employed as a folk medicine for treating various types of hepatitis and jaundice. The purpose of this study was to evaluate the hepatoprotective effects of anthraquinones extract from M. angustifolia root (AEMA) in carbon tetrachloride- (CCl4-) induced liver injury in mice and identify the main bioactive components. Results indicated that AEMA pretreatment could significantly, in a dose-dependent manner, attenuate the increased levels of ALT and AST in mice serum induced by CCl4. At doses of 100 and 200 mg/kg, AEMA exhibited significant suppression of the elevated hepatic levels of malondialdehyde (MDA), as well as marked upregulatory effects on the activities of antioxidant enzymes including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mice exposed to CCl4. However, AEMA treatment had no effect on the antioxidant enzyme catalase (CAT) or the nonenzymatic antioxidant glutathione (GSH). Furthermore, two anthraquinone constituents were isolated from AEMA and identified as soranjidiol and rubiadin-3-methyl ether. Soranjidiol exhibited similar protective effects to those of AEMA on liver damage induced by CCl4. Overall, our research clearly demonstrated the hepatoprotective effects of the AEMA, and anthraquinones, particularly soranjidiol, should be considered as the main hepatoprotective principles of M. angustifolia. In addition, the underlying mechanism may be, at least in part, related to its antioxidant properties.

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Hepatoprotective effect of chiisanoside from Acanthopanax sessiliflorus against LPS/D‐GalN‐induced acute liver injury by inhibiting NF‐κB and activating Nrf2/HO‐1 signaling pathways

Cited by 26 publications

References 34 publications

S‐allyl cysteine, an active ingredient of garlic, attenuates acute liver dysfunction induced by lipopolysaccharide/d‐galactosamine in mouse: Underlying mechanisms

S‐allyl cysteine, an active ingredient of garlic, attenuates acute liver dysfunction induced by lipopolysaccharide/d‐galactosamine in mouse: Underlying mechanisms

Curcumin and α/β-Adrenergic Antagonists Cotreatment Reverse Liver Cirrhosis in Hamsters: Participation of Nrf-2 and NF-κB

Anthraquinones Extract from Morinda angustifolia Roxb. Root Alleviates Hepatic Injury Induced by Carbon Tetrachloride through Inhibition of Hepatic Oxidative Stress

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