Fucosterol Protects against Concanavalin A-Induced Acute Liver Injury: Focus on P38 MAPK/NF-<i>κ</i>B Pathway Activity

Mo, Wenhui; Wang, Chengfen; Li, Jingjing; Chen, Kan; Xia, Yujing; Li, Sainan; Xu, Ling; Wang, Wenwen; Guo, Chuanyong

doi:10.1155/2018/2824139

Cited by 29 publications

(28 citation statements)

References 38 publications

(45 reference statements)

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“…The fact that 23 is able to inhibit the production of pro-inflammatory molecules suggests that it could be used for the treatment of other inflammatory diseases. This suggestion was confirmed by the findings of Mo et al [150], where it was observed that fucosterol 23 attenuated serum liver enzyme levels, hepatic necrosis, and apoptosis induced by TNF-α, IL-6, and IL-1β. In fact, a dosage of 50 mg/kg (b.w.)…”

Section: Fucosterolsupporting

confidence: 77%

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Seaweed Secondary Metabolites with Beneficial Health Effects: An Overview of Successes in In Vivo Studies and Clinical Trials

et al. 2019

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Macroalgae are increasingly viewed as a source of secondary metabolites with great potential for the development of new drugs. In this development, in vitro studies are only the first step in a long process, while in vivo studies and clinical trials are the most revealing stages of the true potential and limitations that a given metabolite may have as a new drug. This literature review aims to give a critical overview of the secondary metabolites that reveal the most interesting results in these two steps. Phlorotannins show great pharmaceutical potential in in vivo models and, among the several examples, the anti-dyslipidemia activity of dieckol must be highlighted because it was more effective than lovastatin in an in vivo model. The IRLIIVLMPILMA tridecapeptide that exhibits an in vivo level of activity similar to the hypotensive clinical drug captopril should still be stressed, as well as griffithsin which showed such stunning results over a variety of animal models and which will probably move onto clinical trials soon. Regarding clinical trials, studies with pure algal metabolites are scarce, limited to those carried out with kahalalide F and fucoxanthin. The majority of clinical trials currently aim to ascertain the effect of algae consumption, as extracts or fractions, on obesity and diabetes.Studies focusing on the preparation of macroalgae extracts and their chemical characterization revealed a large range of seaweed compounds with very interesting biological activities including antitumor, anti-inflammatory, antimicrobial, antidiabetic, antivirus, antihypertensive, fat-lowering, and neuroprotective activities [12][13][14][15].The large volume of studies proving the seaweed compound activities in in vitro systems [16][17][18][19] hints the need for further advancements in the knowledge about macroalgae compound efficiency in living systems (in vivo) and their use in the development of pharmaceuticals. In vitro studies are very relevant and yield very important information, but they only represent the first step of a long process, and the results obtained rarely reveal anything about the effects of a compound in vivo, because the responses observed in vitro can be magnified, diminished, or totally different in a more complex and integrated system. In fact, in vivo studies and clinical trials are those which contribute most to truly understanding the real potential of compounds as future pharmaceuticals.In this regard, the present work intends to present insight into the results obtained in the last few years regarding secondary metabolites, such as phlorotannins, halogenated compounds, fucoxanthin, and fucosterol isolated from macroalgae, involved in in vivo studies and clinical trials, identifying the research opportunities and knowledge gaps, to valorize these compounds and their natural resources. The intention is not to present an exhaustive survey of all published works, but rather a selection of authors based on the following criteria: in-depth studies involving pure compounds most characteristic f...

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Section: Fucosterolsupporting

confidence: 77%

“…also inhibited apoptosis and autophagy by upregulating Bcl-2 (12-fold increase), which decreased levels of functional Bax (50%) and Beclin-1 (46%). Furthermore, reduced P38 MAPK and NF-κB signaling were accompanied by PPARγ activation, showing that fucosterol acts by inhibiting P38 MAPK/PPARγ/NF-κB signaling [150].…”

Section: Fucosterolmentioning

confidence: 92%

Seaweed Secondary Metabolites with Beneficial Health Effects: An Overview of Successes in In Vivo Studies and Clinical Trials

et al. 2019

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“…In the current results, PDRN treatment substantially inhibited the secretion of pro-inflammatory cytokines. Inflammation is an adaptive response to cellular or tissue damage, and the MAPK cascade signaling pathway controls the inflammatory response [ 17 ]. MAPK is responsible for the regulatory response of pro-inflammatory cytokine production and modulates various inflammatory mediators in most cells [ 11 , 13 ].…”

Section: Discussionmentioning

confidence: 99%

“…Inflammation and apoptosis are also regulated by MAPK [ 14 , 16 ]. Due to the action of NF-κB and MAPK, they have been proposed as targets of the therapeutic pathway of ALI [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Polydeoxyribonucleotide Exerts Protective Effect Against CCl4-Induced Acute Liver Injury Through Inactivation of NF-κB/MAPK Signaling Pathway in Mice

Jin

Hwang

et al. 2020

IJMS

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Acute liver injury (ALI) causes life-threatening clinical problem, and its underlying etiology includes inflammation and apoptosis. An adenosine A2A receptor agonist, polydeoxyribonucleotide (PDRN), exhibits anti-inflammatory and anti-apoptotic effects by inhibiting the secretion of pro-inflammatory cytokines. In the current study, the protective effect of PDRN against carbon tetrachloride (CCl4)-induced ALI was investigated using mice. For the induction of ALI, mice received intraperitoneal injection of CCl4 twice over seven days. Mice from the PDRN-treated groups received an intraperitoneal injection of 200 μL saline containing PDRN (8 mg/kg), once a day for seven days, starting on day 1 after the first CCl4 injection. In order to confirm that the action of PDRN occurs through the adenosine A2A receptor, 8 mg/kg 3,7-dimethyl-1-propargylxanthine (DMPX), an adenosine A2A receptor antagonist, was treated with PDRN. Administration of CCl4 impaired liver tissue and increased the liver index and histopathologic score. The expression of pro-inflammatory cytokines was increased, and apoptosis was induced by the administration of CCl4. Administration of CCl4 activated nuclear factor-kappa B (NF-κB) and facilitated phosphorylation of signaling factors in mitogen-activated protein kinase (MAPK). In contrast, PDRN treatment suppressed the secretion of pro-inflammatory cytokines and inhibited apoptosis. PDRN treatment inactivated NF-κB and suppressed phosphorylation of signaling factors in MAPK. As a result, liver index and histopathologic score were reduced by PDRN treatment. When PDRN was treated with DMPX, the anti-inflammatory and anti-apoptotic effect of PDRN disappeared. Therefore, PDRN can be used as an effective therapeutic agent for acute liver damage.

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“…Furthermore, ROS and inflammatory factors such as TNF-α, IL-6 and IL-1β can down-regulate PPAR-γ, the status of which is mainly influenced by the mitogen-activated protein kinase (MAPK) family pathway. 20,21 PPAR-γ and activated retinoid X receptor α (RXR-α) form isomeric dimers that regulate the subsequent expression of NF-κB p65 and JAK/STATs, and further affect the regulation of inflammatory factors, apoptosis, and autophagy. 22 Therefore, PPAR-γ is one of the key pathways.…”

Section: Introductionmentioning

confidence: 99%

<p>Bergenin Exerts Hepatoprotective Effects by Inhibiting the Release of Inflammatory Factors, Apoptosis and Autophagy via the PPAR-γ Pathway</p>

Xiang

Chen

et al. 2020

DDDT

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These authors contributed equally to this workObjective: Hepatic ischemia reperfusion (IR) limits the development of liver transplantation technology. The aim of this study was to explore the protective effects of Bergenin on hepatic IR, particularly the elimination of reactive oxygen species (ROS) and activation of the peroxisome proliferators activated receptor γ (PPAR-γ) pathway. Methods: Initial experiments were performed to confirm the non-toxicity of Bergenin. Mice were randomly divided into sham, IR, and IR + Bergenin (10, 20 and 40 mg/kg) groups, and serum and tissue samples were obtained at 2, 8 and 24 h for detection of liver enzymes (ALT and AST), inflammatory factors (TNF-α, IL-6 and IL-1β), ROS, cell death markers (Bcl-2, Bax, Beclin-1 and LC3) and related important pathways (PPAR-γ, P38 MAPK, NF-κB p65 and JAK2/STAT1). Results: Bergenin reduced the release of ROS, down-regulated inflammatory factors, and inhibited apoptosis and autophagy. Additionally, expression of PPAR-γ-related genes was increased and phosphorylation of P38 MAPK, NF-κB p65 and JAK2/STAT1-related proteins was decreased in Bergenin pre-treatment groups in a dose-dependent manner. Conclusion: Bergenin exerts hepatic protection by eliminating ROS, affecting the release of inflammatory factors, and influencing apoptosis-and autophagy-related genes via the PPAR-γ pathway in this model of hepatic IR injury.

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Fucosterol Protects against Concanavalin A-Induced Acute Liver Injury: Focus on P38 MAPK/NF-κB Pathway Activity

Cited by 29 publications

References 38 publications

Seaweed Secondary Metabolites with Beneficial Health Effects: An Overview of Successes in In Vivo Studies and Clinical Trials

Seaweed Secondary Metabolites with Beneficial Health Effects: An Overview of Successes in In Vivo Studies and Clinical Trials

Polydeoxyribonucleotide Exerts Protective Effect Against CCl4-Induced Acute Liver Injury Through Inactivation of NF-κB/MAPK Signaling Pathway in Mice

<p>Bergenin Exerts Hepatoprotective Effects by Inhibiting the Release of Inflammatory Factors, Apoptosis and Autophagy via the PPAR-γ Pathway</p>

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