Protective role of curcumin on aflatoxin B1-induced TLR4/RIPK pathway mediated-necroptosis and inflammation in chicken liver

Li, Sihong; Liu, Ruimeng; Xia, Shun; Wei, Gaoqiang; Ishfaq, Muhammad; Zhang, Yixin; Zhang, Xiuying

doi:10.1016/j.ecoenv.2022.113319

Cited by 48 publications

(37 citation statements)

References 40 publications

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“…Interestingly, danger signals deriving from oxidative stress and lipid peroxidation also seem to activate TLRs, triggering pro-inflammatory cytokines production [ 86 , 87 ]. Previous studies reported the involvement of the TLR family in the modulation of inflammatory and immune responses following AFB1 exposure in human and bovine species, as well as in chicken liver [ 88 , 89 , 90 , 91 ]. Moreover, in mice fed with a diet supplemented with AFB1, the mRNA levels of TLR2 in the liver increased, thus suggesting a possible role of TLR2 in mediating AFB1-stimulated inflammatory responses [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…Notably, an in-vivo experiment made in piglets confirmed the involvement of p38 MAPKs, AP-1 and NF-κB transcription factors in AFB1-induced liver injury [ 39 ]. NF-κB gene expression also resulted in being upregulated in the liver of chickens exposed to AFB1 through the feed [ 90 ]. In the present study, three members of the p38 MAPK family, as well as AP-1 and NF-κB transcription factors, were upregulated by AFB1.…”

Section: Discussionmentioning

confidence: 99%

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Deepening the Whole Transcriptomics of Bovine Liver Cells Exposed to AFB1: A Spotlight on Toll-like Receptor 2

Iori

Pauletto

Bassan

et al. 2022

Toxins

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Aflatoxin B1 (AFB1) is a food contaminant metabolized mostly in the liver and leading to hepatic damage. Livestock species are differently susceptible to AFB1, but the underlying mechanisms of toxicity have not yet been fully investigated, especially in ruminants. Thus, the aim of the present study was to better characterize the molecular mechanism by which AFB1 exerts hepatotoxicity in cattle. The bovine fetal hepatocyte cell line (BFH12) was exposed for 48 h to three different AFB1 concentrations (0.9 µM, 1.8 µM and 3.6 µM). Whole-transcriptomic changes were measured by RNA-seq analysis, showing significant differences in the expression of genes mainly involved in inflammatory response, oxidative stress, drug metabolism, apoptosis and cancer. As a confirmatory step, post-translational investigations on genes of interest were implemented. Cell death associated with necrosis rather than apoptosis events was noted. As far as the toxicity mechanism is concerned, a molecular pathway linking inflammatory response and oxidative stress was postulated. Toll-Like Receptor 2 (TLR2) activation, consequent to AFB1 exposure, triggers an intracellular signaling cascade involving a kinase (p38β MAPK), which in turn allows the nuclear translocation of the activator protein-1 (AP-1) and NF-κB, finally leading to the release of pro-inflammatory cytokines. Furthermore, a p38β MAPK negative role in cytoprotective genes regulation was postulated. Overall, our investigations improved the actual knowledge on the molecular effects of this worldwide relevant natural toxin in cattle.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Deepening the Whole Transcriptomics of Bovine Liver Cells Exposed to AFB1: A Spotlight on Toll-like Receptor 2

Iori

Pauletto

Bassan

et al. 2022

Toxins

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“…The necrosis in the liver may be caused by the effects of aflatoxin B1 and other toxic metabolites, which affect the lipids of the plasma membrane, as it leads to a loss of the integrity of the membrane and thus cell lysis and the occurrence of necrosis. (Li et al, 2022) results showed obvious necrotic characteristics, including cell swelling, rupture of cell and mitochondrial membranes and inflammation in chicken livers. (Owumi et al, 2022) In this study, the liver and kidneys of AFB1-deficient mice showed evidence of focal inflammatory cell infiltration, mild water/balloon hepatocyte degeneration and moderate vesicular steatosis.…”

Section: Histopathological Observations To Clarify the Protective Eff...mentioning

confidence: 94%

Using B.clausii to reduce the effects of aflatoxin B1

AL-Masari

Al-Obaidi

2022

ijhs

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In the experiment, a bacteria (B. clausii) was more efficient, with a percentage of inhibition of 58.03 percent, while a bacteria (B. subtilis) had a percentage of inhibition of (55.28 percent), so it was chosen in our study to test its efficiency as a probiotic to remove toxins in rats. So 12 rats were divided into four groups, each with three rats. The first group was the control group, which was given only food and water, and the second group was given (0.5) ml of aflatoxin poison for each rat. For each rat, the third group received (0.5) ml of B clausii suspension and the fourth group received (0.5) ml of B. clausii suspension + (0.5) ml of aflatoxin toxin) for 21 days. The findings suggest that B.subtilis bacteria have effects. By increasing the weights of male rats inoculated with B.subtilis alone and the group (B.clausii + aflatoxin toxin), B.subtilis bacteria were able to remove a large percentage of the negative effects of aflatoxin.

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“…Additionally, several clinical studies have shown that curcumin has a strong therapeutic potential for treating a few chronic illnesses, including pulmonary, cancer, neurological, cardiovascular, infectious, neoplastic, psychiatric, and metabolic disorders [ 68 ]. Not surprisingly, several in vitro and animal experimental studies confirmed that curcumin supplementation could offer strong protective effects against AFB1-induced liver injury, mutagenicity, hepatocarcinogenicity, renal dysfunction, ileum damage, immune toxicity via regulating multiple above-mentioned targets [ 26 , 34 , 60 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 ]. The detailed molecular pathways are discussed in the section below.…”

Section: Biological Properties Of Curcuminmentioning

confidence: 99%

“…Curcumin (1,7-bis (4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione) is a polyphenolic molecule extracted from the Curcuma longa (turmeric), which has been shown to have anti-inflammatory, anticancer, antioxidative stress, and immunological modulating characteristics [ 23 , 24 ]. Animal experimental or in vitro studies had reported that curcumin supplementation could effectively reduce AFB1-induced liver damage, renal dysfunction, and intestinal damage via inhibiting oxidative stress, apoptosis, inflammation, necrosis, and CYP450 enzyme expression [ 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ]. In addition, several studies also reported that curcumin in combination with black tea could synergistically improve AFB1-induced liver and kidney damage [ 35 ].…”

Section: Introductionmentioning

confidence: 99%

Aflatoxin B1 Toxicity and Protective Effects of Curcumin: Molecular Mechanisms and Clinical Implications

et al. 2022

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One of the most significant classes of mycotoxins, aflatoxins (AFTs), can cause a variety of detrimental outcomes, including cancer, hepatitis, aberrant mutations, and reproductive issues. Among the 21 identified AFTs, aflatoxin B1 (AFB1) is the most harmful to humans and animals. The mechanisms of AFB1-induced toxicity are connected to the generation of excess reactive oxygen species (ROS), upregulation of CYP450 activities, oxidative stress, lipid peroxidation, apoptosis, mitochondrial dysfunction, autophagy, necrosis, and inflammatory response. Several signaling pathways, including p53, PI3K/Akt/mTOR, Nrf2/ARE, NF-κB, NLRP3, MAPKs, and Wnt/β-catenin have been shown to contribute to AFB1-mediated toxic effects in mammalian cells. Curcumin, a natural product with multiple therapeutic activities (e.g., anti-inflammatory, antioxidant, anticancer, and immunoregulation activities), could revise AFB1-induced harmful effects by targeting these pathways. Therefore, the potential therapeutic use of curcumin against AFB1-related side effects and the underlying molecular mechanisms are summarized. This review, in our opinion, advances significant knowledge, sparks larger discussions, and drives additional improvements in the hazardous examination of AFTs and detoxifying the application of curcumin.

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Protective role of curcumin on aflatoxin B1-induced TLR4/RIPK pathway mediated-necroptosis and inflammation in chicken liver

Cited by 48 publications

References 40 publications

Deepening the Whole Transcriptomics of Bovine Liver Cells Exposed to AFB1: A Spotlight on Toll-like Receptor 2

Deepening the Whole Transcriptomics of Bovine Liver Cells Exposed to AFB1: A Spotlight on Toll-like Receptor 2

Using B.clausii to reduce the effects of aflatoxin B1

Aflatoxin B1 Toxicity and Protective Effects of Curcumin: Molecular Mechanisms and Clinical Implications

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