Caffeic acid abrogates 1,3-dichloro-2-propanol-induced hepatotoxicity by upregulating nuclear erythroid-related factor 2 and downregulating nuclear factor-kappa B

2019 ◽  
Vol 38 (9) ◽  
pp. 1092-1101 ◽  
Author(s):  
TO Ajiboye ◽  
RA Ajala-Lawal ◽  
AB Adeyiga
Keyword(s):  
Caffeic Acid ◽  
Nuclear Factor Kappa B ◽  
Protein Carbonyl ◽  
Related Factor ◽  
Nuclear Factor ◽  
Oxidative Stress Biomarkers ◽  
Acid Pretreatment ◽  
Nuclear Factor Kappa ◽  
Phosphoinositide 3 Kinase ◽  
Factor Α

1,3-dichloro-2-propanol is a food-borne contaminant reported to cause liver injury. In this study, we evaluated the protective influence of caffeic acid on 1,3-dichloro-2-propanol-induced hepatotoxicity in rats. Rats were randomized into five groups (A–E). Rats received distilled water or caffeic acid (10 or 20 mg/kg body weight) for 7 days. In addition, rats were challenged with 1,3-dichloro-2-propanol on day 7. Caffeic acid prevented 1,3-dichloro-2-propanol-mediated alterations in alkaline phosphatase, alanine and aspartate aminotransferases, albumin and total bilirubin in the serum of rats. Furthermore, caffeic acid lowered superoxide ion, hydrogen peroxide and cytochrome P2E1 while increasing the activities of superoxide dismutase, catalase and glutathione S-transferase in the liver of 1,3-dichloro-2-propanol-treated rats. Caffeic acid raised the levels of nuclear erythroid-related factor 2 (Nrf-2), protein kinase A and phosphoinositide 3-kinase. Caffeic acid pretreatment annulled 1,3-dichloro-2-propanol-mediated alterations in the oxidative stress biomarkers; caspase-3, glutathione, malondialdehyde, protein carbonyl and fragmented DNA, in the liver of rats. Contrastingly, caffeic acid lowered 1,3-dichloro-2-propanol-mediated increase in the levels of nuclear factor-kappa B (NF-κB), tumour necrosis factor-α, interleukin-1β (IL-1β) and IL-6. In addition, caffeic acid preserved the morphological features of 1,3-dichloro-2-propanol-treated rats. Results from this study revealed that caffeic acid protects against 1,3-dichloro-2-propanol-induced hepatotoxicity by enhancing the cytoprotective enzymes through Nrf-2 while lowering inflammation through NF-κB.

scholarly journals KCHO-1, a Novel Antineuroinflammatory Agent, Inhibits Lipopolysaccharide-Induced Neuroinflammatory Responses through Nrf2-Mediated Heme Oxygenase-1 Expression in Mouse BV2 Microglia Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Dong-Sung Lee ◽  
Wonmin Ko ◽  
Chi-Su Yoon ◽  
Dong-Cheol Kim ◽  
Jinju Yun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Neurodegenerative Diseases ◽  
Heme Oxygenase ◽  
Nuclear Factor Kappa B ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Bv2 Microglia ◽  
Cox 2

The brain is vulnerable to oxidative stress and inflammation that can occur as a result of aging or neurodegenerative diseases. Our work has sought to identify natural products that regulate heme oxygenase (HO)-1 and to determine their mechanism of action in neurodegenerative diseases. KCHO-1 is a novel herbal therapeutic containing 30% ethanol (EtOH) extracts from nine plants. In this study, we investigated the antineuroinflammatory effects of KCHO-1 in lipopolysaccharide- (LPS-) treated mouse BV2 microglia. KCHO-1 inhibited the protein expression of inducible nitric oxide synthase (iNOS), iNOS-derived nitric oxide (NO), cyclooxygenase- (COX-) 2, and COX-2-derived prostaglandin E2 (PGE2) in LPS-stimulated BV2 microglia. It also reduced tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and IL-6 production. This effect was correlated with the suppression of inhibitor of nuclear factor kappa B-α(IκB-α) phosphorylation and degradation and nuclear factor kappa B (NF-κB) translocation and DNA binding. Additionally, KCHO-1 upregulated HO-1 expression by promoting nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) in mouse BV2 microglia. Tin protoporphyrin (SnPP), an HO activity inhibitor, was used to verify the inhibitory effects of KCHO-1 on proinflammatory mediators and proteins associated with HO-1 expression. Our data suggest that KCHO-1 has therapeutic potential in neurodegenerative diseases caused by neuroinflammation.

Immunohaematological status and mRNA expression of the genes encoding interleukin-6, nuclear-factor kappa B, and tumor-necrosis factor-α in the spleen of broilers supplemented with dietary rutin

2019 ◽  
Vol 59 (8) ◽  
pp. 1454 ◽  
Author(s):  
Ashraf Awad ◽  
Asmaa W. Zaglool ◽  
Samah R. Khalil
Keyword(s):  
Interleukin 6 ◽  
Nuclear Factor Kappa B ◽  
Lymphoid Organ ◽  
Feed Additive ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Immune Parameters ◽  
Genes Encoding ◽  
Factor Α ◽  
Necrosis Factor

Rutin, also known as vitamin P or rutoside, has been explored for many pharmacological activities. Apples, tea leaves, and many other plants contain rutin as one of the active constituents. Haematological, immunological indices and the expression of inflammatory cytokine genes in spleen tissue were assessed to investigate the influence of different levels of dietary rutin supplement (0.25, 0.5, or 1 g/kg diet) on the immune response of broilers. After 6 weeks, rutin-fed chickens showed an increase in the haematological indices, including the number of blood lymphocytes. Similarly, serum total protein and globulin were also elevated. By contrast, serum cholesterol, triglycerides and liver enzymes were lower in the experimental birds than in the control birds. Moreover, compared with the control birds, there was no significant change in the bilirubin concentration, either total or direct, and kidney-function indices in response to rutin supplementation in the experimental birds. Among the immune parameters examined, lysozyme activity, nitric oxide concentrations, and immunologlobulin M (IgM) production were significantly higher in rutin-fed birds than in the control birds; however, there was no significant effect of rutin at any concentration on the IgG and IgA concentrations and lymphoid organ weight. Of the cytokine-encoding genes studied, the genes encoding interleukin-6, nuclear-factor kappa B, and tumour-necrosis factor-α were upregulated in the spleen of the experimental birds, while the expression of interferon gamma-encoding gene was unaffected in the experimental birds. Here, rutin promoted the immune strength in birds mainly at 1 g/kg diet, suggesting that rutin is a promising feed additive for broilers.

Sanguinarine Ameliorates Diabetic Nephropathy in Rats through Nuclear Factor-Kappa B and Nuclear-Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Pathways

2021 ◽  
Vol 19 (4) ◽  
pp. 398-404
Author(s):  
Jiao Zhong
Keyword(s):  
Diabetic Nephropathy ◽  
Heme Oxygenase ◽  
Nuclear Factor Kappa B ◽  
Kidney Injury ◽  
Diabetic Rats ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Related Complication ◽  
Nuclear Factor Kappa

Alkaloids - derived from natural plants - were widely used for therapy in diabetes or diabetes-related complications. Sanguinarine, a benzophenanthridine alkaloid derived from Sanguinaria canadensis, has been identified as a potential drug for type 2 diabetes. However, the role of sanguinarine on diabetes-related complication, diabetic nephropathy, has not been reported yet. In a rat model of diabetic nephropathy we have demonstrated increased levels of 24 h urinary proteins, serum creatinine, and blood urea nitrogen, as well as series of degenerative changes in the kidney tissues. Oral administration with sanguinarine to diabetic rats diminished kidney injury markers and improved the tissue morphology. Furthermore, sanguinarine attenuated increase in the levels of tumor necrosis factor-α and interleukin-6 through downregulation of phosphonuclear factor-kappa B and phosphorylated inhibitor of nuclear factor kappa-B. Lastly, sanguinarine reversed the effects of streptozotocin on levels of reactive oxygen species, malonaldehyde, superoxide dismutase, and glutathione peroxidase through upregulation of nuclear factor erythropoietin-2-related factor 2, heme oxygenase 1 and NAD(P)H quinone dehydrogenase 1 in kidney of rats. In conclusion, sanguinarine ameliorates diabetic nephropathy in rats through inactivation of nuclear factor-kappa B and activation of nuclear-factor erythroid 2-related factor 2 pathways.

Baicalin Inhibits Kidney Inflammation in Mice with Diabetic Nephropathy by Modulating Toll-like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway

2020 ◽  
Vol 19 (1) ◽  
pp. 115-119
Author(s):  
Benyong Wang ◽  
Ning Zhao ◽  
Pingyue Ma ◽  
Qunhong Xu ◽  
Qi Chen
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Nuclear Factor Kappa B ◽  
Kidney Tissue ◽  
Control Group ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nuclear Factor Kappa ◽  
Factor Α

We have explored the effect of baicalin, an anti-inflammatory agent, on the outcome of diabetic nephropathy. To this end, we used 6 weeks old C57BL/6J male diabetic mice exhibiting nephropathy. The treatment with baicalin exhibited significant improvement in the renal function, histopathological changes, and expression of inflammatory markers. Moreover, the expression of interleukin-6, tumor necrosis factor-α, and interleukin-1β in kidney tissue of the mice in baicalin group were significantly downregulated compared to the control group (P ‹ 0.05). The expression of toll-like receptor 4, myeloid differentiation factor 88, and nuclear factor-kappa B proteins in the kidney of baicalin-treated mice were remarkably downregulated compared to the control group. Taken together, we conclude that baicalin may exert its protective effect on kidney by inhibiting inflammation through toll-like receptor 4/nuclear factor-kappa B signaling pathway in mice with diabetic nephropathy.

scholarly journals FABP5 enhances malignancies of lower-grade gliomas via canonical activation of NF-κB signaling

2020 ◽  
Author(s):  
Jia Wang ◽  
Wahafu Alafate ◽  
Yichang Wang ◽  
Wei Wu ◽  
Jianyang Xiang ◽  
...  
Keyword(s):  
Nuclear Factor Kappa B ◽  
Epithelial Mesenchymal Transition ◽  
Lower Grade ◽  
Nuclear Factor ◽  
Fatty Acid Binding ◽  
Mesenchymal Transition ◽  
Molecular Stratification ◽  
Nuclear Factor Kappa ◽  
Grade Ii ◽  
Factor Α

Abstract Background Lower-grade gliomas (LGGs) are grade II/III gliomas based on the WHO classification with significant genetic heterogeneity and clinical properties. Traditional histological classification of gliomas has been challenged by the improvement of molecular stratification, however, the reproducibility and diagnostic accuracy of LGGs classification remain poor. Methods In this study, we derived all relevant data of LGGs including TCGA and CGGA databases from official websites. Bioinformatic analyses unveiled the clinical significance of FABP5 and its potential downstream targets. IHC, qRT-PCR and western blot assays were further conducted to validate those bioinformatic findings. Moreover, lentiviral transduction assays were performed to evaluate the function of FABP5 in patient-derived cell lines. Results We identified fatty acid binding protein 5 (FABP5) as one of the most enriched genes in malignant LGGs and elevated FABP5 revealed severe outcomes in LGGs. Functionally, lentiviral suppression of FABP5 reduced malignant characters including proliferation, cloning formation, migration, invasion and TMZ resistance, contrarily, the malignancies of LGGs were enhanced by exogenous overexpression of FABP5. Mechanistically, epithelial-mesenchymal transition (EMT) was correlated to FABP5 expression in LGGs and tumor necrosis factor α (TNFα)-dependent NF-κB signaling was involved in this process. Furthermore, FABP5 induced phosphorylation of inhibitor of nuclear factor kappa-B kinase α (IKKα) thus activated nuclear factor kappa-B (NF-κB) signaling. Conclusion Taken together, our study indicated that FABP5 enhances malignancies of LGGs through canonical activation of NF-κB signaling, which could be used as individualized prognostic biomarker and potential therapeutic target of LGGs.

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