Inhibition of MAP kinases and down regulation of TNF-α, IL-β and COX-2 genes by the crude extracts from marine bacteria

Krishnaveni, M.; Jayachandran, S

doi:10.1016/j.biopha.2008.09.005

Cited by 15 publications

(7 citation statements)

References 39 publications

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“…TNF-α is a key mediator in many experimental liver injury models, which could mediate acute and chronic inflammation and infection [ 45 , 46 ]. It could promote cytokines generation and inflammation reaction by stimulating neutrophils and macrophages, ultimately resulting in liver cell necrosis or apoptosis [ 47 ]. In addition to promoting inflammation, causing fever outside, IL-1β can stimulate development and differentiation of the immune system [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Maltol, a Food Flavoring Agent, Attenuates Acute Alcohol-Induced Oxidative Damage in Mice

Han

et al. 2015

Nutrients

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The purpose of this study was to evaluate the hepatoprotective effect of maltol, a food-flavoring agent, on alcohol-induced acute oxidative damage in mice. Maltol used in this study was isolated from red ginseng (Panax ginseng C.A Meyer) and analyzed by high performance liquid chromatography (HPLC) and mass spectrometry. For hepatoprotective activity in vivo, pretreatment with maltol (12.5, 25 and 50 mg/kg; 15 days) drastically prevented the elevated activities of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and triglyceride (TG) in serum and the levels of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) in liver tissue (p < 0.05). Meanwhile, the levels of hepatic antioxidant, such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were elevated by maltol pretreatment, compared to the alcohol group (p < 0.05). Histopathological examination revealed that maltol pretreatment significantly inhibited alcohol-induced hepatocyte apoptosis and fatty degeneration. Interestingly, pretreatment of maltol effectively relieved alcohol-induced oxidative damage in a dose-dependent manner. Maltol appeared to possess promising anti-oxidative and anti-inflammatory capacities. It was suggested that the hepatoprotective effect exhibited by maltol on alcohol-induced liver oxidative injury may be due to its potent antioxidant properties.

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Section: Discussionmentioning

confidence: 99%

Maltol, a Food Flavoring Agent, Attenuates Acute Alcohol-Induced Oxidative Damage in Mice

Han

et al. 2015

Nutrients

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“…The p38 kinase pathway is known to regulate wide-ranging proinflammatory responses, including stimulation of proinflammatory genes (36,37), induction of COX-2 (38), increases in iNOS expression (39), increases in adhesion molecule expression (40)(41)(42), and proliferation of inflammatory cells (43)(44)(45)(46). The p38 kinase is both upregulated and activated in intestinal tissue of patients with IBD, and inhibition of p38 kinase inhibits the secretion of inflammatory cytokines in intestinal tissue and in lamina propria mononuclear cells isolated from IBD patients (47,48).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of IL-1β Modulation of Intestinal Epithelial Barrier Involves p38 Kinase and Activating Transcription Factor-2 Activation

Al–Sadi

Guo

et al. 2013

The Journal of Immunology

121

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The defective intestinal epithelial tight junction (TJ) barrier has been postulated to be an important pathogenic factor contributing to intestinal inflammation. It has been shown that the proinflammatory cytokine IL-1β causes an increase in intestinal permeability; however, the signaling pathways and the molecular mechanisms involved remain unclear. The major purpose of this study was to investigate the role of the p38 kinase pathway and the molecular processes involved. In these studies, the in vitro intestinal epithelial model system (Caco-2 monolayers) was used to delineate the cellular and molecular mechanisms, and a complementary in vivo mouse model system (intestinal perfusion) was used to assess the in vivo relevance of the in vitro findings. Our data indicated that the IL-1β increase in Caco-2 TJ permeability correlated with an activation of p38 kinase. The activation of p38 kinase caused phosphorylation and activation of p38 kinase substrate, activating transcription factor (ATF)-2. The activated ATF-2 translocated to the nucleus where it attached to its binding motif on the myosin L chain kinase (MLCK) promoter region, leading to the activation of MLCK promoter activity and gene transcription. Small interfering RNA induced silencing of ATF-2, or mutation of the ATF-2 binding motif prevented the activation of MLCK promoter and MLCK mRNA transcription. Additionally, in vivo intestinal perfusion studies also indicated that the IL-1β increase in mouse intestinal permeability required p38 kinase–dependent activation of ATF-2. In conclusion, these studies show that the IL-1β–induced increase in intestinal TJ permeability in vitro and in vivo was regulated by p38 kinase activation of ATF-2 and by ATF-2 regulation of MLCK gene activity.

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“…The marine environments are enriched with both biological and chemical diversity and covers more than 70% of the biosphere ( Jaiganesh et al, 2012). Earlier studies reported isolation, identification and characterization of many marine bacteria that are capable of producing bioactive molecules active against inflammation and cancer (Krishnaveni et al, 2009;Moushumi et al, 2012;Lalitha et al, 2016Lalitha et al, , 2018. In the present study, MB8 was isolated from deep Bacillus safensis sea sediment of Bay of Bengal, India.…”

Section: Discussionmentioning

confidence: 99%

Bioactive compound isolated from marine Bacillus safensis MB8 and their cytotoxicity potential

Perumal¹

2020

Asian J Pharm Pharmacol

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Background: Marine bacteria represent a potential source for the production of medically useful compounds against cancer, diabetes, inflammation, infection, etc. In the present study, isolation, characterization and identification of Objectives: bioactive compound from marine MB8. Breast cancer (MCF-7) cell lines to determine the Bacillus safensis Methods: cytotoxicity activity of bioactive compound produced from marine MB8. Bacillus safensis Results: Marine Bacillus safensis MB8 (Genbank accession no. KJ531643) isolated from deep sea sediments of the Bay of Bengal, India, produced a bioactive compound, Bis (2-ethylhexyl) benzene-1,2-dicarboxylate (BEHBD) with a molecular formula of C H O. The molecular 24 38 4 ion m/z 391 (M). The MTT assay based cytotoxicity assessment of BEHBD in MCF-7 cancer cells revealed the IC peak at + 50 to be 49.8µg/ml. The acridine-orange and ethidium bromide (AO/EB) staining of the BEHBD treated cancer cells showed typical characteristic of apoptosis such as nuclear condensation, cell shrinkage and formation of apoptotic bodies. Conclusion: Potent cytotoxicity compound of Bis (2-ethylhexyl) benzene-1, 2-dicarboxylate (BEHBD) produced from marine MB8. It was undoubtedly confirmed to BEHBD is a proved cytotoxicity compound. This is the first Bacillus safensis reported to BEHBD produced by marine MB8.

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Inhibition of MAP kinases and down regulation of TNF-α, IL-β and COX-2 genes by the crude extracts from marine bacteria

Cited by 15 publications

References 39 publications

Maltol, a Food Flavoring Agent, Attenuates Acute Alcohol-Induced Oxidative Damage in Mice

Maltol, a Food Flavoring Agent, Attenuates Acute Alcohol-Induced Oxidative Damage in Mice

Mechanism of IL-1β Modulation of Intestinal Epithelial Barrier Involves p38 Kinase and Activating Transcription Factor-2 Activation

Bioactive compound isolated from marine Bacillus safensis MB8 and their cytotoxicity potential

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