Insights antifibrotic mechanism of methyl palmitate: Impact on nuclear factor kappa B and proinflammatory cytokines

Mantawy, Eman M.; Tadros, Mariane G.; Awad, Azza S.; Hassan, Dina A.; El‐Demerdash, Ebtehal

doi:10.1016/j.taap.2011.10.016

Cited by 44 publications

(37 citation statements)

References 52 publications

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“…Raised liver enzyme levels in CCL 4 -injected mice could be attributed to the damaged hepatocellular structural integrity [41]. Similarly, other authors have reported a significant increase in liver enzymes in rats subjected to CCl 4 intoxication [42,43]. According to our findings, treatment of mice with tempol significantly counteracted the hepatotoxic effect of CCl 4 reported in the form of a significant reduction of serum levels of AST, ALT, and total bilirubin compared to CCl 4 intoxicated group.…”

Section: Discussionsupporting

confidence: 80%

Experimental evidence for the therapeutic potential of tempol in the treatment of acute liver injury

et al. 2015

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Oxidative stress is one of the mechanisms involved in the acute carbon tetrachloride (CCl4)-induced hepatotoxicity. Since 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl, known as tempol, has powerful antioxidant properties, we investigated its potential hepatoprotective effects and the underlying mechanisms that may add further benefits for its clinical usefulness using an acute model of CCl4-induced hepatotoxicity. One hour after CCl4 induction of acute hepatotoxicity, mice were treated with a daily dose of 20 mg/kg/day tempol for 3 days. It was found that treatment of animals with tempol significantly negated the pathological changes in liver function parameters as well as histology induced by CCl4. In addition, tempol significantly ameliorated CCl4-induced lipid peroxidation and GSH depletion, and improved catalase activity. Furthermore, tempol alleviated the inflammation induced by CCl4 as indicated by reducing the liver expression level of nuclear factor-kappa B (NF-κB) and tumor necrosis factor-α (TNF-α). Finally, tempol significantly reduced expression level of the B-cell lymphoma-2 protein (Bcl-2) and active caspase-3 which are known markers of apoptosis. In conclusion, the present study provides important evidences for the promising hepatoprotective effects of tempol that can be explained by amelioration of oxidative stress mainly through replenishment of GSH, restoration of antioxidant enzyme activities, and reduction of lipid peroxides alongside its anti-inflammatory properties.

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Section: Discussionsupporting

confidence: 80%

Experimental evidence for the therapeutic potential of tempol in the treatment of acute liver injury

et al. 2015

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“…These results are in accordance with other findings showing that histopathological alternations in the liver tissue are accompanied with an increase in the levels of serum levels of AST and ALT [29,30]. However, the elevated levels of serum marker enzymes may explain cell membrane break down and cell death [31].…”

Section: Discussionsupporting

confidence: 93%

Ameliorative Effects of Pomegranate Peel Extract on Hepatotoxicity Induced by Carbon Tetrachloride in Mice

2016

International Journal of Research Studies in Biosciences

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“…The case is similar with IL-1β. IL-1β, which acts synergistically with TNF-α in activation of NF-κB, is upregulated following bleomycin administration [33]. Transient overexpression of IL-1β induces lung injury and pulmonary fibrosis in the late stages of the experimental setting, while inhibition of IL-1β prevented the fibrosing reaction induced by bleomycin in mice [34].…”

Section: Resultsmentioning

confidence: 99%

Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury

Zheng

Guo

Xiao-ju

et al. 2014

IJMS

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Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF. Here, we investigated the effect of corilagin on lung injury following bleomycin exposure in an animal model of pulmonary fibrosis. Corilagin abrogated bleomycin-induced lung fibrosis as assessed by H&E; Masson’s trichrome staining and lung hydroxyproline content in lung tissue. Corilagin reduced the number of apoptotic lung cells and prevented lung epithelial cells from membrane breakdown, effluence of lamellar bodies and thickening of the respiratory membrane. Bleomycin exposure induced expression of MDA, IKKα, phosphorylated IKKα (p-IKKα), NF-κB P65, TNF-α and IL-1β, and reduced I-κB expression in mice lung tissue or in BALF. These changes were reversed by high-dose corilagin (100 mg/kg i.p) more dramatically than by low dose (10 mg/kg i.p). Last, corilagin inhibits TGF-β1 production and α-SMA expression in lung tissue samples. Taken together, these findings confirmed that corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-β1 signaling. Corilagin may serve as a promising therapeutic agent for pulmonary fibrosis.

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Insights antifibrotic mechanism of methyl palmitate: Impact on nuclear factor kappa B and proinflammatory cytokines

Cited by 44 publications

References 52 publications

Experimental evidence for the therapeutic potential of tempol in the treatment of acute liver injury

Experimental evidence for the therapeutic potential of tempol in the treatment of acute liver injury

Ameliorative Effects of Pomegranate Peel Extract on Hepatotoxicity Induced by Carbon Tetrachloride in Mice

Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury

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