Chemopreventive role of arabinoxylan rice bran, MGN-3/Biobran, on liver carcinogenesis in rats

El-Din, Nariman K. Badr; Ali, Doaa A.; Othman, Reem; French, Samuel W.; Ghoneum, Mamdooh

doi:10.1016/j.biopha.2020.110064

Cited by 23 publications

(19 citation statements)

References 35 publications

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“…Neuronal loss can be caused by mitochondrial dysfunction via the regulation of proapoptotic proteins like caspase-3 and Bax and antiapoptotic proteins like Bcl-2 [ 14 , 15 , 20 ]. The ability of Biobran to exert a protective effect against STZ-induced apoptosis is in accordance with our earlier studies showing that Biobran treatment upregulated Bax expression, activated caspase-3, and downregulated Bcl-2 expression; these well-established molecular events in apoptosis have shown that Biobran can protect against glandular stomach carcinogenesis in rats [ 49 ], inhibit hepatocarcinogenesis in rats [ 50 ], and enhance fractionated X-ray irradiation's anticancer effects for Ehrlich solid tumor-bearing mice [ 59 ].…”

Section: Discussionsupporting

confidence: 90%

Protective Effect of Biobran/MGN‐3 against Sporadic Alzheimer’s Disease Mouse Model: Possible Role of Oxidative Stress and Apoptotic Pathways

Ghoneum

Sayed

2021

Oxidative Medicine and Cellular Longevity

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Alzheimer’s disease (AD) is a debilitating and irreversible brain disease that affects an increasing number of aged individuals, mandating the development of protective nutraceuticals. Biobran/MGN-3, an arabinoxylan from rice bran, has potent antioxidant, antiaging, and immunomodulatory effects. The aim of the present study was to investigate the protective effect of Biobran against sporadic Alzheimer’s disease (SAD). SAD was induced in mice via intracerebroventricular injection of streptozotocin (STZ) (3 mg/kg). STZ-treated mice were administered with Biobran for 21 days. The effects of Biobran on memory and learning were measured via the Morris water maze, novel object recognition, and Y-maze tests. Biomarkers for apoptosis, oxidative stress, and amyloidogenesis were measured using ELISA and western blot analysis. Histopathological examination was performed to confirm neuronal damage and amyloid-beta deposition. Biobran reversed the spatial memory deficit in SAD-induced mice, and it increased the expression of glutathione, reduced malondialdehyde, decreased IL-6, decreased intercellular adhesion molecule-1 (ICAM-1), and significantly increased nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidant response element (ARE). Moreover, Biobran exerted a protective effect against amyloid-beta-induced apoptosis via the suppression of both cleaved caspase-3 and the proapoptotic protein Bax and via the upregulation of the antiapoptotic protein Bcl-2. Furthermore, it reduced the expression of forkhead box class O proteins. It could be concluded from this study that Biobran may be a useful nutritional antioxidant agent for protection against SAD through its activation of the gene expression of Nrf2/ARE, which in turn modulates the apoptotic and amyloidogenic pathways.

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Section: Discussionsupporting

confidence: 90%

Protective Effect of Biobran/MGN‐3 against Sporadic Alzheimer’s Disease Mouse Model: Possible Role of Oxidative Stress and Apoptotic Pathways

Ghoneum

Sayed

2021

Oxidative Medicine and Cellular Longevity

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“…The mean body weight of HCC group (group III) was less than the other three groups with no stastistically significant reduction that might be related to the toxic effect of CCL4 and DEN and the decrease of the appetite. Similar studies related to HCC reported body weight reduction and tissue destruction (Singh et al, 2018;Badr El-Din et al, 2020) as compared to the control group.…”

Section: Discussionsupporting

confidence: 72%

The Apoptotic Effect of Trichinella spiralis Infection Against Experimentally Induced Hepatocellular Carcinoma

Elhasawy

Ashour

Elsaka

et al. 2021

Asian Pac J Cancer Prev

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Background: Hepatocellular carcinoma (HCC) is the sixth most common type of cancer. Prognosis of HCC remains unsatisfactory. Therefore, developing new therapeutic modalities is still mandatory. Tumor biotherapy is a novel concept developed as a therapeutic strategy for cancer treatment. There is a similarity between the regulatory mechanism of Trichinella spiralis nurse cell formation and tumor cell apoptosis signal regulation. Objectives: Induction of apoptosis by T. spiralis can represent a new strategy for tumor treatment. Methods: Experimental animals were divided in four groups; negative control (GI), T. spiralis infected (GII), induced HCC (GIII) and HCC then infected with T. spiralis (GIV). The apoptotic effect of T. spiralis infection was assessed by histopathological and immunohistochemical staining of B-cell lymphoma 2 (Bcl-2). Results: We found higher survival rate of rats and decreased weight of their livers with no nodules in HCC-T. spiralis group as compared to HCC group. Improvement of the dysplastic changes and increased apoptotic bodies which was confirmed by decreased expression of Bcl-2 reported in HCC-T. spiralis group. Conclusion: Trichinella-induced apoptosis can be a contributing mechanism of the anti-tumor effect of T. spiralis infection. Our results showed a certain level of decreased progression of the tumor in HCC-T. spiralis group as indicated by increased rate of apoptosis and subsequently had a positive impact on the survival of rats.

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“…Natural compounds, including rice bran, with anti-carcinogenic effects induce apoptosis and thus reduce the accumulation of mutated cells, but simultaneously inhibit inflammation and regenerative proliferation ( Badr El-Din, Ali, Othman, French, & Ghoneum, 2020 ). Many environmental carcinogens dysregulate the cycles of cell death and proliferation by regulating pro- and anti-apoptotic proteins such as Bax, Bcl-2, caspases and other signaling cascades.…”

Section: Mechanisms Of Pro-tumorigenic Activity By Carcinogensmentioning

confidence: 99%

Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

129

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Inflammation in the tumor microenvironment is a hallmark of cancer and is recognized as a key characteristic of carcinogens. However, the failure of resolution of inflammation in cancer is only recently being understood. Products of arachidonic acid and related fatty acid metabolism called eicosanoids, including prostaglandins, leukotrienes, lipoxins, and epoxyeicosanoids, critically regulate inflammation, as well as its resolution. The resolution of inflammation is now appreciated to be an active biochemical process regulated by endogenous specialized pro-resolving lipid autacoid mediators which combat infections and stimulate tissue repair/regeneration. Environmental and chemical human carcinogens, including aflatoxins, asbestos, nitrosamines, alcohol, and tobacco, induce tumor-promoting inflammation and can disrupt the resolution of inflammation contributing to a devastating global cancer burden. While mechanisms of carcinogenesis have focused on genotoxic activity to induce mutations, nongenotoxic mechanisms such as inflammation and oxidative stress promote genotoxicity, proliferation, and mutations. Moreover, carcinogens initiate oxidative stress to synergize with inflammation and DNA damage to fuel a vicious feedback loop of cell death, tissue damage, and carcinogenesis. In contrast, stimulation of resolution of inflammation may prevent carcinogenesis by clearance of cellular debris via macrophage phagocytosis and inhibition of an eicosanoid/cytokine storm of pro-inflammatory mediators. Controlling the host inflammatory response and its resolution in carcinogen-induced cancers will be critical to reducing carcinogen-induced morbidity and mortality. Here we review the recent evidence that stimulation of resolution of inflammation, including pro-resolution lipid mediators and soluble epoxide hydrolase inhibitors, may be a new chemopreventive approach to prevent carcinogen-induced cancer that should be evaluated in humans.

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Chemopreventive role of arabinoxylan rice bran, MGN-3/Biobran, on liver carcinogenesis in rats

Cited by 23 publications

References 35 publications

Protective Effect of Biobran/MGN‐3 against Sporadic Alzheimer’s Disease Mouse Model: Possible Role of Oxidative Stress and Apoptotic Pathways

Protective Effect of Biobran/MGN‐3 against Sporadic Alzheimer’s Disease Mouse Model: Possible Role of Oxidative Stress and Apoptotic Pathways

The Apoptotic Effect of Trichinella spiralis Infection Against Experimentally Induced Hepatocellular Carcinoma

Carcinogenesis: Failure of resolution of inflammation?

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