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    Induction of liver fibrosis by CCl4 mediates pathological alterations in the spleen and lymph nodes: The potential therapeutic role of propolis
    (Elsevier, 2021) Sayed, Eman A.; Badr, Gamal; Hassan, Khadiga Abdel-Hameed; Waly, Hanan; Ozdemir, Betul; Mahmoud, Mohamed H.; Alamery, Salman
    In an animal models, carbon tetrachloride (CCl4) is a carcinogenic agent that causes liver fibrosis. The current study aims to investigate whether induction in liver-fibrosis by CCl4 in the mouse model could promote the initiation of fibrosis in lymph node and spleen due to sustained increase of inflammatory signals and also aimed to clarify the protective therapeutic effects of propolis. The male mice (BALB/c) were categorized into three experimental sets and each group involved 15 mice. Control group falls into first group; group-II and group-III were injected with CCl4 to induce liver-fibrosis and oral supplementation with propolis was provided in group-III for 4-weeks. A major improvement with hepatic collagen and alpha-smooth muscle actin (alpha-SMA) production was aligned with the activation of liver fibrosis from CCl4. Mice treated with CCl4 exhibited collagen deposition towards liver sections, pathological alterations in spleen and lymph node architectures, and a significantly increase the circulation of both T&B cells in secondary lymphoid organs. Mechanically, the secondary lymphoid organs treated with CCl4 in mice exposed a positive growth in alpha-SMA and collagen expression, increased in proinflammatory cytokine levels and a significant increase in TGF-beta, NO and ROS levels. A manifest intensification in the expression of Nrf2, COX-2, and eNOS and upregulation of ASK1 and P38 phosphorylation. Interestingly, addition of propolis-treated CCl4 mice, substantially suppressed deposition of liver collagen, repealed inflammatory signals and resorted CCl4-mediated alterations in signaling cascades, thereby repairing the architectures of the secondary lymphoid organs. Our findings revealed benefits of propolis against fibrotic complications and enhancing secondary lymphoid organ architecture. (C) 2020 The Author(s). Published by Elsevier B.V. on behalf of King Saud University.
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    The therapeutic mechanisms of propolis against CCl4-mediated liver injury by mediating apoptosis of activated hepatic stellate cells and improving the hepatic architecture through PI3K/AKT/mTOR, TGF-?/Smad2, Bcl2/BAX/P53 and iNOS signaling pathways
    (Cell Physiol Biochem Press GmbH & Co KG, 2019) Badr, Gamal; Sayed, Eman Abdo; Waly, Hanan; Hassan, Khadiga Abdel-Hameed; Mahmoud, Mohamed H.; Selamoglu, Zeliha
    Background/Aims: Propolis is one of the most promising natural products, exhibiting not only therapeutic but also prophylactic actions. Propolis has several biological and pharmacological properties, including hepatoprotective activities. The present study aimed to investigate the underlying molecular mechanisms of propolis against CCl4-mediated liver fibrosis. Methods: Three groups of male BALB/c mice (n=15/group) were used: group 1 comprised control mice; groups 2 and 3 were injected with CCl4 for the induction of liver fibrosis. Group 3 was then orally supplemented with propolis (100 mg/kg body weight) for four weeks. Different techniques were used to monitor the antifibrotic effects of propolis, including histopathological investigations using H&E, Masson's trichrome and Sirius red staining; Western blotting; flow cytometry; and ELISA. Results: We found that the induction of liver fibrosis by CCl4 was associated with a significant increase in hepatic collagen and ?-smooth muscle actin (?-SMA) expression. Moreover, CCl4-treated mice also exhibited histopathological alterations in the liver architecture. Additionally, the liver of CCl4-treated mice exhibited a marked increase in proinflammatory signals, such as increased expression of HSP70 and increased levels of proinflammatory cytokines and ROS. Mechanistically, the liver of CCl4-treated mice exhibited a significant increase in the phosphorylation of AKT and mTOR; upregulation of the expression of BAX and cytochrome C; downregulation of the expression of Bcl2; a significant elevation in the levels of TGF-? followed by increased phosphorylation of SMAD2; and a marked increase in the expression of P53 and iNOS. Interestingly, oral supplementation of CCl4-treated mice with propolis significantly abolished hepatic collagen deposition, abrogated inflammatory signals and oxidative stress, restored CCl4-mediated alterations in the signaling cascades, and hence repaired the hepatic architecture nearly to the normal architecture observed in the control mice. Conclusion: Our findings revealed the therapeutic potential and the underlying mechanisms of propolis against liver fibrosis. © 2019 The Author(s).