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  1. Article ; Online: Melissa officinalis extract palliates redox imbalance and inflammation associated with hyperthyroidism-induced liver damage by regulating Nrf-2/ Keap-1 gene expression in γ-irradiated rats.

    Kawara, Ragaa Sm / Moawed, Fatma Sm / Elsenosi, Yakout / Elmaksoud, Hussein Abd / Ahmed, Esraa S A / Abo-Zaid, Omayma Ar

    BMC complementary medicine and therapies

    2024  Volume 24, Issue 1, Page(s) 71

    Abstract: Background: Melissa officinalis (MO) is a well-known medicinal plant species used in the treatment of several diseases; it is widely used as a vegetable, adding flavour to dishes. This study was designed to evaluate the therapeutic effect of MO Extract ... ...

    Abstract Background: Melissa officinalis (MO) is a well-known medicinal plant species used in the treatment of several diseases; it is widely used as a vegetable, adding flavour to dishes. This study was designed to evaluate the therapeutic effect of MO Extract against hyperthyroidism induced by Eltroxin and γ-radiation.
    Methods: Hyperthyroidism was induced by injecting rats with Eltroxin (100 µg/kg/ day) for 14 days and exposure to γ-radiation (IR) (5 Gy single dose). The hyperthyroid rats were orally treated with MO extract (75 mg/kg/day) at the beginning of the second week of the Eltroxin injection and continued for another week. The levels of thyroid hormones, liver enzymes and proteins besides the impaired hepatic redox status and antioxidant parameters were measured using commercial kits. The hepatic gene expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its inhibitor Kelch-like ECH-associated protein-1(Keap-1) in addition to hepatic inflammatory mediators including tumor necrosis factor-α (TNF- α), Monocyte chemoattractant protein-1 (MCP-1) and fibrogenic markers such as transforming growth factor-beta1 (TGF-β1) were determined.
    Results: MO Extract reversed the effect of Eltroxin + IR on rats and attenuated the thyroid hormones. Moreover, it alleviated hyperthyroidism-induced hepatic damage by inhibiting the hepatic enzymes' activities as well as enhancing the production of proteins concomitant with improving cellular redox homeostasis by attenuating the deranged redox balance and modulating the Nrf2/Keap-1 pathway. Additionally, MO Extract alleviated the inflammatory response by suppressing the TNF- α and MCP-1 and prevented hepatic fibrosis via Nrf2-mediated inhibition of the TGF-β1/Smad pathway.
    Conclusion: Accordingly, these results might strengthen the hepatoprotective effect of MO Extract in a rat model of hyperthyroidism by regulating the Nrf-2/ Keap-1 pathway.
    MeSH term(s) Animals ; Rats ; Gene Expression ; Hyperthyroidism/complications ; Hyperthyroidism/drug therapy ; Inflammation/metabolism ; Liver ; Melissa/chemistry ; NF-E2-Related Factor 2/metabolism ; Oxidation-Reduction ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Thyroid Hormones/metabolism ; Thyroxine/genetics ; Thyroxine/metabolism ; Transforming Growth Factor beta1/metabolism ; Liver Diseases/etiology ; Liver Diseases/therapy
    Chemical Substances NF-E2-Related Factor 2 ; Plant Extracts ; Thyroid Hormones ; Thyroxine (Q51BO43MG4) ; Transforming Growth Factor beta1
    Language English
    Publishing date 2024-02-01
    Publishing country England
    Document type Journal Article
    ISSN 2662-7671
    ISSN (online) 2662-7671
    DOI 10.1186/s12906-024-04370-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Melissa officinalis extract suppresses endoplasmic reticulum stress-induced apoptosis in the brain of hypothyroidism-induced rats exposed to γ-radiation.

    Abo-Zaid, Omayma Ar / Moawed, Fatma Sm / Taha, Eman Fs / Ahmed, Esraa S A / Kawara, Ragaa Sm

    Cell stress & chaperones

    2023  Volume 28, Issue 6, Page(s) 709–720

    Abstract: The purpose of this study was to demonstrate the neuroprotective effect of Melissa officinalis extract (MEE) against brain damage associated with hypothyroidism induced by propylthiouracil (PTU) and/or γ-radiation (IR) in rats. Hypothyroidism induction ... ...

    Abstract The purpose of this study was to demonstrate the neuroprotective effect of Melissa officinalis extract (MEE) against brain damage associated with hypothyroidism induced by propylthiouracil (PTU) and/or γ-radiation (IR) in rats. Hypothyroidism induction and/or exposure to IR resulted in a significant decrease in the serum levels of T3 and T4 associated with increased levels of lipid peroxidation end product, malondialdehyde (MDA), and nitrites (NO) in the brain tissue homogenate. Also, hypothyroidism and /or exposure to IR markedly enhance the endoplasmic reticulum stress by upregulating the gene expressions of the protein kinase RNA-like endoplasmic reticulum kinase (PERK), activated transcription factor 6 (ATF6), endoplasmic reticulum-associated degradation (ERAD), and CCAAT/enhancer-binding protein homologous protein (CHOP) in the brain tissue homogenate associated with a proapoptotic state which indicated by the overexpression of Bax, BCl2, and caspase-12 that culminates in brain damage. Meanwhile, the PTU and /or IR-exposed rats treated with MEE reduced oxidative stress and ERAD through ATF6. Also, the MEE treatment prevented the Bax and caspase-12 gene expression from increasing. This treatment in hypothyroid animals was associated with neuronal protection as indicated by the downregulation in the gene expressions of the microtubule-associated protein tau (MAPT) and amyloid precursor protein (APP) in the brain tissue. Furthermore, the administration of MEE ameliorates the histological structure of brain tissue. In conclusion, MEE might prevent hypothyroidism-induced brain damage associated with oxidative stress and endoplasmic reticulum stress.
    MeSH term(s) Rats ; Animals ; Melissa/metabolism ; Endoplasmic Reticulum-Associated Degradation ; bcl-2-Associated X Protein/metabolism ; Caspase 12/metabolism ; Brain/metabolism ; Apoptosis ; Hypothyroidism/drug therapy ; Hypothyroidism/metabolism ; Hypothyroidism/pathology ; Endoplasmic Reticulum Stress
    Chemical Substances bcl-2-Associated X Protein ; Caspase 12 (EC 3.4.22.-)
    Language English
    Publishing date 2023-06-27
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1362749-1
    ISSN 1466-1268 ; 1355-8145
    ISSN (online) 1466-1268
    ISSN 1355-8145
    DOI 10.1007/s12192-023-01363-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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