Browsing by Author "E Abdel Moneim, Ahmed"

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    Cinnamic acid Attenuates Cisplatin-Induced Hepatotoxicity and Nephrotoxicity
    (Journal of Basic and Environmental Sciences, 2016) A Tohamy, Amany; M Aref, Ahmed; E Abdel Moneim, Ahmed; H Sayed, Romissaa
    We investigated the effects of cinnamic acid (CA, 20 mg/kg body weight) oncisplatin (CP)-induced hepto and nephrotoxicity in mice. CP (5 mg/kg bwt)wasinjected intraperitoneally and CA was given by gastric gavage for 5 days pre-andpost-CP injection. After 5 days of CP injection, CP-induced injuries of the hepaticand renal tissues which were evidenced (i) histopathological damage of the hepaticandrenal tissues, (ii) as increases in liver and kidney function parameters, (iii) asincreases in lipid peroxidation and nitric oxide, and (iv) as decrease in glutathionecontent. In contrast, the oral administration of CA concurrently to CP intoxicatedmice brought back lipid peroxidation, nitric oxide, glutathione levels to nearnormalcy. Moreover, the histological observations evidenced that CA effectivelyrescues the liver and kidney from CP mediated oxidative damage. Therefore,cinnamic acid can be considered a potential candidate for protection of hepato-andnephrotoxicity induced by cisplatin.
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    The Potential Role ofAzadirachta indicaTreatment onCisplatin-Induced Hepatotoxicity and Oxidative Stressin Female Rats
    (Hindawi, 2013) M Aref, Ahmed; A Dkhil, Mohamed; Al-Quraishy, Saleh; S Othman, Mohamed; M. El-Deib, Kamal; E Abdel Moneim, Ahmed
    Azadirachta indica A. Juss. (neem, family: Meliaceae) is perhaps the most commonly used traditional medicinal plant of India. In this study we investigated the protective effect of methanolic neem leaves extract (MNLE; 500 mg/Kg bwt) on rats treated with cisplatin (CDDP)-induced hepatotoxicity. Adult rats were randomly divided into four groups. CDDP was given to rats by intraperitoneal injection, while MNLE was given by oral gavage for 5 days after the CDDP injection. The injury and oxidative stress caused by CDDP on the liver and the effect of MNLE were evaluated by measuring (a) histological changes, (b) tissue biochemical oxidant and antioxidant parameters, and (c) investigating apoptosis markers immunohistochemically and by real time PCR. After treatment with MNLE, the histological damage and apoptosis induction caused by cisplatin were improved. Malondialdehyde and nitric oxide were significantly decreased; the antioxidant system, namely, glutathione content, glutathione-S-transferase, glutathione peroxidase, catalase, and superoxide dismutase activities were significantly elevated. In conclusion, MNLE may have a potential role when combined with cisplatin in chemotherapy to alleviate cisplatin-induced damage and oxidative stress in liver
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    Rutin and Selenium Co-administration Reverse 3-Nitropropionic Acid-Induced Neurochemical and Molecular Impairments in a Mouse Model of Huntington’s Diseas
    (SPRINGER, 2020) S Abdelfattah, Mohamed; EA Badr, Sherif; A Lotfy, Sally; H Attia, Gouda; M Aref, Ahmed; E Abdel Moneim, Ahmed; B Kassab, Rami
    Systemic administration of 3-nitropropionic acid (3-NPA) is commonly used to induce Huntington’s disease (HD)-like symptoms in experimental animals. Here, the potential neuroprotective efficiency of rutin and selenium (RSe) co-administration on 3-NPA-induced HD-like symptoms model in mice was investigated. 3-NPA injection evoked severe alterations in redox status, as indicated via increased striatal malondialdehyde and nitric oxide levels, accompanied by a decrease in levels of antioxidant molecules including glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase. Moreover, 3-NPA potentiated inflammatory status by enhancing the production of interleukin-1β, tumor necrosis factor-α, and myeloperoxidase activity. Pro-apoptotic cascade was also recorded in the striatum as evidenced through upregulation of cleaved caspase-3 and Bax, and downregulation of Bcl-2. 3-NPA activated astrocytes as indicated by the upregulated glial fibrillary acidic protein and inhibited brain-derived neurotrophic factor. Furthermore, perturbations in cholinergic and monoaminergic systems were observed. RSe provided neuroprotective effects by preventing body weight loss, oxidative stress, neuroinflammation, and the apoptotic cascade. RSe inhibited the activation of astrocytes, increased brain-derived neurotrophic factor, and improved cholinergic and monoaminergic transmission following 3-NPA intoxication. Taken together, RSe co-administration may prevent or delay the progression of HD and its associated impairments through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory effects