Browsing by Author "Abdelhamid A.M."

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    Amitriptyline attenuates bleomycin-induced pulmonary fibrosis: modulation of the expression of NF-κβ, iNOS, and Nrf2
    (Springer Verlag, 2019) Zaafan M.A.; Haridy A.R.; Abdelhamid A.M.; Pharmacology and Toxicology Department; Faculty of Pharmacy; October University for Modern Sciences and Arts (MSA); 6th of October; Egypt; Biochemistry Department; Faculty of Pharmacy; October University for Modern Sciences and Arts (MSA); 6th of October; Egypt
    Amitriptyline is a tricyclic antidepressant that was suggested to have antifibrotic potential. The current study aimed to investigate the modulatory effects of amitriptyline on bleomycin-induced pulmonary fibrosis in rats. Rats were randomly assigned into 4 groups: normal control, bleomycin control, amitriptyline+bleomycin, and amitriptyline only treated group. Lung injury was evaluated through the histological examination and immunohistochemical detection of ?-smooth muscle actin (?-SMA) in lung tissue, in addition to the biochemical assessment of pulmonary contents of hydroxyproline and transforming growth factor beta-1 (TGF-?1). In addition, the following parameters were investigated for studying the possible mechanisms of amitriptyline antifibrotic effect: inducible nitric oxide synthase (iNOS), nuclear factor-?? (NF-??), tumor necrosis factor-alpha (TNF-?), serpine-1, p53, nuclear factor erythroid 2-related factor 2 (Nrf2), lipid peroxides, and reduced glutathione (GSH). Amitriptyline exhibited potent antifibrotic effect that was reflected upon the histopathological examination and through its ability to suppress all the fibrotic parameters. Amitriptyline successfully suppressed the expression of NF-??, Nrf2, iNOS, and p53 in lung tissues besides the inhibition of other oxidative stress and inflammatory mediators. Amitriptyline could be a promising treatment to pulmonary fibrosis. Amitriptyline not only prevents the depression and its drawbacks in patients suffering from pulmonary fibrosis but also it can suppress fibrosis through variable mechanisms mainly via inhibition of NF-??/TNF-?/TGF-? pathway in addition to inhibition of Nrf2 and iNOS expression. � 2018, Springer-Verlag GmbH Germany, part of Springer Nature.
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    The protective effect of Korean red ginseng against rotenone-induced parkinsons disease in rat model: Modulation of nuclear factor- and caspase-3
    (Bentham Science Publishers, 2019) Zaafan M.A.; Abdelhamid A.M.; Ibrahim S.M.; Pharmacology & Toxicology Department; Faculty of Pharmacy; MSA University; Egypt; Biochemistry Department; Faculty of Pharmacy; MSA University; Egypt
    Objective: Korean red ginseng was reported to have many biological effects like the antioxidant and the anti-inflammatory activities. Oxidative stress and neuro-inflammation play major roles in the pathogenesis of Parkinsons disease (PD). The current study aimed to investigate the protective effects of ginseng on rotenone-induced PD in rats. Methods: Rats were randomly allocated into 4 groups: Normal rats, rotenone control, ginseng+rotenone and ginseng only treated rats. The severity of PD was evaluated through locomotor activity perceived in the open field test, histological examination and immunohistochemical detection of amyloid-? in brain tissues, in addition to the biochemical assessment of tyrosine hydroxylase activity in brain tissues. Moreover, the following parameters were investigated for studying the possible mechanisms of ginseng neuroprotective effect: Nuclear factor-?? (NF-??), tumor necrosis factor-alpha (TNF-?), caspase- 3, lipid peroxides and reduced glutathione (GSH). Results: Ginseng exhibited potent neuroprotective effect that was reflected upon the histopathological examination, marked improvement in the locomotor activity and through its ability to suppress the amyloid-? deposition in the cortex and striatum along with significant increase in the tyrosine hydroxylase activity. Ginseng successfully inhibited the NF-?? inflammatory pathway in brain tissues beside the inhibition of other oxidative stress and inflammatory mediators. Furthermore, it exhibited antiapoptotic effect via the inhibition of caspase-3 expression. Conclusion: Ginseng could be a promising treatment in PD. It can suppress dopaminergic neuron degeneration through variable mechanisms mainly via inhibition of NF-?? pathway in addition to inhibition of oxidative stress and apoptosis. 2019 Bentham Science Publishers.