Browsing by Author "Zaafan M.A."

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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.
Eicosapentaenoic acid and vitamin e against doxorubicin-induced cardiac and renal damages: Role of cytochrome c and inos
(Academy of Medical Sciences of I.R. Iran, 2018) Fayez A.M.; Zaafan M.A.; Pharmacology and Toxicology Department; Faculty of Pharmacy; October University for Modern Sciences; Arts; Egypt
Background: The current study aimed to evaluate the mechanisms involved in protection against doxorubicin-induced cardiac and renal toxicities upon treatment with eicosapentaenoic acid and vitamin E. Methods: Rats were randomly assigned to 4 groups: normal control, doxorubicin inducted control, eicosapentaenoic acid treated group and a final group pretreated with vitamin E. Lipid peroxidation, reduced glutathione (GSH) and tumor necrosis factor-alpha (TNF-?) contents as well as glutathione peroxidase (GPx), superoxide dismutase (SOD) and myeloperoxidase (MPO) activities were assessed. Moreover, hearts were used for immunohistochemical detection of the pro-apoptotic protein cytochrome c expression, while the kidneys were used for detection of inducible nitric oxide synthase (iNOS) expression. Results: Eicosapentaenoic acid and vitamin E produced significant protection from doxorubicin-induced cardiac and renal toxicities. The suggested mechanisms for protection included decreased cytochrome c and iNOS expression as well as markedly decreased lipid peroxides and TNF-? contents accompanied with increased GSH content as compared to the doxorubicin control group. Moreover, there was marked increase in GPx and SOD activities accompanied by significant suppression of MPO activity. Conclusion: The present study demonstrated the potent protective effects of eicosapentaenoic acid and vitamin E from doxorubicin induced cardiac and renal toxicities through their potent anti-oxidant, anti-inflammatory and anti-apoptotic properties. Hence, eicosapentaenoic acid and vitamin E could be promising protective agents against doxorubicintoxicity. � 2019, Academy of Medical Sciences of I.R. Iran. All rights reserved.
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.
Pyrrolidinedithiocarbamate attenuates bleomycin-induced pulmonary fibrosis in rats: Modulation of oxidative stress, fibrosis, and inflammatory parameters
(Taylor and Francis Ltd, 2016) Zaafan M.A.; Zaki H.F.; El-Brairy A.I.; Kenawy S.A.; Pharmacology & Toxicology Department; Faculty of Pharmacy; October University for Modern Sciences and Arts; Cairo; Egypt; Pharmacology & Toxicology Department; Faculty of Pharmacy; Cairo University; Giza; Egypt
Objective: The current study aimed to investigate the modulatory effects of pyrrolidinedithiocarbamate (PDTC; 100. mg/kg) on bleomycin-induced pulmonary fibrosis (5�mg/kg; intratracheal) in rats. Materials and Methods: Rats were randomly assigned to three groups: normal control, bleomycin control, and PDTC-treated groups. Lung injury was evaluated through histological examination, immunohistochemical detection of inducible nitric oxide synthase (iNOS) in lung tissue and evaluating the total and differential leucocytes count in bronchoalveolar lavage fluid. Lung tissue was used for biochemical assessment of lung content of hydroxyproline, transforming growth factor beta-1 (TGF-?1), tumor necrosis factor-alpha (TNF-?) as well as analysis of lipid peroxides, reduced glutathione (GSH), and total nitrite contents. Results: PDTC attenuated bleomycin-induced pulmonary fibrosis as evidenced by histological observations, decreased iNOS expression and prevention of bleomycin-induced altered total and differential leukocytes count. Additionally, PDTC caused a significant decrease in lung contents of hydroxyproline, TGF-?1, TNF-?, lipid peroxides, and total nitrite coupled with increase in lung GSH content as compared to bleomycin control group. Conclusion: PDTC attenuated bleomycin-induced pulmonary fibrosis in rats via its anti-inflammatory, antioxidant, and antifibrotic activities. � 2016 Taylor & Francis.