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Articles by Ayman M. Mahmoud
Total Records ( 2 ) for Ayman M. Mahmoud
  Ayman M. Mahmoud , Mousa O. Germoush and Ayman S. Soliman
  The antituberculosis drug-induced hepatotoxicity is a leading cause of liver injury in many countries. The current study aimed to investigate the possible protective effects of the isoquinoline alkaloid berberine against isoniazid (INH)-induced hepatotoxicity in rats. The experimental rats received 100 mg kg-1 b.wt. INH and concurrently administered berberine at doses of 25 and 50 mg kg-1 orally for 45 days. To evaluate the hepatoprotective effects of berberine, serum markers of the liver function, serum pro-inflammatory cytokines and liver oxidant/antioxidant biomarkers were assayed. In addition, gene expression levels of inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB) and peroxisome proliferator-activated receptor gamma (PPARγ) were determined. INH induced hepatic damage evidenced by the significantly elevated serum transaminases, serum pro-inflammatory cytokines and liver lipid peroxidation and nitric oxide levels. Consequently, serum albumin, liver glutathione and activities of the antioxidant enzymes were significantly declined. Further, INH administration produced a significant upregulation of liver iNOS and NF-κB and downregulation PPARγ mRNA expressions. Concurrent supplementation of berberine restored the altered markers to an almost normal state, in a dose-dependent manner. In conclusion , Berberine  protects against INH-induced oxidative stress and inflammation leading to liver injury. The protective effects of berberine can be attributed to its ability to upregulate PPARγ and subsequently suppress NF-κB, iNOS and release of the pro-inflammatory cytokines.
  Gadh Al-Basher , Jamaan S. Ajarem , Ahmed A. Allam and Ayman M. Mahmoud
  Objective: Perinatal nicotine exposure induces malformations and imbalances the prooxidant/antioxidant status. The present study aimed to investigate the possible protective effects of green tea extract against perinatal nicotine-induced alterations in mice newborns. Materials and Methods: Pregnant mice received 0.25 mg k–1 nicotine on gestational day 12 to postnatal day 15. A control group received an equal volume of saline. Both control and nicotine exposed mice received 50 mg k–1 green tea on gestational day 1 to postnatal day 15. Results: Mice born to nicotine-exposed dams showed significantly decreased body weight at days 10, 15 and 20 after birth. Nicotine administration provoked chromatolysis in cerebral neurocytes and oxidative stress, evidenced by elevated lipid peroxidation and declined antioxidants, in newborn mice. Green tea supplementation significantly prevented body weight reduction, histological alterations and oxidative stress. In addition, nicotine significantly increased blood glucose and cholesterol, erythrocytes, leukocytes and platelets, an effect that was significantly reversed following green tea supplementation. Conclusion: Green tea protects against perinatal nicotine-induced oxidative stress and hematologic, histologic and metabolic alterations. Therefore, green tea may be considered a potential candidate for attenuating smoking/nicotine-induced alterations in newborns.
 
 
 
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