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- 저자 : Abdulmannan Fadel (검색결과 2 건)
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Yazan Ranneh,Faisal Ali,Abdah Md Akim,Hasiah Abd. Hamid,Huzwah Khazaai,Abdulmannan Fadel 한국응용생명화학회 2017 Applied Biological Chemistry (Appl Biol Chem) Vol.60 No.3
The inflammation process in the human body plays a central role in the pathogenesis of many chronic diseases. In addition, reactive oxygen species (ROS) exert potentially a decisive role in human body, particularly in physiological and pathological process. The chronic inflammation state could generate several types of diseases such as cancer, atherosclerosis, diabetes mellitus and arthritis, especially if it is concomitant with high levels of pro-inflammatory markers and ROS. The respiratory burst of inflammatory cells during inflammation increases the production and accumulation of ROS. However, ROS regulate various types of kinases and transcription factors such nuclear factor-kappa B which is related to the activation of pro-inflammatory genes. The exact crosstalk between pro-inflammatory markers and ROS in terms of pathogenesis and development of serious diseases is still ambitious. Many studies have been attempting to determine the mechanistic mutual relationship between ROS and proinflammatory markers. Therefore hereby, we review the hypothetical relationship between ROS and pro-inflammatory markers in which they have been proposed to initiate cancer, atherosclerosis, diabetes mellitus and arthritis.
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Mahmoud, Ayman M.,Alqahtani, Sultan,Othman, Sarah I.,Germoush, Mousa O.,Hussein, Omnia E.,Al-Basher, Gadh,Khim, Jong Seong,Al-Qaraawi, Maha A.,Al-Harbi, Hanan M.,Fadel, Abdulmannan,Allam, Ahmed A. Hindawi 2017 Oxidative medicine and cellular longevity Vol.2017 No.-
<P>Hyperammonemia is a serious complication of liver disease and may lead to encephalopathy and death. This study investigated the effects of <I>Commiphora molmol</I> resin on oxidative stress, inflammation, and hematological alterations in ammonium chloride- (NH<SUB>4</SUB>Cl-) induced hyperammonemic rats, with an emphasis on the glutamate-NO-cGMP and Nrf2/ARE/HO-1 signaling pathways. Rats received NH<SUB>4</SUB>Cl and <I>C. molmol</I> for 8 weeks. NH<SUB>4</SUB>Cl-induced rats showed significant increase in blood ammonia, liver function markers, and tumor necrosis factor-alpha (TNF-<I>α</I>). Concurrent supplementation of <I>C. molmol</I> significantly decreased circulating ammonia, liver function markers, and TNF-<I>α</I> in hyperammonemic rats. <I>C. molmol</I> suppressed lipid peroxidation and nitric oxide and enhanced the antioxidant defenses in the liver, kidney, and cerebrum of hyperammonemic rats. <I>C. molmol</I> significantly upregulated Nrf2 and HO-1 and decreased glutamine and nitric oxide synthase, soluble guanylate cyclase, and Na<SUP>+</SUP>/K<SUP>+</SUP>-ATPase expression in the cerebrum of NH<SUB>4</SUB>Cl-induced hyperammonemic rats. Hyperammonemia was also associated with hematological and coagulation system alterations. These alterations were reversed by <I>C. molmol</I>. Our findings demonstrated that <I>C. molmol</I> attenuates ammonia-induced liver injury, oxidative stress, inflammation, and hematological alterations. This study points to the modulatory effect of <I>C. molmol</I> on glutamate-NO-cGMP and Nrf2/ARE/HO-1 pathways in hyperammonemia. Therefore, <I>C. molmol</I> might be a promising protective agent against hyperammonemia.</P>
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