scholarly journals Nitric Oxide Inhibits Lipopolysaccharide-Induced Inducible Nitric Oxide Synthase Expression and Its Own Production Through the cGMP Signaling Pathway in Murine Microglia BV-2 Cells

2010 ◽  
Vol 113 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Yasuhiro Yoshioka ◽  
Nobuo Takeda ◽  
Akiko Yamamuro ◽  
Atsushi Kasai ◽  
Sadaaki Maeda
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Signaling Pathway ◽  
Inducible Nitric Oxide Synthase ◽  
Cgmp Signaling ◽  
Murine Microglia ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Modulation of oxidative–nitrosative stress and inflammatory response by rapamycin in target and distant organs in rats exposed to hindlimb ischemia–reperfusion: the role of mammalian target of rapamycin

2019 ◽  
Vol 97 (12) ◽  
pp. 1193-1203
Author(s):  
Zumrut Kocak ◽  
Meryem Temiz-Resitoglu ◽  
Demet Sinem Guden ◽  
Ozden Vezir ◽  
Nehir Sucu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Signaling Pathway ◽  
Inducible Nitric Oxide Synthase ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion ◽  
Mammalian Target Of Rapamycin ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Mammalian target of rapamycin (mTOR) has been recognized with potential immunomodulatory properties playing an important role in various physiopathological processes including ischemia–reperfusion (I/R) injury. I/R injury stimulate reactive oxygen and nitrogen species by activating nicotinamide adenine dinucleotide phosphate oxidase and inducible nitric oxide synthase, respectively. Controversial results have been obtained in different I/R models following localized I/R; however, the precise role of the mTOR signaling pathway remains undefined. The objective of the current study was to evaluate the role of the mTOR in oxidative–nitrosative stress and inflammation in hindlimb I/R-induced injury in target and remote organ injuries. In rats subjected to I/R, an increased expression of ribosomal protein S6 (rpS6), inhibitor κB (IκB)-α, nuclear factor-κB (NF-κB) p65, inducible nitric oxide synthase, cyclooxygenase 2, gp91phox, and levels of tumor necrosis factor α, nitrite, nitrotyrosine, malondialdehyde and the activities of myeloperoxidase and catalase in the tissues and (or) sera were detected. Treatment with rapamycin, a selective inhibitor of mTOR, reversed all the I/R-induced changes as manifested by its anti-inflammatory and antioxidant effects in kidney and gastrocnemius muscle of rats. Collectively, these findings suggest that rapamycin protects against I/R-induced oxidative–nitrosative stress and inflammation leading to organ injuries via suppression of mTOR/IκB-α/NF-κB signaling pathway.

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