• Biomedical Science Letters
• /
• v.24 no.2
• /
• pp.102-107
• /
• 2018

Toll-like receptors (TLRs) play an important role for host defense against invading pathogens. The activation of TLRs signaling leads to the activation of $NF-{\kappa}B$ and the expression of pro-inflammatory gene products such as cytokines and inducible nitric oxide synthase (iNOS). To evaluate the therapeutic potential of cardamonin, which is a naturally occurring chalcone from Alpinia species (zingiberaceous plant species), $NF-{\kappa}B$ activation and iNOS expression induced by MALP-2 (TLR2 and TLR6 agonist) or LPS (TLR4 agonist) were examined. Cardamonin inhibited the activation of $NF-{\kappa}B$ induced by MALP-2 or LPS. Cardamonin also suppressed the iNOS expression induced by MALP-2 or LPS. These results suggest that cardamonin has the specific mechanism for anti-inflammatory responses by regulating of TLRs signaling pathway.

• Biomedical Science Letters
• /
• v.23 no.2
• /
• pp.104-110
• /
• 2017

Inflammation is a pathophysiological process that is known to be involved in numerous diseases. Microbial infection or tissue injury activates inflammatory responses, resulting in the induction of proinflammatory proteins including inducible nitric oxide synthase (iNOS). Aster yomena is used in traditional Korean remedies. Here, we investigated the effects of ethanol extracts of Aster yomena (EAY) on the expression of iNOS induced by ovalbumin (OVA), one of the major egg allergens, or lipopolysaccharide (LPS), a Toll-like receptor 4 agonist. EAY inhibited OVA- or LPS-induced $NF-{\kappa}B$ activation. EAY also suppressed OVA- or LPS-induced iNOS expression and nitrite production. These results suggest that EAY has the specific mechanism for anti-inflammatory responses and the potential to be developed as a potent anti-inflammatory and anti-allergic drug.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.05a
• /
• pp.50-50
• /
• 2003

Nitric oxide (NO) has been studied and found to be an important intracellular modulator. The excess NO produced by the inducible nitric-oxide synthase (iNOS) is implicated in various inflammatory diseases and cellular injury. Inflammatory cytokines such as TNF- or IL-6 increase intracellular ceramide and ceramide may induce NO production and inflammation. (omitted)

• Proceedings of the PSK Conference
• /
• 2002.10a
• /
• pp.293.2-293.2
• /
• 2002

Bisphenol A ［BPA. 2.2-bis(4-hydroxyphenyl)propane］ is reported to have estrogenic activity: however. its influence on cytokine production or immune system function remains unclear. In this study. we investigated the effects of BPA on the production of nitric oxide (NO) and tumor necrosis factor-a (TNF-a), and on the level of inducible nitric oxide synthase (iNOS) and TNF-a gene expression in mouse macrophages. BPA alone did not affect NO or TNF-a production. (omitted)

• Biomedical Science Letters
• /
• v.29 no.2
• /
• pp.66-74
• /
• 2023

Triglyceride (TG) accumulation can cause monocytic death and suppress innate immunity. However, the signaling pathways involved in this phenomenon are not fully understood. This study aimed to examine whether inducible nitric oxide synthase (iNOS) is involved in the TG-induced death of THP-1 monocytes. Results showed that iNOS was upregulated in TG-treated THP-1 monocytes, and iNOS inhibition blocked TG-induced monocytic death. In addition, TG-induced poly (ADP-ribose) polymerase (PARP) cleavage and caspase-3 and -7 activation were suppressed by iNOS inhibition. Furthermore, the expression of X-linked inhibitor of apoptosis protein (XIAP) and survivin, which inhibit caspase-3 and -7, was reduced in TG-treated THP-1 monocytes, but iNOS inhibition recovered the TG-induced downregulation of XIAP and survivin expression. Considering that TG-induced monocytic death is triggered by caspase2 and -8, we investigated whether caspase-2 and -8 are linked to the TG-induced expression of iNOS in THP-1 monocytes. When the activities of caspase-2 and -8 were inhibited by specific inhibitors, the TG-induced upregulation of iNOS and downregulation of XIAP and survivin were restored in THP-1 monocytes. These results suggest that TG-induced monocytic death is mediated by the caspase-2/caspase-8/iNOS/XIAP and survivin/executioner caspase/PARP pathways.

• YAKHAK HOEJI
• /
• v.43 no.2
• /
• pp.214-220
• /
• 1999

Present study was aimed to examine whether indomethacin affected the production of NO in the rat paw exudate by carrageenin. Paw edema and nitrite/nitrate levels in the paw exudate were maximal after 4 h and remained elevated up to 10 h, whereas indomethacin (10 mg/kg, po) significantly inhibited the carrageenin-induced paw edema and levels of nitrate in the paw exudate. However, paw edema and nitrite/nitrite levels were increased thereafter for 10 h. Indomethacin also enhanced the expression of iNOS mRNA and protein 4 h after carrageenin infection. Indomethacin inhibited the level of $PGE_2$ in the paw exudate in a time-dependent manner. These results suggest the possibility that indomethacin may potentiate expression of iNOS and subsequently increase nitrite/nitrate level in the late phase of carrageenin-induced rat paw inflammation possibly by suppressing cycloxygenase activity.

• Journal of Korean Society for Atmospheric Environment
• /
• v.18 no.E2
• /
• pp.121-128
• /
• 2002

This study was carried out to investigate if nitric oxide synthase (NOS) inhibitors modulate airway inflammation induced by diesel exhaust particles (DEP). N$\^$G/-nitro-L-arginine methyl ester (L-NAME), a potent constitutive NOS (cNOS) inhibitor, and aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, were administered to mice in their drinking water for 7 weeks. Airway inflammation was elicited by the repeated intratracheal administration of DEP. The results showed that macrophages, inflammatory eosinophils and neutrophils in bronchoalveolar lavage (BAL) fluids by intratracheal DEP instillation were significantly suppressed in the mice treated with two NOS inhibitors toghther with DEP. The suppression of these cells was more effective in AG treated groups than in L -NAME treated groups. NOS inhibitor treatment also reduced interleukin -5 (IL-5 in the BAL fluids and lung homogenates. Additionally, it was found that eosinophil peroxidase (EPO) activity in the BAL fluids was also decreased by NOS inhibitor treatment. These results suggest that nitric oxide (NO) is produced in airway inflammation by repeated DEP instillation, and that iNOS inhibition as well as cNOS inhibition can play a modulating role in this airway inflammation by DEP.

• Journal of Life Science
• /
• v.16 no.2 s.75
• /
• pp.192-198
• /
• 2006

Epidemiological studies have demonstrated an association between exposure to diesel exhaust particles (DEP) and adverse cardiopulmonary effects. Despite the epidemiological proof, the pathogenesis of DEP-related pulmonary diseases remain poorly understood. So, comprehensive in vivo and in vitro researches are required to know the effects of DEP on diverse lung diseases. Alveolar macrophages (AM) and airway epithelial cells are known as important cellular targets in DEP-induced lung diseases. Other studies have shown that nitric oxide (NO) is involved in particle matter induced lung injury. The present study was undertaken to determine whether DEP has an synergistic effects on lipopolysaccharide (LPS)-induced NO formation and inducible nitric oxide synthase (iNOS) with nitrotyrosilated-protein formation in cultured primary alveolar macrophages. The formation of NO was determined through the Griess reaction in the cultured medium and iNOS with nitrotyrosilated-proteins are analyzed by immunohistochemical staining and Western analysis. The results indicate that DEP exposure does not induce NO formation by itself, however DEP showed significant synergistic effects on LPS-induced NO formation. So, our results suggest that DEP inhalation could aggravate inflammatory lung disease through NO formation.

• The Korean Journal of Physiology and Pharmacology
• /
• v.10 no.6
• /
• pp.337-341
• /
• 2006

The present study was designed to investigate the protein expression of nitric oxide synthase (NOS) and guanylyl cyclase (GC) activity in ischemia/perfusion (I/R) renal injury in rats. Renal I/R injury was experimentally induced by clamping the both renal pedicle for 40 min in Sprague-Dawley male rats. The renal expression of NOS isoforms was determined by Western blot analysis, and the activity of guanylyl cyclase was determined by the amount of guanosine 3', 5'-cyclic monophosphate (cGMP) formed in response to sodium nitroprusside (SNP), NO donor. I/R injury resulted in renal failure associated with decreased urine osmolality. The expression of inducible NOS (iNOS) was increased in I/R injury rats compared with controls, while endothelial NOS (eNOS) and neuronal NOS (nNOS) expression was decreased. The urinary excretion of NO metabolites was decreased in I/R injury rats. The cGMP production provoked by SNP was decreased in the papilla, but not in glomerulus. These results indicate an altered regulation of NOS expression and guanylyl cyclase activity in I/R-induced nephropathy.

• Asian-Australasian Journal of Animal Sciences
• /
• v.18 no.5
• /
• pp.626-631
• /
• 2005

Nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) is involved in cell apoptosis, which contributes to luteal regression and luteolysis in some species. In large domestic animals, no direct evidence for the relationship between NO and cell apoptosis in the process of corpus luteum regression is reported. The present study was conducted to investigate the localization of iNOS on porcine corpora lutea (CL) during the oestrus cycle and its relation to cell DNA fragmentation and CL regression. According to morphology, four luteal phases throughout the estrous cycle were defined as CL1, CL2, CL3 and CL4. By isoform-specific antibody against iNOS, the immunochemial staining was determined. Luteal cell DNA fragmentation was determined by flow cytometry. The results showed that no positive staining for iNOS was in CL1 and that iNOS was produced but limited to the periphery of CL2, while in the CL3, the spreading immunochemical staining was found inside the CL. No iNOS positive staining was detected in CL4. Meanwhile, DNA fragmentation increased dramatically when CL developed from CL2 to CL3 (p<0.05). In CL4, higher proportion of luteal cells still had fragmented DNA than that of luteal cells from CL1 or CL2 (p<0.05). These results indicate that iNOS expression is closely related to luteal cell apoptosis and then to luteal regression.