scholarly journals Ameliorative Effects of Allium sativum Extract on iNOS Gene Expression and NO Production in Liver of Streptozotocin + Nicotinamide-Induced Diabetic Rats

2017 ◽  
Vol 33 (2) ◽  
pp. 147-153 ◽  
Author(s):  
Nasrin Ziamajidi ◽  
Hamid Behrouj ◽  
Roghayeh Abbasalipourkabir ◽  
Fatemeh Lotfi
Keyword(s):  
Gene Expression ◽  
Allium Sativum ◽  
Diabetic Rats ◽  
No Production ◽  
Inos Gene ◽  
Inos Gene Expression

scholarly journals Effects of Lycopene, Indole-3-Carbinol, and Luteolin on Nitric Oxide Production and iNOS Expression are Organ-Specific in Rats

2010 ◽  
Vol 61 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Evita Rostoka ◽  
Sergejs Isajevs ◽  
Larisa Baumane ◽  
Aija Line ◽  
Karina Silina ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Cortex ◽  
Natural Compounds ◽  
Inos Expression ◽  
No Production ◽  
Nitric Oxide Production ◽  
Inos Gene ◽  
Organ Specific ◽  
The Brain ◽  
Inos Gene Expression

Effects of Lycopene, Indole-3-Carbinol, and Luteolin on Nitric Oxide Production and iNOS Expression are Organ-Specific in RatsNatural compounds are known to modify NO content in tissues; however, the biological activity of polyphenol-rich food often does not correspond to the effects of individual polyphenols on NO synthase activity. The aim of this study was to see how natural compounds luteolin, indole-3-carbinol, and lycopene modify NO production in rat tissues and change the expression of the iNOS gene and protein. Indole-3-carbinol produced multiple effects on the NO level; it significantly decreased NO concentration in blood, lungs, and skeletal muscles and increased it in the liver. Indole-3-carbinol enhanced lipopolyssaccharide (LPS)-induced NO production in all rat organs. It decreased iNOS gene expression in the brain cortex of animals that did not receive LPS and up-regulated it in the LPS-treated animals. Lycopene increased the iNOS gene transcription rate in the brain cortex of LPS-treated animals. Luteolin did not modify NO production in any organ of LPS-untreated rats, nor did it affect gene expression in the liver. In the brain it slightly decreased iNOS gene expression. Luteolin decreased NO production in the blood of LPS-treated animals and the number of iNOS-positive cells in these animals. Our results suggest that changes in tissue NO levels caused by natural compounds cannot be predicted from their effect on NOS expression or activity obtained in model systems. This stresses the importance of direct measurements of NO and NOS expression in animal tissues.

scholarly journals Impacts of garlic extract on testicular oxidative stress and sperm characteristics in type 1 and 2 diabetic rats: An experimental study

2021 ◽  
pp. 929-942
Author(s):  
Fatemeh Lotf ◽  
Nasrin Ziamajidi ◽  
Roghayeh Abbasalipourkabir ◽  
Mohammad Taghi Goodarzi ◽  
Sara Soleimani Asl
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Sperm Quality ◽  
Diabetic Rats ◽  
Garlic Extract ◽  
Inos Gene ◽  
Total Antioxidant ◽  
Total Oxidative Status ◽  
Inos Gene Expression

Background: Hyperglycemia damages various tissues such as the testes through oxidative stress and inflammation, which can eventually lead to infertility. Objective: Garlic extract effects on the testicular tissue of diabetic rats were investigated. Materials and Methods: In this experimental study, 36 male Wistar rats (8-wk old, weighing 230-300 gr) were randomly divided into 6 groups (n = 6/each) including; C: control rats, G: received 0.4 gr of garlic extract/100 gr body weight, D1: Streptozotocin-induced-diabetic rats or type 1, D1+G: D1 rats that were treated with garlic, D2: Streptozotocin + nicotinamide-induced-diabetic rats or type 2, D2+G: D2 rats treated with garlic. At the end of the study, serum testosterone was assayed by ELISA. Also, sperm quality and quantity were evaluated. For determination of oxidative stress status, total antioxidant capacity, total oxidative status, lipid peroxidation, and thiol groups were assayed in the testis tissues of the rats by colorimetric methods. Also, inducible nitric oxide synthase (iNOS) gene expression and the protein level of interleukin-1-1β (IL-1β) were determined by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Results: In diabetic rats, glucose, total oxidative status and lipid peroxidation, iNOS gene expression, and IL-1β were higher than in non-diabetic rats, whereas testosterone, total antioxidant capacity and thiol groups, and sperm quality were significantly lower compared with control rats. These alterations were normalized by garlic intervention. Conclusion: In diabetic rats, garlic was associated with reduced glucose, oxidative stress, IL-1β, and iNOS gene expression and increased testosterone and sperm quality. So, the results suggest that garlic can reduce the severity of damage in testicular tissues of diabetic rats through its hypoglycemic, antioxidant, and anti-inflammatory properties. Key words: Diabetes mellitus, Garlic, Oxidative stress, Inflammation, Testis.

scholarly journals Essential amino acid tryptophan inhibits induction of inducible nitric oxide synthase gene expression in interleukin-1β stimulated hepatocytes

2019 ◽  
Vol 2 (7) ◽  
pp. 170
Author(s):  
Takumi Tsuda ◽  
Hirokazu Miki ◽  
Richi Nakatake ◽  
Tatsuma Sakaguchi ◽  
Masahiko Hatta ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Inos Expression ◽  
No Production ◽  
Inos Gene ◽  
Oxide Synthase ◽  
Inos Gene Expression ◽  
Inducible Nitric Oxide

Background/objective: Tryptophan exerts protective effects against a variety of organ inflammation and injury, including liver. However, there are few scientific reports about the mechanisms involved in the action. Pro-inflammatory cytokine interleukin (IL)-1β stimulates the induction of inducible nitric oxide synthase (iNOS) expression and NO production in cultured hepatocytes (“in vitro liver injury model”), and the prevention of iNOS expression and NO production is considered to be an indicator of liver protection. This study aimed to examine whether tryptophan influences the induction of iNOS gene expression and the mechanisms.Methods: Tryptophan was added into primary cultures of rat hepatocytes stimulated by IL-1β. The iNOS induction, NO production and its signaling pathway were analyzed.Results: IL-1β induced iNOS gene expression, which was followed by iNOS expression and NO production. Tryptophan inhibited the expression of iNOS mRNA and protein, and decreased the production of NO. Transfection experiments with iNOS promoter-luciferase constructs revealed that tryptophan reduced the activities of iNOS mRNA synthesis and its stability. Tryptophan blocked two essential signaling pathways, the activation of nuclear factor (NF)-κB and upregulation of type I IL-1receptor (IL-1RI).Conclusions: Results indicate that tryptophan can prevent the NO production by the inhibition of iNOS gene expression, in part through NF-κB activation and IL-1RI upregulation, in inflamed hepatocytes. Tryptophan may be a potential therapeutic treatment in injured organs, including liver.Key words: tryptophan, inducible nitric oxide synthase, nitric oxide, cultured hepatocytes, nuclear factor-κB, type I interleukin-1 receptor

scholarly journals Peroxidation of n-3 Polyunsaturated Fatty Acids Inhibits the Induction of iNOS Gene Expression in Proinflammatory Cytokine-Stimulated Hepatocytes

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Yoshiro Araki ◽  
Miho Matsumiya ◽  
Takashi Matsuura ◽  
Masaharu Oishi ◽  
Masaki Kaibori ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Proinflammatory Cytokine ◽  
No Production ◽  
Hepatic Inflammation ◽  
Inos Gene ◽  
Anti Inflammatory ◽  
Inos Gene Expression

Eicosapentaenoic acid and docosahexaenoic acid (EPA/DHA), n-3 polyunsaturated fatty acids (PUFAs), have a variety of biological activities including anti-inflammatory and anticancer effects. We hypothesized that their peroxidized products contributed in part to anti-inflammatory effects. In the liver, the production of nitric oxide (NO) by inducible nitric oxide synthase (iNOS) has been implicated as one of the factors in hepatic inflammation and injury. We examined whether the peroxidation of EPA/DHA influences the induction of iNOS and NO production in proinflammatory cytokine-stimulated cultured hepatocytes, which isin vitroliver inflammation model. Peroxidized EPA/DHA inhibited the induction of iNOS and NO production in parallel with the increased levels of their peroxidation, whereas unoxidized EPA/DHA had no effects at all. Peroxidized EPA/DHA reduced the activation of transcription factor, NF-κB, and the expression of the iNOS antisense transcript, which are involved in iNOS promoter transactivation (mRNA synthesis) and its mRNA stabilization, respectively. These findings demonstrated that peroxidized products of EPA/DHA suppressed the induction of iNOS gene expression through both of the transcriptional and posttranscriptional steps, leading to the prevention of hepatic inflammation.

Wogonin but not Nor-wogonin inhibits lipopolysaccharide and lipoteichoic acid-induced iNOS gene expression and NO production in macrophages

2007 ◽  
Vol 7 (8) ◽  
pp. 1054-1063 ◽  
Author(s):  
Guan-Cheng Huang ◽  
Jyh-Ming Chow ◽  
Shing-Chuan Shen ◽  
Liang-Yo Yang ◽  
Cheng-Wei Lin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipoteichoic Acid ◽  
No Production ◽  
Inos Gene ◽  
Inos Gene Expression

scholarly journals Modifications of expression of genes and proteins involved in DNA repair and nitric oxide metabolism by carbatonides [disodium-2,6-dimethyl-1,4-dihydropyridine- 3,5-bis(carbonyloxyacetate) derivatives] in intact and diabetic rats

2017 ◽  
Vol 68 (3) ◽  
pp. 212-227 ◽  
Author(s):  
Kristīne Ošiņa ◽  
Elina Leonova ◽  
Sergejs Isajevs ◽  
Larisa Baumane ◽  
Evita Rostoka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Repair ◽  
Diabetic Rats ◽  
Dna Breaks ◽  
Inos Gene ◽  
Expression Of Genes ◽  
Nitric Oxide Metabolism ◽  
Vis Spectroscopy ◽  
Type 1 Dm ◽  
Inos Gene Expression

Abstract Studies on the pathogenesis of diabetes mellitus complications indicate that the compounds reducing free radicals and enhancing DNA repair could be prospective as possible remedies. Carbatonides, the disodium-2,6-dimethyl-1,4- dihydropyridine-3,5-bis(carbonyloxyacetate) derivatives, were tested for these properties. EPR spectroscopy showed that metcarbatone was an effective scavenger of hydroxyl radicals produced in the Fenton reaction, etcarbatone, and propcarbatone were less effective, styrylcarbatone was ineffective. UV/VIS spectroscopy revealed that styrylcarbatone manifested a hyperchromic effect when interacting with DNA, while all other carbatonides showeda hypochromic effect. Rats with streptozotocin induced type 1 DM were treated with metcarbatone, etcarbatone or styrylcarbatone (all compounds at doses 0.05 mg kg-1 or 0.5 mg kg-1) nine days after the DM approval. Gene expression levels in kidneys and blood were evaluated by quantitative RT-PCR; protein expression - immunohistochemically in kidneys, heart, sciatic nerve, and eyes; DNA breakage - by comet assay in nucleated blood cells. Induction of DM induced DNA breaks; metcarbatone and styrylcarbatone (low dose) alleviated this effect. Metcarbatone and etcarbatone up-regulated mRNA and protein of eNOS in kidneys of diabetic animals; etcarbatone also in myocardium. Etcarbatone reduced the expression of increased iNOS protein in myocardium, nerve, and kidneys. iNos gene expression was up-regulated in kidneys by etcarbatone and metcarbatone in diabetic animals. In blood, development of DM increased iNos gene expression; etcarbatone and metcarbatone normalised it. Etcarbatone up-regulated the expression of H2AX in kidneys of diabetic animals but decreased the production of c-PARP1. Taken together, our data indicate that carbatonides might have a potential as drugs intended to treat DM complications.

scholarly journals Anti-Inflammatory Effects of Abeliophyllum distichum Nakai (Cultivar Okhwang 1) Callus through Inhibition of PI3K/Akt, NF-κB, and MAPK Signaling Pathways in Lipopolysaccharide-Induced Macrophages

Processes ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 1071
Author(s):  
Tae-Won Jang ◽  
Jae-Ho Park
Keyword(s):  
Gene Expression ◽  
Polymerase Chain Reaction ◽  
Signaling Pathways ◽  
Chain Reaction ◽  
Inos Gene ◽  
Polymerase Chain ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Abeliophyllum Distichum ◽  
Inos Gene Expression

One of the Korean endemic plants, Abeliophyllum distichum Nakai (Oleaceae), contains acteoside, which is a glycoside exhibiting neuroprotective, anti-inflammation effects and antibacterial capacities. We conducted an investigation on the effects of the callus of A. distichum (cultivar Okhwang 1, CAO) on pro-inflammatory mediators released following nuclear factor-кB (NF-кB), phosphatidylinositol 3-kinase/Akt (PI3K-Akt) and mitogen-activated protein kinase (MAPK) signal activation in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Immunoblotting was employed to find out the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide (iNOS), and activation of MAPK molecules, NF-κB and Akt. Cytokines, COX-2, and iNOS gene expression were assessed using polymerase chain reaction techniques. Cytokines, COX-2, and iNOS gene expression were assessed using polymerase chain reaction techniques. High-performance liquid chromatography revealed that CAO was rich in acteoside and isoacteoside. As a result, CAO inhibited the generation of NO, cytokines, COX-2, and iNOS expression. Further, translocation to the nuclear of NF-κB p65 and degradation of the inhibitor of NF-кB (IкB) were alleviated by suppressing phosphorylation. Additionally, CAO significantly impacted MAPK pathway activation by potentially reducing phosphorylation of MAPKs. These results indicate that the anti-inflammatory effect of CAO is mediated via the inhibition of MAPK, PI3K/Akt, and NF-κB signaling pathways, probably via glycosides, phenolics, and flavonoids bioactivity derived from plants. CAO can serve as a potential anti-inflammatory agent, which alleviates inflammation factors and act through specific cell signaling pathways.

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