scholarly journals Vasodilator Effects on Canine Basilar Artery Induced by Intracisternal Interleukin-1β

1997 ◽  
Vol 17 (12) ◽  
pp. 1337-1345 ◽  
Author(s):  
Koji Osuka ◽  
Yoshio Suzuki ◽  
Yasuo Watanabe ◽  
Aclan Dogan ◽  
Masakazu Takayasu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Basilar Artery ◽  
Systemic Blood Pressure ◽  
Interleukin 1Β ◽  
Zinc Protoporphyrin ◽  
Dependent Manner ◽  
Nitric Oxide Metabolism ◽  
Canine Basilar Artery ◽  
Cox 2 ◽  
Nitric Oxide Metabolites

The effect of interleukin-1β (IL-1β) on a cerebral artery was investigated in anesthetized dogs. Intracisternal administration of IL-1β (0.03 and 0.3 μg) dilated the canine basilar artery in a dose-dependent manner, without affecting systemic blood pressure or heart rate. The increase in diameter induced by 0.3 μg of IL-1β was 28.4% ± 13.4% of control at 2 hours and was inhibited by 30 μg of the IL-1β receptor antagonist, zinc protoporphyrin (4.5% ± 13.5%, P < 0.05). Interleukin-1β did not affect the concentration of nitric oxide metabolites in CSF. However, there was an increase in the concentration of eicosanoids in CSF, and the elevation of 6-keto-PGF1α paralleled the vasodilation. Pretreatment with 30 μg of the selective inducible cyclooxygenase (COX-2) inhibitor NS-398 also inhibited the IL-1β-induced vasodilation significantly (5.9% ± 9.4% at 2 hours, P < 0.01). Western blot analysis revealed the expression of a 68-kD COX-2-like protein in basilar artery extracts. These findings suggest that the IL-1β-induced vasodilator effect is linked to the prostaglandin cascade, predominantly to prostaglandin I2, by induction of COX-2, but not to the stimulation of nitric oxide metabolism.

scholarly journals Oleifolioside A, a New Active Compound, Attenuates LPS-Stimulated iNOS and COX-2 Expression through the Downregulation of NF-κB and MAPK Activities in RAW 264.7 Macrophages

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Hai Yang Yu ◽  
Kyoung-Sook Kim ◽  
Young-Choon Lee ◽  
Hyung-In Moon ◽  
Jai-Heon Lee
Keyword(s):  
Nitric Oxide ◽  
Mapk Signaling ◽  
Binding Activity ◽  
Prostaglandin E ◽  
Raw 264.7 ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Raw 264.7 Macrophages ◽  
Dendropanax Morbifera ◽  
Cox 2

Oleifolioside A, a new triterpenoid compound isolated fromDendropanax morbiferaLeveille (D. morbifera), was shown in this study to have potent inhibitory effects on lipopolysaccharide (LPS-)stimulated nitric oxide (NO) and prostaglandin E2(PGE2) production in RAW 264.7 macrophages. Consistent with these findings, oleifolioside A was further shown to suppress the expression of LPS-stimulated inducible nitric oxide synthase (iNOS) and cyclooxigenase-2 (COX-2) in a dose-dependent manner at both the protein and mRNA levels and to significantly inhibit the DNA-binding activity and transcriptional activity of NF-κB in response to LPS. These results were found to be associated with the inhibition of the degradation and phosphorylation of IκB-αand subsequent translocation of the NF-κB p65 subunit to the nucleus. Inhibition of NF-κB activation by oleifolioside A was also shown to be mediated through the prevention of p38 MAPK and ERK1/2 phosphorylation. Taken together, our results suggest that oleifolioside A has the potential to be a novel anti-inflammatory agent capable of targeting both the NF-κB and MAPK signaling pathways.

Expression and Function of Recombinant Endothelial Nitric Oxide Synthase Gene in Canine Basilar Artery

1997 ◽  
Vol 80 (3) ◽  
pp. 327-335 ◽  
Author(s):  
Alex F.Y. Chen ◽  
Timothy O’Brien ◽  
Masato Tsutsui ◽  
Hiroyuki Kinoshita ◽  
Vincent J. Pompili ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Basilar Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Canine Basilar Artery ◽  
And Function ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Anti-Oxidative and Anti-Inflammatory Activity of Kenya Grade AA Green Coffee Bean Extracts

2020 ◽  
Author(s):  
In-Chul LEE ◽  
Jae-Sook LEE ◽  
Jeong-Hyun LEE ◽  
Yeona KIM ◽  
Wi-Young SO
Keyword(s):  
Nitric Oxide ◽  
Coffee Bean ◽  
Dependent Manner ◽  
Green Coffee ◽  
Cosmetic Products ◽  
Concentration Dependent Manner ◽  
Total Polyphenol ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Green Coffee Bean

Background: Kenya AA green coffee bean extracts were tested for natural ingredients used for anti-oxidative and anti-inflammatory purposes in cosmetic products Methods: Anti-oxidative activities were measured by total polyphenol, 1,1-diphenyl-2-picrylhydrazyl (DPPH), and the 2,2′-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assays. Anti-inflammatory activities were evaluated via nitric oxide (NO) assays, and through quantification of inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) protein expression by western blotting. Data analyses were performed using independent Student’s t-tests, with statistical significance set at P < 0.05. Results: Total polyphenol content of water and ethanol extract was 169.0 ± 3.1 mg and 300.34 ± 16.6 mg tannic acid/g dry weight, respectively. The DPPH and ABTS radical scavenging activities of all the extracts were significantly increased in a concentration-dependent manner. Kenya AA green coffee bean extracts were toxic at a concentration of 1,000 µg/mL in RAW 264.7 cells. Anti-inflammatory activity as determined by NO assay showed that lipopolysaccharide (LPS)-induced NO was significantly inhibited following treatment with Kenya AA green coffee bean extracts in a concentration-dependent manner. iNOS and COX-2 protein expression was also significantly inhibited following treatment. Conclusion: These results highlight the potential of Kenya AA green coffee bean extracts as a naturally active anti-inflammatory agent in cosmetic products.

Endothelial L-arginine pathway and relaxations to vasopressin in canine basilar artery

1993 ◽  
Vol 264 (2) ◽  
pp. H413-H418 ◽  
Author(s):  
F. Cosentino ◽  
J. C. Sill ◽  
Z. S. Katusic
Keyword(s):  
Nitric Oxide ◽  
Basilar Artery ◽  
Isometric Tension ◽  
Nitric Oxide Donor ◽  
Basal Tone ◽  
Basilar Arteries ◽  
Canine Basilar Artery ◽  
Subsequent Activation ◽  
Oxide Synthase

Experiments were designed to determine the role of the L-arginine pathway in endothelium-dependent relaxations to vasopressin. The effects of L-arginine analogues NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-monomethyl-L-arginine (L-NMMA) on basal and vasopressin-induced activity of nitric oxide synthase were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (37 degrees C, pH 7.4). Radioimmunoassay was used to determine the level of guanosine 3',5'-cyclic monophosphate (cGMP). All experiments were performed in the presence of indomethacin, a cyclooxygenase inhibitor. L-NAME and L-NMMA caused endothelium-dependent contractions and inhibited basal production of cGMP. In contrast, L-NNA did not affect basal tone or basal production of cGMP. L-Arginine analogues inhibited relaxations to vasopressin but did not affect relaxations to a nitric oxide donor, molsidomine (SIN-1). The effects of L-NNA, L-NAME, and L-NMMA were reversed in the presence of L-arginine. The relaxations to vasopressin were associated with an increase of cGMP levels in the arterial wall. This effect of vasopressin was inhibited in the presence of L-NNA. These studies suggest that the relaxations to vasopressin are mediated by activation of the endothelial L-arginine pathway, leading to increased production of nitric oxide, with subsequent activation of guanylate cyclase in smooth muscle cells. In canine basilar artery, L-NAME and L-NMMA are nonselective inhibitors of both basal and stimulated production of nitric oxide, whereas L-NNA selectively inhibits vasopressin-induced activation of the L-arginine pathway.

scholarly journals NITRIC OXIDE METABOLISM FEATURES UNDER CONDITIONS OF EXPERIMENTAL INFECTED RADIATION-INDUCED SKIN INJURIES DEVELOPMENT AND THEIR TREATMENT WITH PHOTODYNAMIC THERAPY

2020 ◽  
Vol 73 (8) ◽  
pp. 1655-1658
Author(s):  
Mykola V. Krasnoselskyi ◽  
Elena S. Pushkar ◽  
Larisa I. Simonova-Pushkar ◽  
Mykhailo S. Myroshnychenko
Keyword(s):  
Nitric Oxide ◽  
Staphylococcus Aureus ◽  
Photodynamic Therapy ◽  
Blood Serum ◽  
Skin Ulcer ◽  
Skin Injuries ◽  
Skin Ulcers ◽  
Nitric Oxide Metabolism ◽  
Radiation Induced ◽  
Nitric Oxide Metabolites

The aim: To follow-up nitric oxide content values in rat serum at the development of Staphylococcus aureus infected radiation skin injuries and their photodynamic therapy. Materials and methods: Eighty WAG male rats were studied in an experiment. Four groups were identified for evaluation. Group 1 included unaffected intact rats (n=20). Group 2 involved rats (n=20) with a modeled radiation-induced ulcer of the skin. The rats (n=20) with a modeled radiation-induced skin ulcer followed by infecting with Staphylococcus aureus were referred to group 3. Group 4 included rats (n=20) with Staphylococcus aureus infected radiation skin ulcer exposed to photodynamic therapy. Rats of groups 1-4 were sampled for biochemical blood examination on days 7, 14, 21, 30 and 45. Total nitric oxide metabolites (nitrites and nitrates) were measured according to V.A. Metelskaya et al. method. Results: Infectious agent (Staphylococcus aureus) present in skin ulcer impairs nitric oxide metabolism in rat blood serum that manifested in decreased total nitric oxide metabolites content on day 7, followed by its increase within days 14 to 45. While photodynamic therapy exposed on the Staphylococcus aureus infected radiation skin ulcer, total nitric oxide metabolites in blood serum had increased by day 7, but days 14 to 45 level was compliant with physiological norm. Conclusions: Infecting radiation skin ulcers with Staphylococcus aureus causes impaired nitric oxide metabolism, while photodynamic therapy helps to normalize the metabolism of the above-mentioned chemical compound that can improve healing of radiation skin ulcers.

scholarly journals Promoting effect of Se-allylselenocysteine on 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin tumorigenesis

2020 ◽  
Vol 9 ◽  
Author(s):  
An-Chin Cheng ◽  
Wan-Ru Jiang ◽  
Yu-Hsuan Hsiao ◽  
Vladimir Badmaev ◽  
Chi-Tang Ho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Positive Control ◽  
Positive Control Group ◽  
Raw 264.7 Cells ◽  
Control Group ◽  
Dependent Manner ◽  
Promoting Effect ◽  
Skin Tumorigenesis ◽  
Cox 2 ◽  
Anti Inflammatory

Se-allylselenocysteine (ASC), an analogue of garlic compound, has been shown to inhibit mammary carcinogenesis in vivo and cell growth in vitro. However, the function of ASC on anti-inflammatory effects remains largely unknown. Therefore, we investigated whether ASC has an anti-inflammatory effect on lipopolysaccharide (LPS) -induced inflammation or an anti-tumour effect promoting on DMBA/TPA-induced skin tumorigenesis and tried to elucidate the mechanisms involved. Herein, the results showed that ASC inhibited LPS-induced production of nitric oxide (NO) with a decreased protein level of inducible nitric oxide synthase (iNOS) in RAW 264.7 cells. However, ASC enhanced LPS-induced cyclooxygenase-2 (COX-2) protein levels and mRNA expression. Interestingly, we found for the first time that topical application of ASC on the dorsal skin of DMBA-initiated and TPA-promoted mice significantly accelerated skin tumorigenesis and raised tumour multiplicity as compared to the positive control group (DMBA/TPA). The number of tumours that were 1–3 mm, 3–5 mm, and >5 mm in size per mouse increased in a dose-dependent manner in the ASC pre-treated groups. Pre-treatment with ASC showed a significant increase in the expression of COX-2 compared with the positive control group. In summary, that ASC may modulate the COX-2 protein expression and promoting DMBA/TPA-induced skin cancer in mice.

scholarly journals A Protective Role for Heme Oxygenase Expression in Pancreatic Islets Exposed to Interleukin-1β**This work was supported by NIH Grant DK-25705 (to S.G.L.).

Endocrinology ◽  
1998 ◽  
Vol 139 (10) ◽  
pp. 4155-4163 ◽  
Author(s):  
Jing Ye ◽  
Suzanne G. Laychock
Keyword(s):  
Nitric Oxide ◽  
Protective Effect ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Heme Oxygenase ◽  
Protoporphyrin Ix ◽  
Interleukin 1Β ◽  
Zinc Protoporphyrin ◽  
Inhibitory Effects ◽  
Isolated Pancreatic Islets

Abstract Heme oxygenase (HO)-1 expression was investigated in rat isolated pancreatic islets. Freshly isolated islets showed no evidence of HO-1 expression. After a 20-h culture, there was a small increase in HO-1 in control islets, and interleukin-1β (IL-1β) induced HO-1 expression above control levels. NG-monomethyl-l-arginine inhibited the IL-1β-induced increase in HO-1. Sodium nitroprusside-generated nitric oxide also increased HO-1 expression. CoCl2 induced a concentration- and time-dependent increase in HO-1, but not heat shock protein 70, expression. Cobalt chloride (CoCl2) protected islets from the inhibitory effects of IL-1β on glucose-stimulated insulin release and glucose oxidation. Nickel chloride did not mimic the effects of CoCl2. An inhibitor of HO-1 activity, zinc-protoporphyrin IX (ZnPP), prevented the protective effect of CoCl2 on insulin release with IL-1β but did not affect HO-1 expression or the inhibitory response to IL-1β alone. ZnPP also inhibited the protective effect of hemin in IL-1β-treated islets. CoCl2 inhibited the marked increase in islet nitrite production in response to IL-1β. Cobalt-protoporphyrin IX (CoPP), which increased HO expression and activity, also protected islets from the inhibitory effects of IL-1β, even though IL-1β largely blocked the CoPP-induced increase in HO-1 expression. In βHC9 cells, CoCl2 increased HO-1 expression and HO activity, whereas CoPP directly activated HO. ZnPP inhibited basal and CoCl2-stimulated HO activity. Thus, increased HO-1 expression and/or HO activity in response to CoCl2, CoPP, and hemin, seems to mediate protective responses of pancreatic islets against IL-1β. HO-1 may be protective of β-cells because of the scavenging of free heme, the antioxidant effects of the end-product bilirubin, or the generation of carbon monoxide, which might have insulin secretion-promoting effects and inhibitory effects on nitric oxide synthase.

Asiatic Acid Attenuates Osteoarthritis by Regulating NF-κB Signaling Pathway in Chondrocytes

2020 ◽  
Author(s):  
Zhengmeng Yang ◽  
Lu Feng ◽  
Xiaoting Zhang ◽  
Weiping Lin ◽  
Bin Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Articular Chondrocytes ◽  
Cartilage Damage ◽  
Luciferase Assay ◽  
No Production ◽  
Asiatic Acid ◽  
Dependent Manner ◽  
Cox 2 ◽  
Dose Dependent

Abstract Background: Natural small molecules have become more attractive as alternatives to non-steroidal anti-inflammatory drugs in osteoarthritis (OA) treatments. This study aims to investigate the effects of Asiatic acid (AA) on OA in chondrocytes and the surgery-induced OA animal model. Methods: Cytotoxicity of AA in primary rat articular chondrocytes was determined. Chondrocytes were pretreated with AA at the safe concentrations and subsequently treated with IL-1β. The production of inflammatory mediators including nitric oxide (NO), nitric oxide synthase (iNOS), as well as cyclooxygenase (COX)-2, and the expression of chondrogenic and hypertrophic markers including Sox 9, Aggrecan, Col 2a1, and matrix metalloproteinase-13 (MMP13) in the cells were measured. The effect of AA on nuclear factor-kappa B (NF-κB) signaling pathway was further determined by dual luciferase assay and western blot. The surgery-induced OA animals were treated with AA or saline for 6 weeks. The pathological changes in the affected joints were measured by micro-CT and histological analysis. Results: We found a broad safety spectrum of AA from 0 to 25 μM. A dose-dependent inhibitory effect of AA on NO production, as well as iNOS and COX-2 expression were found. Meanwhile, AA promoted chondrogenesis and inhibited hypertrophy in chondrocyte treated with IL-1β. In addition, AA inhibited NF-κB signaling pathway with a dose-dependent manner. Furthermore, results from animal study revealed that AA prevented articular cartilage damage as well as subchondral bone remodeling in the surgery-induced OA animal.

Similar responsiveness of smooth muscle of the canine basilar artery to EDRF and nitric oxide

1989 ◽  
Vol 257 (4) ◽  
pp. H1235-H1239 ◽  
Author(s):  
Z. S. Katusic ◽  
J. J. Marshall ◽  
H. A. Kontos ◽  
P. M. Vanhoutte
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Basilar Artery ◽  
Inhibitory Effect ◽  
Relaxing Factor ◽  
Basilar Arteries ◽  
Canine Basilar Artery ◽  
Endothelium Derived Relaxing Factor ◽  
Ly 83583 ◽  
Hemoglobin M

Experiments were designed to compare the reactivity of canine basilar arteries to endothelium-derived relaxing factor (EDRF) and nitric oxide. Preparations with endothelium activated by bradykinin were used to study relaxations induced with EDRF, whereas the inhibitory effect of nitric oxide was studied in preparations without endothelium. All experiments were performed in the presence of indomethacin. EDRF- and nitric oxide-induced relaxations were significantly augmented in the presence of superoxide dismutase plus catalase but were reduced in the presence of methylene blue, LY 83583, and hemoglobin. M & B 22984 did not affect relaxations to either EDRF or nitric oxide. These results indicate that in the canine basilar artery EDRF is not an oxygen-derived free radical. The similar responsiveness of the basilar artery to EDRF and nitric oxide is consistent with the proposal that in the canine basilar artery nitric oxide is the factor.

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