scholarly journals Gastroprotective Effect of Juanislamin on Ethanol-Induced Gastric Lesions in Rats: Role of Prostaglandins, Nitric Oxide and Sulfhydryl Groups in the Mechanism of Action

Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2246
Author(s):  
María Elena Sánchez-Mendoza ◽  
Yaraset López-Lorenzo ◽  
Leticia Cruz-Antonio ◽  
Arturo Cruz-Oseguera ◽  
Jazmín García-Machorro ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mechanism Of Action ◽  
Gastrointestinal Disorder ◽  
Sulfhydryl Groups ◽  
Dependent Manner ◽  
Gastric Lesions ◽  
Reference Drug ◽  
Ulcer Disease ◽  
Gastroprotective Effect

Peptic ulcer disease, the most common gastrointestinal disorder, is currently treated with several types of drugs, but all have severe side effects. The aim of the present study was to evaluate the gastroprotective activity of juanislamin, isolated from Calea urticifolia, in a rat model of ethanol-induced gastric lesions. Thirty minutes after orally administering a given dose of juanislamin (from 1 to 30 mg/kg) or carbenoxolone (the reference drug, at 1–100 mg/kg) to rats, 1 mL of ethanol was applied, and the animals were sacrificed 2 h later. The stomachs were removed and opened to measure the total area of lesions in each. To examine the possible participation of prostaglandins, nitric oxide and/or sulfhydryl groups in the mechanism of action of juanislamin, the rats received indomethacin, NG-Nitro-l-arginine methyl ester hydrochloride (l-NAME) or N-ethylmaleimide pretreatment, respectively, before being given juanislamin and undergoing the rest of the methodology. Juanislamin inhibited gastric lesions produced by ethanol in a non-dose-dependent manner, showing the maximum gastroprotective effect (100%) at 10 mg/kg. The activity of juanislamin was not modified by pretreatment with indomethacin, l-NAME or N-ethylmaleimide. In conclusion, juanislamin protected the gastric mucosa from ethanol-induced damage, and its mechanism of action apparently does not involve prostaglandins, nitric oxide or sulfhydryl groups.

scholarly journals Gastroprotection of Calein D against Ethanol-Induced Gastric Lesions in Mice: Role of Prostaglandins, Nitric Oxide and Sulfhydryls

Molecules ◽  
2019 ◽  
Vol 24 (3) ◽  
pp. 622 ◽  
Author(s):  
María Sánchez-Mendoza ◽  
Yaraset López-Lorenzo ◽  
Leticia Cruz-Antonio ◽  
Audifás-Salvador Matus-Meza ◽  
Yolanda Sánchez-Mendoza ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Oral Treatment ◽  
Control Group ◽  
Peptic Ulcers ◽  
Gastric Lesions ◽  
Gastroprotective Activity ◽  
Reference Drug ◽  
Sulfhydryl Compounds

Peptic ulcers are currently treated with various drugs, all having serious side effects. The aim of this study was to evaluate the gastroprotective activity of calein D (from Calea urticifolia), a sesquiterpene lactone with a germacrane skeleton. Gastric lesions were induced in mice by administering ethanol (0.2 mL) after oral treatment with calein D at 3, 10 and 30 mg/kg, resulting in 13.15 ± 3.44%, 77.65 ± 7.38% and 95.76 ± 2.18% gastroprotection, respectively, to be compared with that of the control group. The effect found for 30 mg/kg of calein D was not reversed by pretreatment with NG-nitro-l-arginine methyl ester (l-NAME, 70 mg/kg, ip), indomethacin (10 mg/kg, sc) or N-ethylmaleimide (NEM, 10 mg/kg, sc). Hence, the mechanism of action of calein D does not involve NO, prostaglandins or sulfhydryl compounds. Calein D was more potent than carbenoxolone, the reference drug. The findings for the latter are in agreement with previous reports.

scholarly journals Phaseolin Attenuates Lipopolysaccharide-Induced Inflammation in RAW 264.7 Cells and Zebrafish

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 420
Author(s):  
Su-Jung Hwang ◽  
Ye-Seul Song ◽  
Hyo-Jong Lee
Keyword(s):  
Nitric Oxide ◽  
Nuclear Translocation ◽  
Raw 264.7 Cells ◽  
Network Pharmacology ◽  
Raw 264.7 ◽  
Dependent Manner ◽  
Bioactive Constituents

Kushen (Radix Sophorae flavescentis) is used to treat ulcerative colitis, tumors, and pruritus. Recently, phaseolin, formononetin, matrine, luteolin, and quercetin, through a network pharmacology approach, were tentatively identified as five bioactive constituents responsible for the anti-inflammatory effects of S. flavescentis. However, the role of phaseolin (one of the primary components of S. flavescentis) in the direct regulation of inflammation and inflammatory processes is not well known. In this study, the beneficial role of phaseolin against inflammation was explored in lipopolysaccharide (LPS)-induced inflammation models of RAW 264.7 macrophages and zebrafish larvae. Phaseolin inhibited LPS-mediated production of nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS), without affecting cell viability. In addition, phaseolin suppressed pro-inflammatory mediators such as cyclooxygenase 2 (COX-2), interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) in a dose-dependent manner. Furthermore, phaseolin reduced matrix metalloproteinase (MMP) activity as well as macrophage adhesion in vitro and the recruitment of leukocytes in vivo by downregulating Ninjurin 1 (Ninj1), an adhesion molecule. Finally, phaseolin inhibited the nuclear translocation of nuclear factor-kappa B (NF-κB). In view of the above, our results suggest that phaseolin could be a potential therapeutic candidate for the management of inflammation.

scholarly journals Toxoplasma gondii Cyclophilin 18-Mediated Production of Nitric Oxide Induces Bradyzoite Conversion in a CCR5-Dependent Manner

2009 ◽  
Vol 77 (9) ◽  
pp. 3686-3695 ◽  
Author(s):  
Hany M. Ibrahim ◽  
Hiroshi Bannai ◽  
Xuenan Xuan ◽  
Yoshifumi Nishikawa
Keyword(s):  
Nitric Oxide ◽  
Toxoplasma Gondii ◽  
Inflammatory Responses ◽  
Interleukin 12 ◽  
Dependent Manner ◽  
Independent Manner ◽  
Necrosis Factor Alpha ◽  
Parasite Multiplication ◽  
Factor Alpha

ABSTRACT Toxoplasma gondii modulates pro- and anti-inflammatory responses to regulate parasite multiplication and host survival. Pressure from the immune response causes the conversion of tachyzoites into slowly dividing bradyzoites. The regulatory mechanisms involved in this switch are poorly understood. The aim of this study was to investigate the immunomodulatory role of T. gondii cyclophilin 18 (TgCyp18) in macrophages and the consequences of the cellular responses on the conversion machinery. Recombinant TgCyp18 induced the production of nitric oxide (NO), interleukin-12 (IL-12), and tumor necrosis factor alpha through its binding with cysteine-cysteine chemokine receptor 5 (CCR5) and the production of gamma interferon and IL-6 in a CCR5-independent manner. Interestingly, the treatment of macrophages with TgCyp18 resulted in the inhibition of parasite growth and an enhancement of the conversion into bradyzoites via NO in a CCR5-dependent manner. In conclusion, T. gondii possesses sophisticated mechanisms to manipulate host cell responses in a TgCyp18-mediated process.

scholarly journals Gastroprotection of Suaveolol, Isolated from Hyptis suaveolens, against Ethanol-Induced Gastric Lesions in Wistar Rats: Role of Prostaglandins, Nitric Oxide and Sulfhydryls

Molecules ◽  
2012 ◽  
Vol 17 (8) ◽  
pp. 8917-8927 ◽  
Author(s):  
Carlos Vera-Arzave ◽  
Leticia Cruz Antonio ◽  
Jesús Arrieta ◽  
Gerardo Cruz-Hernández ◽  
Antonio Magdiel Velázquez-Méndez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Wistar Rats ◽  
Gastric Lesions ◽  
Hyptis Suaveolens

Adrenomedullin acts in the lateral parabrachial nucleus to increase arterial blood pressure through mechanisms mediated by glutamate and nitric oxide

2008 ◽  
Vol 295 (1) ◽  
pp. R38-R44 ◽  
Author(s):  
Adrian Geambasu ◽  
Teresa L. Krukoff
Keyword(s):  
Nitric Oxide ◽  
Calcium Channel ◽  
Male Rats ◽  
Parabrachial Nucleus ◽  
Dependent Manner ◽  
Pressor Effect ◽  
Arterial Blood ◽  
Lateral Parabrachial Nucleus ◽  
Nos Inhibitors

Adrenomedullin (ADM) acts in a site-specific manner within autonomic centers of the brain to modulate mean arterial pressure (MAP). To determine the role of ADM in the pontine autonomic center, the lateral parabrachial nucleus (LPBN), we used urethane-anesthetized adult Sprague-Dawley male rats to test the hypothesis that ADM increases MAP at this site through glutamate- and nitric oxide (NO)-dependent mechanisms. ADM microinjected into the LPBN increased MAP in a dose-dependent manner. The pressor effect of ADM (0.01 pmol) had a peak value of 11.9 ± 1.9 mmHg at 2 min and lasted for 7 min. We demonstrated that ADM's effect is receptor mediated by blocking the effect with the ADM receptor antagonist, ADM22-52. We showed that glutamate mediates ADM's pressor response, as this response was blocked using coinjections of ADM with dizolcipine hydrogen maleate or 6-cyano-7-nitroquinoxaline-2,3-dione, N-methyl-d-aspartate (NMDA) and non-NMDA glutamate receptor antagonists, respectively. We tested the roles of NO with coinjections of ADM with either N5-(1-iminoethyl)-l-ornithine or 7-nitroindazole monosodium salt, nonspecific and neuronal NO synthase (NOS) inhibitors, respectively; both inhibitors blocked ADM's pressor effect. Finally, we studied the role of calcium influx in ADM's pressor effect, as intracellular calcium is important in both glutamate and NO neurotransmission. ADM's effect was blocked when nifedipine, an L-type calcium channel blocker, was coinjected with ADM into the LPBN. This study is the first to show that ADM acts in the LPBN to increase MAP through mechanisms dependent on activation of ionotropic glutamate receptors, neuronal and endothelial NOS-mediated NO synthesis, and L-type calcium channel activation.

Role of Nitric Oxide towards Vasodilator Effects of Substance P and ATP in Human Forearm Vessels

1997 ◽  
Vol 92 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Masanari Shiramoto ◽  
Tsutomu Imaizumi ◽  
Yoshitaka Hirooka ◽  
Toyonari Endo ◽  
Takashi Namba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Dependent Manner ◽  
Human Forearm ◽  
Before And After ◽  
Dose Dependent

1. It has been shown in animals that substance P as well as acetylcholine releases endothelium-derived nitric oxide and evokes vasodilatation and that ATP-induced vasodilatation is partially mediated by nitric oxide. The aim of this study was to examine whether vasodilator effects of substance P and ATP are mediated by nitric oxide in humans. 2. In healthy volunteers (n = 35), we measured forearm blood flow by a strain-gauge plethysmograph while infusing graded doses of acetylcholine, substance P, ATP or sodium nitroprusside into the brachial artery before and after infusion of NG-monomethyl-l-arginine (4 or 8 μmol/min for 5 min). In addition, we measured forearm blood flow while infusing substance P before and during infusion of l-arginine (10 mg/min, simultaneously), or before and 1 h after oral administration of indomethacin (75 mg). 3. Acetylcholine, substance P, ATP or sodium nitroprusside increased forearm blood flow in a dose-dependent manner. NG-Monomethyl-l-arginine decreased basal forearm blood flow and inhibited acetylcholine-induced vasodilatation but did not affect substance P-, ATP-, or sodium nitroprusside-induced vasodilatation. Neither supplementation of l-arginine nor pretreatment with indomethacin affected substance P-induced vasodilatation. 4. Our results suggest that, in the human forearm vessels, substance P-induced vasodilatation may not be mediated by either nitric oxide or prostaglandins and that ATP-induced vasodilatation may also not be mediated by nitric oxide.

Gastroprotective effects of goniothalamin against ethanol and indomethacin-induced gastric lesions in rats: Role of prostaglandins, nitric oxide and sulfhydryl compounds

2014 ◽  
Vol 224 ◽  
pp. 206-212 ◽  
Author(s):  
Débora Barbosa Vendramini-Costa ◽  
Karin Maia Monteiro ◽  
Leilane Hespporte Iwamoto ◽  
Michelle Pedroza Jorge ◽  
Sirlene Valério Tinti ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Lesions ◽  
Sulfhydryl Compounds

scholarly journals Gastroprotective effect of ethylacetate fraction of the leaves of Hannoa klaineana on aspirin and histamine-induced gastric ulcer in rats

2020 ◽  
Vol 8 (1) ◽  
pp. 70
Author(s):  
Ibrahim Abubakar ◽  
Hassan Muhammad Yankuzo ◽  
Yusha'u Shuaibu Baraya ◽  
Mu'azu Abubakar Gusau
Keyword(s):  
Protective Effect ◽  
Ph Value ◽  
Gastrointestinal Diseases ◽  
Gastric Volume ◽  
Total Acidity ◽  
Gastric Lesions ◽  
Ulcer Index ◽  
Ulcer Disease ◽  
Gastroprotective Effect ◽  
Ulcer Model

Background: Peptic ulcer disease remains endemic in our society affecting about four million people every year worldwide. Hannoa klaineana is used traditionally in the treatment of various gastrointestinal diseases including ulcer.Aim: This study aims at evaluating the gastroprotective effect of ethylacetate fraction of the leaves of Hannoa klaineana (Simaroubaceae).Methods: The gastroprotective effect of ethylacetate fraction of the Hannoa klaineana (50, 100 and 200mg/kg b.wt) was evaluated using aspirin and histamine induced ulcer models.Results: In aspirin-induced ulcer model, the ethylacetate fraction of the Hannoa klaineana demonstrated significant (p<0.001) decreased in mean ulcer index with the maximum protective effect (99.84%) at 200 mg/kg against the gastric damages. While histamine-induced ulcer model, the solvent fraction significantly (p<0.001) decreased mean ulcer index with the protective effect up to 99.83% against the gastric lesions. In both models, a significant (p<0.001) increased in pH value coupled with significant (p<0.001) decreased in gastric volume, free and total acidity in rats pre-treated with varying doses of the ethylacetate fraction was found.Conclusion: The mechanism of gastroprotective effects of ethylacetate fraction of the Hannoa klaineana could be attributed to its ability to stimulate prostaglandins secretion or possess prostaglandins like-substances or suppression of histamine-induced vasospastic effect and gastric secretion.   

Sign in / Sign up

Export Citation Format

Share Document