Gastroprotective effect of a flavone from <i>Lonchocarpus araripensis</i> Benth. (Leguminosae) and the possible mechanism

Campos, Deive A.; Lima, Almi F.; Ribeiro, Saulo Rodrigo L; Silveira, Edilberto R.; Pessoa, Otília Deusdênia Loiola; Rao, V. S. N.; Santos, Flávia Almeida

doi:10.1211/jpp.60.3.0016

Cited by 8 publications

(4 citation statements)

References 27 publications

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“…ATP-sensitive potassium channels (K + ATP ) provide a gastric defense by inhibiting neutrophil activation and superoxide production and by enhancing gastric microcirculation [40]. Our data, however, demonstrate that K + ATP channels are not involved in the mechanism of action of EC because the blockade of these channels with glibenclamide did not reverse the gastroprotective effects of EC.…”

Section: Discussionmentioning

confidence: 72%

Morphologic and Pharmacological Investigations in the Epicatechin Gastroprotective Effect

Rozza

Hiruma-Lima

Tanimoto

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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Previous studies of the gastroprotective activity of plants have highlighted the importance of the polyphenolic compound epicatechin (EC) in the treatment of gastric ulcers. This paper aimed to evaluate and characterize the gastroprotective mechanism of action of EC using male rats. The gastroprotective action of EC was analyzed in gastric ulcers induced by ethanol or indomethacin. The involvement of sulfhydryl (SH) groups, K+ ATP channels, α 2 adrenoceptors, gastric antisecretory activity, and the amount of mucus in the development of gastric ulcers were investigated. The lowest effective dose of EC providing gastroprotective effects was 50 mg/kg in the ethanol-induced gastric ulcers and 25 mg/kg in the indomethacin-induced gastric ulcers. The gastroprotection seen upon treatment with EC was significantly decreased in rats pretreated with a SH compound reagent or an α 2-receptor antagonist, but not with a K+ ATP channel blocker. Furthermore, oral treatment with EC increased mucus production and decreased H+ secretion. Immunohistochemistry demonstrated the involvement of superoxide dismutase (SOD), nitric oxide (NO), and heat shock protein-70 (HSP-70) in the gastroprotection. These results demonstrate that EC provides gastroprotection through reinforcement of the mucus barrier and neutralization of gastric juice and this protection occurs through the involvement of SH compounds, α 2-adrenoceptors, NO, SOD, and HSP-70.

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Section: Discussionmentioning

confidence: 72%

Morphologic and Pharmacological Investigations in the Epicatechin Gastroprotective Effect

Rozza

Hiruma-Lima

Tanimoto

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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“…NO increases cyclic guanosine monophosphate levels, leading to activation of the ATP sensitive potassium channels (K + ATP ), in a sequence of events that ends in gastroprotection [ 37 ]. K + ATP channels mediate gastroprotection through the stimulation of gastric microcirculation and the inhibition of neutrophil activation and subsequent superoxide production [ 38 ]. Blocking NO production or K + ATP channels reversed the gastroprotection offered by B. holophylla .…”

Section: Discussionmentioning

confidence: 99%

Antiulcerogenic Activity and Toxicity ofBauhinia holophyllaHydroalcoholic Extract

Rozza

Cesar

Pieroni

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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Several species of Bauhinia are used in traditional medicine for the treatment of gastrointestinal diseases, diabetes, and inflammation, among other conditions. The aim of this study was to investigate the antiulcer effect of a hydroalcoholic extract from the leaves of B. holophylla. The chemical profile of the extract was determined by HPLC-PAD-ESI-IT-MS. A dose-effect relation was constructed using the ethanol-induced gastric ulcer model in male Wistar rats. Histological analyses and studies of antioxidant and anti-inflammatory activities were performed in stomach samples. The involvement of SH compounds, NO, K+ ATP channels, and α 2-adrenergic receptors in the gastroprotective effect was evaluated. A toxicity study was performed with a single oral dose of 5000 mg/kg. The extract was composed mainly of cyanoglucoside and flavonol-O-glycosides derivatives of quercetin and myricetin. SH compounds, NO release, K+ ATP channel activation, and presynaptic α 2-adrenergic receptor stimulation each proved to be involved in the antiulcer effect. The levels of GSH and activity of GR and GPx were increased, and the levels of TNF-α, IL-6 and IL-10 were modulated. There was an antidiarrheal effect and there were no signs of toxicity. B. holophylla presents antiulcer activity mainly by decreasing oxidative stress and attenuating the inflammatory response, without inducing side effects.

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“…In addition, a saline-treated group (normal control) was included. In another experimental setting, mice were treated with capsazepine (TRPV1 receptor antagonist; 5 mg ⅐ kg (Campos et al, 2008). Ethanol at 50% (0.5 ml 25 g Ϫ1 p.o.)…”

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confidence: 99%

Hydrogen Sulfide Prevents Ethanol-Induced Gastric Damage in Mice: Role of ATP-Sensitive Potassium Channels and Capsaicin-Sensitive Primary Afferent Neurons

Medeiros

Bezerra²,

Gomes³

et al. 2009

J Pharmacol Exp Ther

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The aim of this study was to evaluate the protective effect of hydrogen sulfide (H 2 S) on ethanol-induced gastric lesions in mice and the influence of ATP-sensitive potassium (K ATP ) channels, capsaicin-sensitive sensory afferent neurons, and transient receptor potential vanilloid (TRPV) 1 receptors on such an effect. Saline and L-cysteine alone or with propargylglycine, sodium hydrogen sulfide (NaHS), or Lawesson's reagent were administrated for testing purposes. For other experiments, mice were pretreated with glibenclamide, neurotoxic doses of capsaicin, or capsazepine. Afterward, mice received L-cysteine, NaHS, or Lawesson's reagent. After 30 min, 50% ethanol was administrated by gavage. After 1 h, mice were sacrificed, and gastric damage was evaluated by macroscopic and microscopic analyses. L-Cysteine, NaHS, and Lawesson's reagent treatment prevented ethanol-induced macroscopic and microscopic gastric damage in a dose-dependent manner. Administration of propargylglycine, an inhibitor of endogenous H 2 S synthesis, reversed gastric protection induced by L-cysteine. Glibenclamide reversed L-cysteine, NaHS, or Lawesson's reagent gastroprotective effects against ethanol-induced macroscopic damage in a dose-dependent manner. Chemical ablation of sensory afferent neurons by capsaicin reversed gastroprotective effects of L-cysteine or H 2 S donors (NaHS or Lawesson's reagent) in ethanol-induced macroscopic gastric damage. Likewise, in the presence of the TRPV1 antagonist capsazepine, the gastroprotective effects of L-cysteine, NaHS, or Lawesson's reagent were also abolished. Our results suggest that H 2 S prevents ethanol-induced gastric damage. Although there are many mechanisms through which this effect can occur, our data support the hypothesis that the activation of K ATP channels and afferent neurons/TRPV1 receptors is of primary importance.

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Gastroprotective effect of a flavone from Lonchocarpus araripensis Benth. (Leguminosae) and the possible mechanism

Cited by 8 publications

References 27 publications

Morphologic and Pharmacological Investigations in the Epicatechin Gastroprotective Effect

Morphologic and Pharmacological Investigations in the Epicatechin Gastroprotective Effect

Antiulcerogenic Activity and Toxicity ofBauhinia holophyllaHydroalcoholic Extract

Hydrogen Sulfide Prevents Ethanol-Induced Gastric Damage in Mice: Role of ATP-Sensitive Potassium Channels and Capsaicin-Sensitive Primary Afferent Neurons

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