Ethanolic extract of roots from Arctium lappa L. accelerates the healing of acetic acid-induced gastric ulcer in rats: Involvement of the antioxidant system

Silva, Luísa Mota da; Allemand, Alexandra; Mendes, Dayse; Santos, Ana Cristina dos; André, Eunice; Souza, Lauro Mera de; Cipriani, Thales R.; Dartora, Nessana; Marques, Maria Consuelo Andrade; Baggio, Cristiane Hatsuko; Werner, Maria Fernanda de Paula

doi:10.1016/j.fct.2012.09.026

Cited by 77 publications

(42 citation statements)

References 41 publications

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“…These findings showed that the complex had the ability to stimuli the mucus secretion. In agreement with several studies [33], [34], [69], [70], [77], our investigation revealed that the exposure of gastric mucosa to oxidative stress was restricted through the oral administration of omeprazole (5.790×10 −5 M/kg) or the complex as a pre-treatment. The involvement of formation of PGE-2 in the gastroprotective mechanisms was previously investigated with conflicting evidences [25], [29], [33], [34].…”

Section: Discussionsupporting

confidence: 92%

Gastroprotection Studies of Schiff Base Zinc (II) Derivative Complex against Acute Superficial Hemorrhagic Mucosal Lesions in Rats

et al. 2013

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BackgroundThe study was carried out to assess the gastroprotective effect of the zinc (II) complex against ethanol-induced acute hemorrhagic lesions in rats.Methodology/Principal FindingThe animals received their respective pre-treatments dissolved in tween 20 (5% v/v), orally. Ethanol (95% v/v) was orally administrated to induce superficial hemorrhagic mucosal lesions. Omeprazole (5.790×10−5 M/kg) was used as a reference medicine. The pre-treatment with the zinc (II) complex (2.181×10−5 and 4.362×10−5 M/kg) protected the gastric mucosa similar to the reference control. They significantly increased the activity levels of nitric oxide, catalase, superoxide dismutase, glutathione and prostaglandin E2, and decreased the level of malondialdehyde. The histology assessments confirmed the protection through remarkable reduction of mucosal lesions and increased the production of gastric mucosa. Immunohistochemistry and western blot analysis indicated that the complex might induced Hsp70 up-regulation and Bax down-regulation. The complex moderately increased the gastroprotectiveness in fine fettle. The acute toxicity approved the non-toxic characteristic of the complex (<87.241×10−5 M/kg).Conclusion/SignificanceThe gastroprotective effect of the zinc (II) complex was mainly through its antioxidant activity, enzymatic stimulation of prostaglandins E2, and up-regulation of Hsp70. The gastric wall mucus was also a remarkable protective mechanism.

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Section: Discussionsupporting

confidence: 92%

Gastroprotection Studies of Schiff Base Zinc (II) Derivative Complex against Acute Superficial Hemorrhagic Mucosal Lesions in Rats

et al. 2013

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“…Treatment of peptic ulcers focuses on eliminating pain, healing ulceration and preventing recurrence. Pharmacological intervention has historically been directed at the suppression of peptic acid secretion and more recently the eradication of Helicobacter pylori (Castillo‐Juárez et al, ; da Silva et al, ). However, currently available pharmacological treatments are not completely effective and can provoke adverse reactions.…”

Section: Introductionmentioning

confidence: 99%

Gastroprotective effect of calealactone B: Lack of involvement of prostaglandins, nitric oxide and sulfhydryls

Sánchez-Mendoza

López-Lorenzo

Matus-Meza

et al. 2017

Drug Development Research

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Hit, Lead & Candidate Discovery The gastroprotective effect of calealactone B, isolated from Calea urticifolia was assessed in an ethanol-induced model of gastric lesioning. The possible involvement of prostaglandins, nitric oxide (NO) and sulfhydryl groups in the mechanism of action of calealactone B was also assessed. Calealactone B inhibited ethanol-induced gastric injuries with a maximal effect (95.3 ± 2.6%) at 30 mg kg . A similar value was obtained at 10 mg kg (83.5 ± 7.7%). Meanwhile, the reference anti-ulcer drug, carbenoxolone, an 11β-hydroxysteroid dehydrogenase (11β-HSD) inhibitor administered at 30 mg kg showed 63.5 ± 9.4% gastroprotection. Hence, calealactone B was more potent than carbenoxolone. Pretreatment with indomethacin, L-NAME or NEM did not reverse the effects of calealactone B, indicating that prostaglandins, NO and sulfhydryl compounds do not participate in its mechanism of action.

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“…It was observed that acetic acid injury occurs by alteration of multiple factors such as growth factors, NO, iNOS activity, and antioxidant properties (Kobayashi and others ). Ulcer healing was a complex process, which involved cell proliferation, replication of epithelial cells at the ulcer margins to reestablish the glandular architecture, angiogenesis in the granulation tissue at the base of the ulcer, and matrix deposition, all ultimately leading to scar formation (da Silva and others ). In current experiments, the efficacy of CCP was comparable to the protective effects of cimetidine, because acidity of the gastric contents secreted, as well as macroscopic and histopathological lesion parameters were reduced when compared to EC group, reinforcing the potential use of CCP for the treatment of gastric ulcers.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Cod (Gadus macrocephalus) Skin Collagen Peptides on Acetic Acid‐Induced Gastric Ulcer in Rats

Niu

Wang

Hou

et al. 2016

Journal of Food Science

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This research was performed to explore the protective effect of cod skin collagen peptides (CCP) on gastric ulcer induced by acetic acid. The CCP were fractionated into low molecular CCP (LMCCP, Mw < 3 kDa) and high molecular CCP (HMCCP, Mw > 3 kDa). In HMCCP and LMCCP, glycine of accounted for about one-third of the total amino acids without cysteine and tryptophan, and hydrophobic amino acids accounted for about 50%. After 21 d CCP treatment (60 or 300 mg/kg, p.o./daily), the healing effects on acetic acid-induced gastric ulcers were evaluated by macroscopic measure, microscopic measure, and immune histochemistry. Moreover, the expression levels of the growth factors, such as vascular endothelial growth factor, epidermal growth factor, transforming growth factor β1 (TGFβ1), and the heat shock protein 70 (HSP70) was detected. The results showed that both LMCCP and HMCCP could significantly decrease the ulcer areas and promote the healing of the lesions. They also could improve the levels of hexosamine, glutathione, superoxide dismutase, and glutathione peroxidase, and reduce the content of malondialdehyde and inducible nitric oxide synthase. In addition, the expression level of TGFβ1 gene and HSP70 mRNA was significantly improved by the treatment. It suggested that CCP could be able to improve symptoms of gastric ulcer and probably be used in the treatment of gastric ulcer.

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Ethanolic extract of roots from Arctium lappa L. accelerates the healing of acetic acid-induced gastric ulcer in rats: Involvement of the antioxidant system

Cited by 77 publications

References 41 publications

Gastroprotection Studies of Schiff Base Zinc (II) Derivative Complex against Acute Superficial Hemorrhagic Mucosal Lesions in Rats

Gastroprotection Studies of Schiff Base Zinc (II) Derivative Complex against Acute Superficial Hemorrhagic Mucosal Lesions in Rats

Gastroprotective effect of calealactone B: Lack of involvement of prostaglandins, nitric oxide and sulfhydryls

Protective Effect of Cod (Gadus macrocephalus) Skin Collagen Peptides on Acetic Acid‐Induced Gastric Ulcer in Rats

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