Ameliorative effect of Boesenbergin A, a chalcone isolated from Boesenbergia rotunda (Fingerroot) on oxidative stress and inflammation in ethanol-induced gastric ulcer in vivo

Mohan, Syam; Hobani, Yahya Hasan; Shaheen, Emad S.; Abou-Elhamd, Alaa Sayed; Abdelhaleem, Aymen; Alhazmi, Hassan A.; Abdelwahab, Siddig Ibrahim

doi:10.1016/j.jep.2020.113104

Cited by 37 publications

(27 citation statements)

References 31 publications

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“…A good explanation for inhibiting oxidative stress was the observed remission of neutrophil infiltration and the decrease of membrane lipid peroxidation level. Ample evidence demonstrated the antioxidants plays a central role in process of GU (Kwiecien et al, 2002;Raish et al, 2018;Mohan, et al, 2020). Our data validated the restoration of Nrf2 along with the prototypical Nrf2 target genes (HO-1 and Nqo1) and the replenish of crucial antioxidation elements (SOD, CAT and GSH) in the wake of RUT treatment.…”

Section: Discussionsupporting

confidence: 77%

Rutaecarpine Ameliorates Ethanol-Induced Gastric Mucosal Injury in Mice by Modulating Genes Related to Inflammation, Oxidative Stress and Apoptosis

Ren

Wei

et al. 2020

Front. Pharmacol.

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Background: Rutaecarpine (RUT), a major quinazolino carboline alkaloid compound from the dry unripe fruit Tetradium ruticarpum (A. Juss.) T. G. Hartley, has various pharmacological effects. The aim of this present study was to investigate the potential gastroprotective effect of rutaecarpine on ethanol-induced acute gastric mucosal injury in mice and associated molecular mechanisms, such as activating Nrf2 and Bcl-2 via PI3K/AKT signaling pathway and inhibiting NF-κB.Methods: Gastric ulcer index and histopathology was carried out to determine the efficacy of RUT in gastric ulceration, and the content of SOD, GSH in serum and CAT, MDA, MPO, TNF-α, IL-6, IL-1β in tissue were measured by kits. Besides, in order to illustrate the potential inflammatory, oxidative, and apoptotic perturbations, the mRNA levels of NF-κB p65, PI3K, AKT, Nrf2, Nqo1, HO-1, Bcl-2 and Bax were analyzed. In addition, the protein expression of NF-κB p65 and Nrf2 in cytoplasm and nucleus, AKT, p-AKT, Bcl-2 Bax and Caspase 3 were analyzed for further verification. Finally, immunofluorescence analysis was performed to further verify nuclear translocation of NF-κB p65.Results: Current data strongly demonstrated that RUT alleviated the gross gastric damage, ulcer index and the histopathology damage caused by ethanol. RUT inhibited the expression and nuclear translocation of NF-κB p65 and the expression of its downstream signals, such as TNF-α, IL-6, IL-1β and MPO. Immunofluorescence analysis also verifies the result. In the context of oxidative stress, RUT improved the antioxidant milieu by remarkably upregulating the expression Nqo1 and HO-1 with activating Nrf2, and could remarkably upregulate antioxidant SOD, GSH, CAT and downregulate levels of MDA. Additionally, RUT activate the expression of Bcl-2 and inhibited the expression of downstream signals Bax and Caspase 3 to promote gastric cellular survival. These were confirmed by RUT activation of the PI3K/AKT pathway manifested by enhanced expression of PI3K and promotion of AKT phosphorylation.Conclusion: Taken together, these results strongly demonstrated that RUT exerted a gastroprotective effect against gastric mucosal injury induced by ethanol. The underlying mechanism might be associated with the improvement of anti-inflammatory, anti-oxidation and anti-apoptosis system.

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Section: Discussionsupporting

confidence: 77%

Rutaecarpine Ameliorates Ethanol-Induced Gastric Mucosal Injury in Mice by Modulating Genes Related to Inflammation, Oxidative Stress and Apoptosis

Ren

Wei

et al. 2020

Front. Pharmacol.

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“…Tarnawski believes that repairing and reconstructing submucosal tissue is the key to the treatment of gastric ulcers. Clinically, a remnant of pathological changes still exists in some of the healed ulcers observed by endoscopy, which gives weight to the determination of functional maturity of the ulcers in addition to the observation of superficial regenerated mucosa under direct endoscopy, to better evaluate the recurrence of the disease [23].…”

Section: Discussionmentioning

confidence: 99%

A Retrospective Trial Exploring Erzhu Yiren Decoction in Gastric Ulcer with Spleen Deficiency and Dampness-Heat

Zhang

Zhaowei

2022

BioMed Research International

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Objective. To assess the efficacy of Erzhu Yiren Decoction in treating gastric ulcer of spleen deficiency and dampness-heat and its effect on serum NO, EGF, and PGE2 levels. Methods. A retrospective study was conducted among 64 patients with gastric ulcers of spleen deficiency and dampness heat admitted to our hospital from September 2019 to May 2020, and they were divided at a ratio of 1 : 1 into an observation group (rabeprazole sodium enteric-coated capsules plus Erzhu Yiren Decoction) and a control group (rabeprazole sodium enteric-coated capsules) based on different treatment methods. The clinical symptom scores, the effective rate of ulcer healing under gastroscopy, the quality of ulcer healing (QOUH), serum nitric oxide (NO), endothelial growth factor (EGF), and prostaglandin E2 (PGE2) levels were compared between the two groups. Results. The clinical symptom scores of the observation group after treatment were significantly lower than those of the control group ( P < 0.001 ). The observation group obtained a remarkably higher efficacy of ulcer healing under gastroscopy than the control group ( P = 0.039 ). The observation group outperformed the control group in terms of the number of patients with excellent and good QOUH ( P = 0.003 , 0.014), but no statistical difference in the number of patients with poor QOUH between the two groups was found ( P > 0.05 ). Serum NO, EGF, and PGE2 levels of the observation group after treatment were significantly better than those of the control group ( P < 0.001 ). Conclusion. Erzhu Yiren Decoction can relieve the clinical symptoms of patients with gastric ulcers of spleen deficiency and dampness heat; improve the serum NO, EGF, and PGE2 levels; optimize the mucosal maturity; and enhance the overall efficacy, which merits clinical promotion.

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“…The rats fasted 24 hours before death but drank freely. 2 h after the last administration, except for the normal control group, all rats were given 5 mL/kg ethanol to induce gastric mucosal injury [ 18 , 19 ]. 1 h later, the rats were anesthetized to death with pentobarbital sodium.…”

Section: Methodsmentioning

confidence: 99%

Gastroprotective Effect of Ethanol Extracts from Bark of Magnolia officinalis on Ethanol-Induced Gastric Mucosal Damage in Rats

Wang

Zhang

et al. 2021

BioMed Research International

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Background. Magnolia officinalis Rehd. and Wils. is widely used in Asian countries because of its multiple pharmacological effects. This study investigated the gastroprotective effect and mechanisms of the ethanol extracts from the bark of Magnolia officinalis (MOE) against ethanol-induced gastric mucosal damage in rats. Methods. MOE was prepared by reflux extraction with 70% ethanol, and its main compounds were analyzed by UPLC-Q-Exactive Orbitrap-MS. DPPH, ABTS, and FRAP methods were used to evaluate the antioxidant capacity of MOE in vitro. The gastroprotective effects of MOE were evaluated by the area of gastric injury, H&E (hematoxylin-eosin), and PAS (periodic acid-Schiff). The mechanism was explored by measuring the levels of cytokines and protein in the NF-κB signaling pathway. Results. 30 compounds were identified from MOE, mainly including lignans and alkaloids. MOE presented a high antioxidant activity in several oxidant in vitro systems. Gastric ulcer index and histological examination showed that MOE reduced ethanol-induced gastric mucosal injury in a dose-dependent manner. MOE pretreatment significantly restored the depleted activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) enzymes, reduced malondialdehyde (MDA), and prostaglandin E2 (PGE2) levels in the gastric tissue in rats. In addition, MOE also inhibited the activation of nuclear factor kappa B (NF-κB) pathway and decreased the production of proinflammatory cytokines. Conclusions. The gastroprotective effect of MOE was attributed to the inhibition of oxidative stress and the NF-κB inflammatory pathway. The results provided substantial evidence that MOE could be a promising phytomedicine for gastric ulcer prevention.

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Ameliorative effect of Boesenbergin A, a chalcone isolated from Boesenbergia rotunda (Fingerroot) on oxidative stress and inflammation in ethanol-induced gastric ulcer in vivo

Cited by 37 publications

References 31 publications

Rutaecarpine Ameliorates Ethanol-Induced Gastric Mucosal Injury in Mice by Modulating Genes Related to Inflammation, Oxidative Stress and Apoptosis

Rutaecarpine Ameliorates Ethanol-Induced Gastric Mucosal Injury in Mice by Modulating Genes Related to Inflammation, Oxidative Stress and Apoptosis

A Retrospective Trial Exploring Erzhu Yiren Decoction in Gastric Ulcer with Spleen Deficiency and Dampness-Heat

Gastroprotective Effect of Ethanol Extracts from Bark of Magnolia officinalis on Ethanol-Induced Gastric Mucosal Damage in Rats

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