Alpha-boswellic acid protects against ethanol-induced gastric injury in rats: involvement of nuclear factor erythroid-2-related factor 2/heme oxygenase-1 pathway

Zhang, Yikai; Jia, Junmei; Ding, Yi; Ma, Yongzheng; Shang, Peijin; Liu, Tianlong; Hui, Guangfei; Wang, Lin; Wang, Mingming; Zhu, Zhihui; Li, Yuwen; Wen, Aidong

doi:10.1111/jphp.12532

Cited by 36 publications

(26 citation statements)

References 40 publications

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“…Another clarification is managed by Hartmann et al [ 9 ] who proposed that BAs possess antioxidant effects restraining MDA production in acute experimental colitis. In addition, previous findings accentuated that BAs evoke antioxidant properties that fortify the Nrf2/HO-1 defense pathway [ 8 , 14 ].…”

Section: Discussionmentioning

confidence: 99%

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Protective Effect of Boswellic Acids against Doxorubicin‐Induced Hepatotoxicity: Impact on Nrf2/HO‐1 Defense Pathway

Barakat

Ahmed

Bahr

et al. 2018

Oxidative Medicine and Cellular Longevity

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The current study aimed to investigate the potential protective role of boswellic acids (BAs) against doxorubicin- (DOX-) induced hepatotoxicity. Also, the possible mechanisms underlying this protection; antioxidant, as well as the modulatory effect on the Nrf2 transcription factor/hem oxygenase-1 (Nrf2/HO-1) pathway in liver tissues, was investigated. Animals were allocated to five groups: group 1: the saline control, group 2: the DOX group, animals received DOX (6 mg/kg, i.p.) weekly for a period of three weeks, and groups 3–5: animals received DOX (6 mg/kg, i.p.) weekly and received protective doses of BAs (125, 250, and 500 mg/kg/day). Treatment with BAs significantly improved the altered liver enzyme activities and oxidative stress markers. This was coupled with significant improvement in liver histopathological features. BAs increased the Nrf2 and HO-1 expression, which provided protection against DOX-induced oxidative insult. The present results demonstrated that BAs appear to scavenge ROS and inhibit lipid peroxidation and DNA damage of DOX-induced hepatotoxicity. The antioxidant efficacy of BAs might arise from its modulation of the Nrf2/HO-1 pathway and thereby protected liver from DOX-induced oxidative injury.

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Section: Discussionmentioning

confidence: 99%

“…AKBA has a structural similarity to ursolic acid, and interestingly, one study affirmed that AKBA has greater antioxidant activity in mice than ursolic acid [ 13 ]. Consequently, it may promote some of its protective effects via activating the Nrf2 pathway, a hypothesis which was proved recently by Zhang et al [ 14 ].…”

Section: Introductionmentioning

confidence: 98%

Protective Effect of Boswellic Acids against Doxorubicin‐Induced Hepatotoxicity: Impact on Nrf2/HO‐1 Defense Pathway

Barakat

Ahmed

Bahr

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…The rat stomach was taken out, and the excised stomach was opened along the greater curvature and then rinsed with ice‐cold PBS. The whole stomach was then laid flat on the clean white paper, and the ulcer index and ulcer inhibition rate were calculated according to our previous description …”

Section: Methodsmentioning

confidence: 99%

“…Another third of rats randomly selected in each group were anesthetized with urethane, and the stomach was excised. Gastric juice acidity and gastric wall mucus (GWM) were detected according to the previously description …”

Section: Methodsmentioning

confidence: 99%

Total triterpenes from the fruits of Chaenomeles speciosa (Sweet) Nakai protects against indomethacin-induced gastric mucosal injury: involvement of TFF1-mediated EGF/EGFR and apoptotic pathways

Zhang

et al. 2020

Journal of Pharmacy and Pharmacology

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Objectives Our previous studies indicated that the triterpenes from the fruits of Chaenomeles speciosa (Sweet) Nakai (TCS) owned effectively therapeutic effects on gastric ulcer patients and animals, but its mechanisms have not been fully understood. The current study was to further investigate its protective effect on indomethacin (IND)-damaged RGM-1 cells and rats, as well as its mechanisms involved. Methods The gastroprotection of TCS was evaluated with IND-induced gastric lesions model in RGM-1 cells and rats. In vitro, the proliferation, migration, mitochondrial viability and apoptosis were assessed. In vivo, ulcer index, ulcer inhibition rate, gastric juice acidity, gastric wall mucus (GWM) and histopathology of gastric mucosa were detected. The gastroprotective effects of TCS through the TFF1-mediated EGF/EGFR and apoptotic pathways were measured by qRT-PCR and Western blot assays. Key findings The results demonstrated that TCS had gastroprotective function, which was related to the amelioration in promoting IND-damaged RGM-1 cell proliferation and migration, hoisting gastric juice acidity and GWM, improving ulcer index and ulcer inhibition rate, attenuating the haemorrhage, oedema, epithelial cell loss and inflammatory cell infiltration of gastric mucosa, upregulating PCNA, Bcl-2, Bcl-xl mRNA and TFF1, EGF, p-EGFR, p-Src, pro-caspase-3, pro-caspase-9 protein expressions, mitochondrial viability, mitochondrial cytochrome c concentration and p-EGFR/EGFR, p-Src/Src, Bcl-2/Bax, Bcl-xl/Bad ratioes, downregulating Bax, Bad, Apaf-1 mRNA and cleaved-caspase-3, cleavedcaspase-9, cleaved PARP-1 protein expressions and cytosol cytochrome c concentration. Conclusions Our present study demonstrated that TCS's gastroprotective effect was closely connected with boosting TFF1 expression, activating TFF1-mediated EGF/EGFR pathway, thus restraining mitochondrial-dependent apoptosis, which provided new insights into interpreting its underlying mechanism and promised to act as a candidate drug to treat gastric mucosal injury.Gastroprotective effects of TCS Yuanyuan Zhang et al.

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“…According to Umemura et al [18], both 2,3-epoxyjuanislamin and calealactone B can activate the Nrf2 system. Upon exposure to an oxidative stimulus, Nrf2 is known to translocate into the nucleus and bind to the antioxidant response element, which regulates the expression of antioxidant enzymes (e.g., CAT, SOD and GPx) involved in the protection of the gastric mucosa [19]. The activation of this system is triggered by the α,β-unsaturated carbonyl groups in the structure of these lactones, as they are susceptible to undergoing a Michael-type reaction [18,20] with the sulfhydryl groups of the cysteine residues of the proteins.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2019

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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.

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Alpha-boswellic acid protects against ethanol-induced gastric injury in rats: involvement of nuclear factor erythroid-2-related factor 2/heme oxygenase-1 pathway

Abstract: These findings demonstrate that α-BA decreases oxidative stress and that the Nrf2/HO-1 pathway might play a role in the gastroprotective action of α-BA in ethanol-induced gastric injury in rats.

Cited by 36 publications

References 40 publications

Protective Effect of Boswellic Acids against Doxorubicin‐Induced Hepatotoxicity: Impact on Nrf2/HO‐1 Defense Pathway

Protective Effect of Boswellic Acids against Doxorubicin‐Induced Hepatotoxicity: Impact on Nrf2/HO‐1 Defense Pathway

Total triterpenes from the fruits of Chaenomeles speciosa (Sweet) Nakai protects against indomethacin-induced gastric mucosal injury: involvement of TFF1-mediated EGF/EGFR and apoptotic pathways

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

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