Interaction between endogenous carbon monoxide and hydrogen sulfide in the mechanism of gastroprotection against acute aspirin-induced gastric damage

Magierowski, Marcin; Magierowska, Katarzyna; Hubalewska-Mazgaj, Magdalena; Adamski, Juliusz; Bakalarz, Dominik; Śliwowski, Zbigniew; Pajdo, Robert; Kwiecień, Sławomir; Brzozowski, Tomasz

doi:10.1016/j.phrs.2016.11.001

Cited by 51 publications

(78 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the day of experiment, aspirin dissolved in 0.2 M HCl solution was administered intragastrically in a dose of 125 mg/kg (1.5 ml per rat) to induce gastric lesions, as described previously [17]. Thirty minutes before aspirin application, rats with capsaicin-induced denervation (series A) and rats without capsaicin-induced denervation (series B) were pretreated intragastrically with (1) 0.9% saline (vehicle control) or dimethyl sulfoxide and saline (1:10), (2) CO-releasing CORM-2 [20], applied in a dose of 5 mg/ kg, which has previously been reported by our group to increase CO content in gastric mucosa and to exert gastroprotection against aspirin-and ethanol-induced gastric damage [17,21], or (3) NaHS, the H 2 S-releasing salt applied intragastrically in a dose of 5 mg/kg, which has been demonstrated to protect gastric mucosa against aspirin-, stress-, or alendronate-induced lesions [17,19,22].…”

Section: Methodsmentioning

confidence: 99%

“…Thirty minutes before aspirin application, rats with capsaicin-induced denervation (series A) and rats without capsaicin-induced denervation (series B) were pretreated intragastrically with (1) 0.9% saline (vehicle control) or dimethyl sulfoxide and saline (1:10), (2) CO-releasing CORM-2 [20], applied in a dose of 5 mg/ kg, which has previously been reported by our group to increase CO content in gastric mucosa and to exert gastroprotection against aspirin-and ethanol-induced gastric damage [17,21], or (3) NaHS, the H 2 S-releasing salt applied intragastrically in a dose of 5 mg/kg, which has been demonstrated to protect gastric mucosa against aspirin-, stress-, or alendronate-induced lesions [17,19,22]. In a separate series (C), rats with intact sensory nerves were pretreated with NaHS or CORM-2 in combination with capsazepine (5 mg/kg intragastrically), a TRPV1 antagonist [23], or N G -nitro-L-arginine (L-NNA, 20 mg/kg intraperitoneally), a nonselective nitric oxide synthase (NOS) inhibitor [24].…”

Section: Methodsmentioning

confidence: 99%

“…Reverse transcription to complementary DNA was performed with a high-capacity complementary DNA reverse transcription kit (Thermo Fisher Scientific, Life Technologies, MA, USA). Expression of b-actin, heme oxygenase 1 (HO-1), cyclooxygenase (COX)-2, inducible NOS (iNOS), interleukin-1b (IL-1b), GPx-1, and SOD-2 was determined by real-time PCR using specific primers [17,22], SG qPCR master mix (29) including SYBR Green (EURx, Gdansk, Poland), and Quant Studio 12K Flex thermal cycler (Thermo Fisher Scientific, MA, USA). To determine a-CGRP mRNA expression, 5 0 -GCTCACCAGGGAGG-CATCAT-3 0 forward primer and 5 0 -ATGCCTGGTA-CAGGAGCAAGA-3 0 reverse primer were used.…”

Section: Methodsmentioning

confidence: 99%

“…Protein expression of b-actin, GPx-1, SOD-1, and iNOS in gastric mucosa was determined by Western blot, as described previously [17,21,22]. Rabbit polyclonal antiiNOS antibody (1:500, ab3523, Abcam, Cambridge, UK), rabbit polyclonal anti-GPx-1 antibody (1:1000, ab22604, Abcam), rabbit polyclonal anti-SOD-1 antibody (1:1000, ab13498, Abcam), and rabbit polyclonal anti-b-actin anitbody (1:1000, 20536-1-AP, Proteintech, Manchester, UK) were used as primary antibodies.…”

Section: Determination Of Protein Expression In Gastric Mucosa By Wesmentioning

confidence: 99%

“…Recently, it has been reported that inhibition of H 2 S generation contributes to the formation of aspirin-induced gastric injury [5]. The CO and H 2 S biosynthesis pathways were both shown to synergistically interact in the mechanism of gastroprotection against NSAID-induced gastric damage via restoration of gastric microcirculation impaired by these drugs [17].…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

et al. 2017

Self Cite

View full text Add to dashboard Cite

Background Aspirin exerts side effects within the gastrointestinal tract. Hydrogen sulfide (H 2 S) and carbon monoxide (CO) have been implicated in gastroprotection but the mechanism of beneficial action of these gaseous mediators against aspirin-induced damage has not been fully studied. We determined the involvement of afferent sensory neurons, calcitonin-gene-related peptide (CGRP), lipid peroxidation, and nitric oxide (NO) biosynthesis in gastroprotection of H 2 S-releasing NaHS and CO-releasing tricarbonyldichlororuthenium(II) dimer (CORM-2) against aspirin-induced injury. Methods Wistar rats with or without capsaicin-induced denervation of sensory neurons were pretreated with vehicle, CORM-2 (5 mg/kg intragastrically), or NaHS (5 mg/kg intragastrically) with or without capsazepine (5 mg/kg intragastrically) or N G -nitro-L-arginine (L-NNA, 20 mg/kg intraperitoneally). The areas of aspirin-induced lesions and gastric blood flow (GBF) were assessed by planimetry and laser flowmetry respectively. Gastric mucosal messenger RNA and/or protein expression of CGRP, heme oxygenase 1, inducible nitric oxide synthase, cyclooxygenase 2, interleukin-1b, glutathione peroxidase 1 (GPx-1), and superoxide dismutase was determined by real-time PCR or Western blot. Malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) content was determined by colorimetric assay. Results Aspirin caused gastric lesions, decreased GBF, and raised MDA content, but pretreatment with NaHS and CORM-2 reduced these effects. Capsaicin-induced denervation or co-treatment with capsazepine reversed the gastroprotective and vasodilatory effects of NaHS but not those of CORM-2. L-NNA reversed NaHS-induced gastroprotection and partly reduced CORM-2-induced gastroprotection. NaHS and CORM-2 decreased MDA and 4-HNE content, restoring GPx-1 protein expression. Conclusions We conclude that H 2 S-but not CO-mediated gastroprotection against aspirin-induced injury involves afferent sensory nerves and partly NO activity. NaHS and CORM-2 prevented aspirin-induced gastric mucosal lipid peroxidation via restoration of microcirculation and antioxidative GPx-1 protein expression.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Determination Of Protein Expression In Gastric Mucosa By Wesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

et al. 2017

Self Cite

View full text Add to dashboard Cite

show abstract

COin Gastrointestinal Physiology and Protection

Magierowska

Magierowski

2022

Carbon Monoxide in Drug Discovery

View full text Add to dashboard Cite

A Single‐Component Dual Donor Enables Ultrasound‐Triggered Co‐release of Carbon Monoxide and Hydrogen Sulfide

Zhang,

Cheng,

Shen

et al. 2023

Angewandte Chemie

View full text Add to dashboard Cite

The development of dual gasotransmitter donors can not only provide robust tools to investigate their subtle interplay under pathophysiological conditions but also optimize therapeutic efficacy. While conventional strategies are heavily dependent on multicomponent donors, we herein report the first ultrasoundresponsive water‐soluble copolymer (PSHF) capable of releasing carbon monoxide (CO) and hydrogen sulfide (H2S) based on singlecomponent sulfur‐substituted 3‐hydroxyflavone (SHF) derivatives. Interestingly, the sulfur substitution can not only greatly improve the ultrasound sensitivity but also enable the co‐release of CO/H2S under mild ultrasound irradiation. The co‐release of CO/H2S gasotransmitters exerts a bactericidal effect against Staphylococcus aureus and demonstrates anti‐inflammatory activity in lipopolysaccharide‐challenged macrophages. Moreover, the excellent tissue penetration of ultrasound irradiation enables the local release of CO/H2S in the joints of septic arthritis rats, exhibiting superior therapeutic efficacy without the need for any antibiotics.

show abstract

Interaction between endogenous carbon monoxide and hydrogen sulfide in the mechanism of gastroprotection against acute aspirin-induced gastric damage

Cited by 51 publications

References 80 publications

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

COin Gastrointestinal Physiology and Protection

A Single‐Component Dual Donor Enables Ultrasound‐Triggered Co‐release of Carbon Monoxide and Hydrogen Sulfide

Contact Info

Product

Resources

About