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Ishii, Masakazu; Shimizu, Shunichi; Nawata, Shuichi; Kiuchi, Yuji; Yamamoto, Toshinori

doi:10.1023/a:1005413511320

Cited by 37 publications

(4 citation statements)

References 25 publications

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“…Oxidative stress induced by high levels of active oxygen plays a major role in GI-R injury. Excess production of oxygen free radicals is a major initiating factor and an independent pathogenic factor of GI-R injury (17,18). Therefore, investigating how to decrease oxidative stress is essential for developing means of protecting the gastric mucosa from attack by deleterious factors.…”

Section: Discussionmentioning

confidence: 99%

“…In mammals, endogenous H 2 S is generated from L-cys under the catalysis of total CBS and CSE, 1/3 of which is in the form of gas while 2/3 is in the form of NaHS. NaHS dissociates in vivo into sodium ions and sulfhydryl group ions and the latter bind with hydrogen ions to generate H 2 S. Thus, H 2 S and NaHS are in dynamic equilibrium (17). L-cys administration is cardioprotective through enhanced myocardial H 2 S generation as a result of CSE activation, which is attenuated by the selective CSE enzyme inhibitor, PAG (23).…”

Section: Discussionmentioning

confidence: 99%

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Protective effect of endogenous hydrogen sulfide against oxidative stress in gastric ischemia-reperfusion injury

Cui

Liu

Zou

et al. 2012

Experimental and Therapeutic Medicine

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Hydrogen sulfide (H2S) is a gaseous signaling molecule, which plays a critical role in a number of physiological and pathological progresses. In order to determine the effect of endogenous H2S on gastric ischemia-reperfusion (GI-R), we evaluated the gastric mucosal damage in rats intraperitoneally injected with DL-propargylglycine (PAG, 50 mg/kg/day) or L-cysteine (L-cys, 50 mg/kg/day) for 7 days before GI-R. GI-R injury was achieved by clamping the celiac artery for 30 min, followed by reperfusion for 60 min. Gastric mucosal damage was macroscopically assessed in the area of injury and deep damage was assessed by histopathological scoring. PAG increased the area of gastric mucosal injury and deep damage compared with that in untreated GI-R rats (P<0.05). While PAG decreased the H2S concentration and cystathionine γ-lyase (CSE) expression in the gastric mucosa, L-cys significantly attenuated the effects of GI-R. Western blot analysis revealed that the increases of malondialdehyde (MDA) and xanthine oxidase (XOD), and decreases of glutathione (GSH), superoxide dismutase (SOD) and the restriction of superoxide (O2−) production in the PAG group were inhibited by L-cys (P<0.05). Endogenous H2S has a protective effect against GI-R in rats by inhibiting oxygen free radical overproduction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective effect of endogenous hydrogen sulfide against oxidative stress in gastric ischemia-reperfusion injury

Cui

Liu

Zou

et al. 2012

Experimental and Therapeutic Medicine

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“…Numerous studies have suggested that excessive production of ROS or oxygen free radicals could be important initiating factors or pathogenic factors mediating GI-R injury (Itoh and Guth, 1985 ; Ishii et al, 2000 ). According to previous studies, we want to investigated whether the GABA B receptor protect the GI-R against the injury through the anti-oxidative stress pathway.…”

Section: Discussionmentioning

confidence: 99%

The Regulatory Effects of Lateral Hypothalamus Area GABAB Receptor on Gastric Ischemia-Reperfusion Injury in Rats

et al. 2017

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HIGHLIGHTS The aim of the research was to determine the functional effects and molecular mechanisms of GABAB receptor on ischemia reperfusion-induced gastric injury in rats.The lateral hypothalamus area GABAB receptor attenuated the ischemia reperfusion-induced gastric injury by up-regulating the production of GABA, GABABR, and down-regulating P-GABABR in the brain.This work would provide a new therapeutic strategy for acute gastric injury.Gastric ischemia-reperfusion (GI-R) injury progression is largely associated with excessive activation of the greater splanchnic nerve (GSN). This study aims to investigate the protective effects of GABAB receptor (GABABR) in the lateral hypothalamic area (LHA) on GI-R injury. A model of GI-R injury was established by clamping the celiac artery for 30 min and then reperfusion for 1 h. The coordinate of FN and LHA was identified in Stereotaxic Coordinates and then the L-Glu was microinjected into FN, GABAB receptor agonist baclofen, or GABAB receptor antagonist CGP35348 was microinjected into the LHA, finally the GI-R model was prepared. The expression of GABABR, P-GABABR, NOX2, NOX4, and SOD in the LHA was detected by western blot, PCR, and RT-PCR. The expression of IL-1β, NOX2, and NXO4 in gastric mucosa was detected by western blot. We found that microinjection of L-Glu into the FN or GABAB receptor agonist (baclofen) into the LHA attenuated GI-R injury. Pretreatment with GABAB receptor antagonist CGP35348 reversed the protective effects of FN stimulation or baclofen into the LHA. Microinjection of baclofen into the LHA obviously reduced the expression of inflammatory factor IL-1β, NOX2, and NOX4 in the gastric mucosa.Conclusion: The protective effects of microinjection of GABABR agonist into LHA on GI-R injury in rats could be mediated by up-regulating the production of GABA, GABABR, and down-regulating P-GABABR in the LHA.

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“…In vitro BH 4 supplementation partially restored eNOS activity, suppressed eNOS-derived ·O 2 − , and improved post-ischemic recovery of NOS-dependent coronary flow [15]. A number of animal studies have also demonstrated the protective effects of BH 4 against in vivo I/R injury in many organs, including the heart, lung, liver, kidney and stomach [16–20]. While in vivo BH 4 supplementation was reported to reduce post-ischemic myocardial injury [16], the extent to which alterations in endogenous BH 4 availability and NOS coupling modulates myocardial salvage following in vivo I/R remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Liposomal tetrahydrobiopterin preserves eNOS coupling in the post-ischemic heart conferring in vivo cardioprotection

Xie

Talukder

Sun

et al. 2015

Journal of Molecular and Cellular Cardiology

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Tetrahydrobiopterin (BH4) is an essential cofactor of nitric oxide synthase (NOS), and reduced BH4 availability leads to endothelial NOS (eNOS) uncoupling and increased reactive oxygen species (ROS) generation. Questions remain regarding the functional state of eNOS and role of BH4 availability in the process of in vivo myocardial ischemia-reperfusion (I/R) injury. Rats were subjected to 60-minutes of in vivo left coronary artery occlusion and varying periods of reperfusion with or without pre-ischemic liposomal BH4 supplementation (1 mg/kg, iv). Myocardial infarction was correlated with cardiac BH4 content, eNOS protein level, NOS enzyme activity, and ROS generation. In the vehicle group, 60-min ischemia drastically reduced myocardial BH4 content in the area at risk (AAR) compared to non-ischemic (NI) area and the level remained lower during early reperfusion followed by recovery after 24-hr reperfusion. Activated eNOS protein level (eNOS Ser1177 phosphorylation) and NOS activity were also significantly reduced during ischemia and/or early reperfusion, but recovered after 24-hr reperfusion. With liposomal BH4 treatment, BH4 levels were identical in the AAR and NI area during ischemia and/or early reperfusion, and were significantly higher than with vehicle. BH4 pre-treatment preserved eNOS Ser1177 phosphorylation and NOS activity in the AAR, and significantly reduced myocardial ROS generation and infarction compared to vehicle. These findings provide direct evidence that in vivo I/R induces eNOS dysfunction secondary to BH4 depletion, and that pre-ischemic liposomal BH4 administration preserves eNOS function conferring cardioprotection with reduced oxidative stress.

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Cited by 37 publications

References 25 publications

Protective effect of endogenous hydrogen sulfide against oxidative stress in gastric ischemia-reperfusion injury

Protective effect of endogenous hydrogen sulfide against oxidative stress in gastric ischemia-reperfusion injury

The Regulatory Effects of Lateral Hypothalamus Area GABAB Receptor on Gastric Ischemia-Reperfusion Injury in Rats

Liposomal tetrahydrobiopterin preserves eNOS coupling in the post-ischemic heart conferring in vivo cardioprotection

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