Carbon monoxide attenuates LPS-induced myocardial dysfunction in rats by regulating the mitochondrial dynamic equilibrium

Zhang, Sheng; Xu, Yanping; Zhu, Jinyuan; Ma, Jie; Niu, Qingsheng; Wang, Xiaohong

doi:10.1016/j.ejphar.2020.173726

Cited by 9 publications

(5 citation statements)

References 51 publications

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“…The increased MAP in rats that were treated with CORM-2 could be attributed to two factors. First, according to our previous study, CORM-2 increased cardiac output and left ventricular ejection fraction and exerted a positive effect on ischemic myocardial mitochondrial function and ultrastructural changes to protect cardiac tissues of lipopolysaccharide (LPS)-stimulated rats [19]. This bene cial effect on cardiac function by CORM-2 treatment might result in the increase of MAP in rats.…”

Section: Discussionmentioning

confidence: 89%

WITHDRAWN: Carbon Monoxide Releasing Molecule-2 Protects Intestinal Mucosal Barrier Function of Rat Undergoing Cardiopulmonary Resuscitation via Attenuation of TNF-α/NF-κB Signaling

Niu

Liu

Zhang

et al. 2021

Preprint

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The unique features of post–cardiac arrest pathophysiology are often superimposed on the disease or injury, causing the cardiac arrest, as well as underlying comorbidities. Exogenous carbon monoxide (CO) was reported to reduce ischemia-reperfusion injury (IRI). This study aimed to assess the effects of CO releasing molecule-2 (CORM-2) on intestinal mucosal barrier function after cardiopulmonary resuscitation (CPR) in rats. For this purpose, we established a rat model of asphyxiation-induced cardiac arrest and resuscitation to study intestinal IRI, and measured the serum level of intestinal fatty-acid binding protein (I-FABP). The expression levels of claudin-3, occludin, ZO-1, tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), and nuclear factor kappa B (NF-κB) p65 were detected by Western blotting. CORM-2 up-regulated the expression levels of tight junction proteins (claudin-3, occludin, and ZO-1) in intestinal mucosa, leading to the reduction of the permeability of intestinal mucosa and reduced the release of proinflammatory cytokines. Besides, the CORM-2 exhibited anti-inflammatory effects by regulating the TNF-α/NF-κB pathway. In conclusion, CORM-2 treatment is clinically significant, preventing intestinal mucosal damage as a result of IRI during CPR.

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Section: Discussionmentioning

confidence: 89%

WITHDRAWN: Carbon Monoxide Releasing Molecule-2 Protects Intestinal Mucosal Barrier Function of Rat Undergoing Cardiopulmonary Resuscitation via Attenuation of TNF-α/NF-κB Signaling

Niu

Liu

Zhang

et al. 2021

Preprint

Self Cite

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“…Another dose of CORM-2, 20 mg/kg, was justified if 10 mg/kg was unsuccessful in diminishing venom activity, as up to 30 mg/kg of CORM-2 in a murine model of acute kidney injury was well tolerated and protected against injury [ 35 ]. CORM-2 doses that result in no toxicity in vivo vary a great deal, with values as small as 5 mg/kg to 50 mg/kg depending on the species [ 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 ]. As has been demonstrated with several venoms and venom enzymes, it is the ruthenium radical of CORM-2 that presumably binds to key amino acid residues, such as histidine, to inhibit activity [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Novel Toxicodynamic Model of Subcutaneous Envenomation to Characterize Snake Venom Coagulopathies and Assess the Efficacy of Site-Directed Inorganic Antivenoms

Nielsen

2023

IJMS

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Venomous snake bite adversely affects millions of people yearly, but few animal models allow for the determination of toxicodynamic timelines with hemotoxic venoms to characterize the onset and severity of coagulopathy or assess novel, site-directed antivenom strategies. Thus, the goals of this investigation were to create a rabbit model of subcutaneous envenomation to assess venom toxicodynamics and efficacy of ruthenium-based antivenom administration. New Zealand White rabbits were sedated with midazolam via the ear vein and had viscoelastic measurements of whole blood and/or plasmatic coagulation kinetics obtained from ear artery samples. Venoms derived from Crotalus scutulatus scutulatus, Bothrops moojeni, or Calloselasma rhodostoma were injected subcutaneously, and changes in coagulation were determined over three hours and compared to samples obtained prior to envenomation. Other rabbits had ruthenium-based antivenoms injected five minutes after venom injection. Viscoelastic analyses demonstrated diverse toxicodynamic patterns of coagulopathy consistent with the molecular composition of the proteomes of the venoms tested. The antivenoms tested attenuated venom-mediated coagulopathy. A novel rabbit model can be used to characterize the onset and severity of envenomation by diverse proteomes and to assess site-directed antivenoms. Future investigation is planned involving other medically important venoms and antivenom development.

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“…In this study, we found that LPS could promote cellular apoptosis. When studying the effect of LPS on myocardial function in rats, the researchers found that LPS stimulation could cause swelling, fragmentation and reduction of cristae density in mitochondrial morphology, as well as a decrease in the activity of mitochondrial complex IV (Zhang, Xu, Zhu, et al., 2020 ). Based on previous research findings, C3G could effectively prevent ultraviolet‐induced apoptosis of HaCaT cells by scavenging ROS (He et al., 2017 ).…”

Section: Resultsmentioning

confidence: 99%

Anti‐inflammatory activity of cyanidin‐3‐O‐glucoside and cyanidin‐3‐O‐glucoside liposomes in THP‐1 macrophages

Hao

Guan

Huang

et al. 2021

Food Science & Nutrition

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Inflammation is a response of the body to stimulation, which may be beneficial or harmful. Inflammation may either be acute or chronic, and is related to the homeostasis of physiological systems in vivo. Inflammation is associated with many diseases and is the basis of most pathological processes. The main causes of inflammation are infection and tissue damage, which can lead to the concentration of leukocytes and plasma proteins (Medzhitov, 2008).Chronic inflammation is involved in many diseases, including diabetes, obesity, atherosclerosis, and cancer (Coussens & Werb, 2002;

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Carbon monoxide attenuates LPS-induced myocardial dysfunction in rats by regulating the mitochondrial dynamic equilibrium

Cited by 9 publications

References 51 publications

WITHDRAWN: Carbon Monoxide Releasing Molecule-2 Protects Intestinal Mucosal Barrier Function of Rat Undergoing Cardiopulmonary Resuscitation via Attenuation of TNF-α/NF-κB Signaling

WITHDRAWN: Carbon Monoxide Releasing Molecule-2 Protects Intestinal Mucosal Barrier Function of Rat Undergoing Cardiopulmonary Resuscitation via Attenuation of TNF-α/NF-κB Signaling

Novel Toxicodynamic Model of Subcutaneous Envenomation to Characterize Snake Venom Coagulopathies and Assess the Efficacy of Site-Directed Inorganic Antivenoms

Anti‐inflammatory activity of cyanidin‐3‐O‐glucoside and cyanidin‐3‐O‐glucoside liposomes in THP‐1 macrophages

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