Annexin A1 peptide Ac2-26 mitigates ventilator-induced lung injury in acute respiratory distress syndrome rats and partly depended on the endothelial nitric oxide synthase pathway

Ju, Yingnan; Sun, Xikun; Xu, Guangxiao; Tai, Qihang

doi:10.1590/acb371203

Cited by 5 publications

(5 citation statements)

References 37 publications

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“…As an important anti-inflammatory factor, IL-10 can inhibit the synthesis of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6 [27]. As an endogenous glucocorticoid-regulated anti-inflammatory [28], Ac2-26 has been indicated to prompt the expression of IL-10 to regulate inflammation [29,30]. These results suggested that Ac2-26 ameliorated liver injury and protected liver function may be associated with anti-inflammation.…”

Section: Discussionmentioning

confidence: 94%

Ac2-26 reduced the liver injury after cardiopulmonary bypass in rats via AKT1/GSK3β/eNOS pathway

Xing,

Liu,

Yang

et al. 2024

J Cardiothorac Surg

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Objective About 10% of patients after cardiopulmonary bypass (CPB) would undergo acute liver injury, which aggravated the mortality of patients. Ac2-26 has been demonstrated to ameliorate organic injury by inhibiting inflammation. The present study aims to evaluate the effect and mechanism of Ac2-26 on acute liver injury after CPB. Methods A total of 32 SD rats were randomized into sham, CPB, Ac, and Ac/AKT1 groups. The rats only received anesthesia, and rats in other groups received CPB. The rats in Ac/AKT1 were pre-injected with the shRNA to interfere with the expression of AKT1. The rats in CPB were injected with saline, and rats in Ac and Ac/AKT1 groups were injected with Ac2-26. After 12 h of CPB, all the rats were sacrificed and the peripheral blood and liver samples were collected to analyze. The inflammatory factors in serum and liver were detected. The liver function was tested, and the pathological injury of liver tissue was evaluated. Results Compared with the sham group, the inflammatory factors, liver function, and pathological injury were worsened after CPB. Compared with the CPB group, the Ac2-26 significantly decreased the pro-inflammatory factors and increased the anti-inflammatory factor, improved liver function, and ameliorated the pathological injury. All the therapeutic effects of Ac2-26 were notably attenuated by the shRNA of AKT1. The Ac2-26 increased the GSK3β and eNOS, and this promotion was inhibited by the shRNA. Conclusion The Ac2-26 significantly treated the liver injury, inhibited inflammation, and improved liver function. The effect of Ac2-26 on liver injury induced by CPB was partly associated with the promotion of AKT1/GSK3β/eNOS.

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Section: Discussionmentioning

confidence: 94%

Ac2-26 reduced the liver injury after cardiopulmonary bypass in rats via AKT1/GSK3β/eNOS pathway

Xing,

Liu,

Yang

et al. 2024

J Cardiothorac Surg

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“…Cunha, 56 et al demonstrated that acute lung injury (ALI), caused by the administration of endotoxin LPS in mice resulted in leukocyte infiltration, exacerbated production of inflammatory mediators and tissue damage. Treatment with Ac2-26 was able to decrease leukocyte migration, especially in the pulmonary connective tissue and alveoli, contributing to the regulation of inflammation.…”

Section: Gutmentioning

confidence: 99%

“…In this context, it has been shown that ANXA1 effectively interrupts the activation of the NF-κB signalling pathway, which is an important transcription factor responsible for the activation of cytokines and chemokines, with a protective effect on the progression of ALI. 56 It is known that one of the pathological mechanisms of posttransplant I/R is the excessive production of ROS. It has been shown that ANXA1, by regulating iNOS (inducible nitric oxide synthase) and eNOS (endothelial nitric oxide synthase) levels, is able to inhibit oxygen stress, TNF-α expression, inflammation and apoptosis and, consequently, improve alveolar-capillary permeability.…”

Section: Gutmentioning

confidence: 99%

Protective effects of endogenous and exogenous Annexin A1 on ischemia-reperfusion-derived injuries

da Costa,

Dias,

Vieira

et al. 2023

IJMBOA

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Ischemia and reperfusion (I/R) injury permeates a variety of diseases, causing significant inflammatory and thrombotic responses. Given its importance, efforts have been made to identify the complex and integrated network of mediators that ensure a timely and spatially regulated inflammatory response, in order to mitigate its deleterious effects on the body. The Annexin A1 protein (ANXA1) and its mimetic peptide Ac2-26 can alleviate the inflammatory process by decreasing adhesion and neutrophil trafficking, inhibiting pro-inflammatory and pro-thrombotic mediators, and regulating the interactions of neutrophil-platelets. In this review, we discuss the anti-inflammatory potential of ANXA1 and its intracellular effects, contrasting the possible long-term permanence of the damage caused by I/R injuries. As a pharmacological approach, the aim is to understand how ANXA1 operates in processes resulting from I/R injuries and its performance as a biomarker and therapeutic target after injury in different tissues and organs.

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“…Knockdown of AnxA1 enhanced the oxidative stress and in ammation in cigarette smoke extract (CSE)-induced bronchial epithelial cells, a chronic obstructive pulmonary disease in vitro model (Yu and Zhang, 2022). In addition, AnxA1 peptide Ac2-26 signi cantly suppressed the activity of NADPH oxidase and malondialdehyde to decrease oxidative stress, lung injury and epithelium apoptosis in acute respiratory distress syndrome rats (Ju et al, 2023). Besides, in the kidney following ischemic injury, AnxA1 limited ROS production and increased antioxidant enzymes to abrogate oxidative stress and attenuate tubular cell death, which nally preserves the kidney against the ischemia (Suliman et al, 2021).…”

Section: Introductionmentioning

confidence: 98%

Annexin A1 conveys neuroprotective function via inhibiting oxidative stress in diffuse axonal injury of rats

Zheng,

Li,

et al. 2023

Preprint

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Purpose Diffuse axonal injury (DAI) is a critical pathological facet of traumatic brain injury (TBI). Oxidative stress plays a significant role in progress of DAI. Annexin A1 has been demonstrated benefit for recovery of neurofunctional outcomes after TBI. However, whether annexin A1 exhibits neuronal protective function through modulating oxidative stress in DAI remains unknown. Methods Expression of annexin A1 was evaluated via real time PCR and western blot analysis in rat brainstem after DAI. Neurological effect of annexin A1 following DAI through quantification of modified neurologic severity score (mNSS) was compared between wild-type and annexin A1-knockout rats. Brain edema and neuronal apoptosis, as well as expression of oxidative factors and inflammatory cytokines was analysed between wild-type and annexin A1 deficiency rats after DAI. Furthermore, mNSS, oxidative and inflammatory cytokines were assayed after timely administration of recombinant annexin A1 for DAI rats. Results In brainstem of DAI, the expression of annexin A1 remarkably increased. Ablation of annexin A1 increased mNSS score and brain water content of rats after DAI. Neuron apoptosis in brainstem after DAI was exaggerated by annexin A1 deficiency. In addition, annexin A1 deficiency significantly upregulated level of oxidative and inflammatory factors in brainstem of DAI rats. Moreover, mNSS decreased by annexin A1 treatment in rats following DAI. Expression of oxidative and inflammatory molecules in rat brainstem subjected to DAI inhibited by annexin A1 administration. Conclusions These results demonstrated that annexin A1 exhibits neuronal protective function in the progression of DAI mainly dependent on suppressing oxidative stress and inflammation.

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Annexin A1 peptide Ac2-26 mitigates ventilator-induced lung injury in acute respiratory distress syndrome rats and partly depended on the endothelial nitric oxide synthase pathway

Cited by 5 publications

References 37 publications

Ac2-26 reduced the liver injury after cardiopulmonary bypass in rats via AKT1/GSK3β/eNOS pathway

Ac2-26 reduced the liver injury after cardiopulmonary bypass in rats via AKT1/GSK3β/eNOS pathway

Protective effects of endogenous and exogenous Annexin A1 on ischemia-reperfusion-derived injuries

Annexin A1 conveys neuroprotective function via inhibiting oxidative stress in diffuse axonal injury of rats

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