DL‐3‐n‐butylphthalide‐induced neuroprotection in rat models of asphyxia‐induced cardiac arrest followed by cardiopulmonary resuscitation

Yang, Song; Yu, Changxiao; Yang, Zhengfei; Cui, Hao; Wu, Yang; Liang, Zhen; Liu, Ying; Shi, Xian; Shao, Fei; Tang, Ziren

doi:10.1002/jcp.30442

Cited by 5 publications

(4 citation statements)

References 29 publications

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“…However, Pei et al and Hurt et al found TRPV1 by western blotting and by immunostaining in primary mouse and rat cardiomyocytes 6 , 34 . Furthermore, TRPV1 localization was demonstrated in murine embryonic stem cells (ESC) and in ESC-derived cardiomyocytes 35 , 36 . While the expression of TRPV1 mRNA in iPSC and unspecified human iPSC-derived cardiac cells was shown recently 37 , to our knowledge our study is the first to describe the expression and localization of the channel protein in hiPSC-CMs.…”

Section: Discussionmentioning

confidence: 99%

TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

Sattler

El‐Battrawy

Cyganek

et al. 2021

Sci Rep

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The non-selective cation channel transient receptor potential vanilloid 1 (TRPV1) is expressed throughout the cardiovascular system. Recent evidence shows a role for TRPV1 in inflammatory processes. The role of TRPV1 for myocardial inflammation has not been established yet. Human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (hiPSC-CM) from 4 healthy donors were incubated with lipopolysaccharides (LPS, 6 h), TRPV1 agonist capsaicin (CAP, 20 min) or the antagonist capsazepine (CPZ, 20 min). TRPV1 expression was studied by PCR and western blotting. TRPV1 internalization was analyzed by immunofluorescence. Interleukin-6 (IL-6) secretion and phosphorylation of JNK, p38 and ERK were determined by ELISA. TRPV1-associated ion channel current was measured by patch clamp. TRPV1-mRNA and -protein were expressed in hiPSC-CM. TRPV1 was localized in the plasma membrane. LPS significantly increased secretion of IL-6 by 2.3-fold, which was prevented by pre-incubation with CPZ. LPS induced TRPV1 internalization. Phosphorylation levels of ERK, p38 or JNK were not altered by TRPV1 stimulation or inhibition. LPS and IL-6 significantly lowered TRPV1-mediated ion channel current. TRPV1 mediates the LPS-induced inflammation in cardiomyocytes, associated with changes of cellular electrophysiology. LPS-induced inflammation results in TRPV1 internalization. Further studies have to examine the underlying pathways and the clinical relevance of these findings.

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Section: Discussionmentioning

confidence: 99%

TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

Sattler

El‐Battrawy

Cyganek

et al. 2021

Sci Rep

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“…DL-3-n-butylphthalide (NBP) is a neuroprotective agent, originally isolated from celery seeds and has been shown to possess therapeutic efficacy in ischemic brain by suppressing neuroinflammation and maintaining the BBB. In rat models of 6-minute asphyxia-induced CA, IV NBP (10 mg/kg) infusion 10 minutes after resuscitation and delivered twice a day for 3 consecutive days improved neurological function up to 72 hours after CA [ 98 ]. NBP treatment reduced neuronal damage alongside ultrastructural mitochondrial damage, reduced apoptosis through the Jun N-terminal kinases and p38 mitogen-activated protein kinases (JNK/p38) pathway, and suppressed inflammatory response through the nuclear factor kappa light chain enhancer of activated B cells (NF-κB pathway).…”

Section: Neuroprotective Approaches In Ca-induced Brain Injurymentioning

confidence: 99%

Neuroprotective Approaches for Brain Injury After Cardiac Arrest: Current Trends and Prospective Avenues

Marasini,

Jia

2024

J Stroke

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With the implementation of improved bystander cardiopulmonary resuscitation techniques and public-access defibrillation, survival after out-of-hospital cardiac arrest (OHCA) has increased significantly over the years. Nevertheless, OHCA survivors have residual anoxia/reperfusion brain damage and associated neurological impairment resulting in poor quality of life. Extracorporeal membrane oxygenation or targeted temperature management has proven effective in improving post-cardiac arrest (CA) neurological outcomes, yet considering the substantial healthcare costs and resources involved, there is an urgent need for alternative treatment strategies that are crucial to alleviate brain injury and promote recovery of neurological function after CA. In this review, we searched PubMed for the latest preclinical or clinical studies (2016–2023) utilizing gas-mediated, pharmacological, or stem cell-based neuroprotective approaches after CA. Preclinical studies utilizing various gases (nitric oxide, hydrogen, hydrogen sulfide, carbon monoxide, argon, and xenon), pharmacological agents targeting specific CA-related pathophysiology, and stem cells have shown promising results in rodent and porcine models of CA. Although inhaled gases and several pharmacological agents have entered clinical trials, most have failed to demonstrate therapeutic effects in CA patients. To date, stem cell therapies have not been reported in clinical trials for CA. A relatively small number of preclinical stem-cell studies with subtle therapeutic benefits and unelucidated mechanistic explanations warrant the need for further preclinical studies including the improvement of their therapeutic potential. The current state of the field is discussed and the exciting potential of stem-cell therapy to abate neurological dysfunction following CA is highlighted.

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“…In one ACA study in pigs, the initial rhythm converted from PEA to VF in 57% of pigs before CPR was begun ( Varvarousi et al, 2015 ). If a shockable rhythm occurs, 2–4 joules (J) could be applied for defibrillation, with 2 J most commonly used in recent rat models ( Hu et al, 2019 ; Yang et al, 2021 ). Electrical defibrillation can also have side effects, with too high defibrillation energy causing heart damage ( Ishigaki et al, 2016 ).…”

Section: Factors To Consider In Establishing An Aca Rat Modelmentioning

confidence: 99%

Rat model of asphyxia-induced cardiac arrest and resuscitation

Zhu

et al. 2023

Front. Neurosci.

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Neurologic injury after cardiopulmonary resuscitation is the main cause of the low survival rate and poor quality of life among patients who have experienced cardiac arrest. In the United States, as the American Heart Association reported, emergency medical services respond to more than 347,000 adults and more than 7,000 children with out-of-hospital cardiac arrest each year. In-hospital cardiac arrest is estimated to occur in 9.7 per 1,000 adult cardiac arrests and 2.7 pediatric events per 1,000 hospitalizations. Yet the pathophysiological mechanisms of this injury remain unclear. Experimental animal models are valuable for exploring the etiologies and mechanisms of diseases and their interventions. In this review, we summarize how to establish a standardized rat model of asphyxia-induced cardiac arrest. There are four key focal areas: (1) selection of animal species; (2) factors to consider during modeling; (3) intervention management after return of spontaneous circulation; and (4) evaluation of neurologic function. The aim was to simplify a complex animal model, toward clarifying cardiac arrest pathophysiological processes. It also aimed to help standardize model establishment, toward facilitating experiment homogenization, convenient interexperimental comparisons, and translation of experimental results to clinical application.

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DL‐3‐n‐butylphthalide‐induced neuroprotection in rat models of asphyxia‐induced cardiac arrest followed by cardiopulmonary resuscitation

Cited by 5 publications

References 29 publications

TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

Neuroprotective Approaches for Brain Injury After Cardiac Arrest: Current Trends and Prospective Avenues

Rat model of asphyxia-induced cardiac arrest and resuscitation

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