Abstract 155: Identification of Decreased Plasma Lysophosphatidylcholine Using Phospholipidomics in Cardiac Arrest: A Novel Therapeutic Application

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Mitsuaki Nishikimi ◽  
Tsukasa Yagi ◽  
Ryosuke Takegawa ◽  
Shoaib Muhammad ◽  
Kei Hayashida ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Brain Function ◽  
Injury Severity ◽  
University Hospital ◽  
Control Group ◽  
Therapeutic Application ◽  
Public Health Burden ◽  
Plasma Phospholipids ◽  
Novel Therapeutic

Introduction: Cardiac arrest (CA) is a significant public health burden with few effective therapies available. Plasma phospholipids are important for proper organ function. We hypothesized that alterations in plasma phospholipids may play an important role in the pathophysiology of CA and normalizing these alterations may be a novel therapeutic application for the treatment of CA. Objective: The aim of this study was to test the phospholipid therapy as a novel therapeutic approach in CA. Methods and Results: We performed phospholipidomics on plasma samples from CA patients and controls from North Shore University Hospital to identify plasma phospholipids that correlate with injury severity. We then confirmed the finding using our rat model of 10 and 14 min of asphyxia-induced CA. Finally, we tested the effect of administering LPC using the same model. From the phospholipids analyzed, lysophosphatidylcholine (LPC) levels were found to be the most significantly decreased in CA patients, which was also associated with survival of patients. The same trend was observed in the rat model where rats after 14 min CA had significantly lower plasma LPC levels than rats after 10 min CA. We also found that LPC levels began to decrease continuously following resuscitation, but not during the ischemic phase of CA. Finally, we found that LPC administration substantially increased rat survival compared to the control group. Rats who survived in the LPC-treated group displayed significantly improved brain function and the neuroprotective effect of LPC is supported by improved brain histology. We also found LPC treatment increased plasma IL-10 levels and decreased IL-6 levels post-CA. Conclusion: Plasma LPC levels inversely correlated with survival and LPC treatment significantly improved brain function and rat survival. This data indicates that the decrease of plasma LPC is a major mechanism responsible for brain damage demonstrating the potential of LPC as a novel therapeutic in CA.

scholarly journals Plasma metabolomics supports the use of long-duration cardiac arrest rodent model to study human disease by demonstrating similar metabolic alterations

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Muhammad Shoaib ◽  
Rishabh C. Choudhary ◽  
Jaewoo Choi ◽  
Nancy Kim ◽  
Kei Hayashida ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Human Disease ◽  
Injury Severity ◽  
Tca Cycle ◽  
Suitable Model ◽  
Metabolic Dysfunction ◽  
Sprague Dawley ◽  
Metabolic Alterations ◽  
Long Duration

AbstractCardiac arrest (CA) is a leading cause of death and there is a necessity for animal models that accurately represent human injury severity. We evaluated a rat model of severe CA injury by comparing plasma metabolic alterations to human patients. Plasma was obtained from adult human control and CA patients post-resuscitation, and from male Sprague–Dawley rats at baseline and after 20 min CA followed by 30 min cardiopulmonary bypass resuscitation. An untargeted metabolomics evaluation using UPLC-QTOF-MS/MS was performed for plasma metabolome comparison. Here we show the metabolic commonality between humans and our severe injury rat model, highlighting significant metabolic dysfunction as seen by similar alterations in (1) TCA cycle metabolites, (2) tryptophan and kynurenic acid metabolites, and (3) acylcarnitine, fatty acid, and phospholipid metabolites. With substantial interspecies metabolic similarity in post-resuscitation plasma, our long duration CA rat model metabolically replicates human disease and is a suitable model for translational CA research.

scholarly journals The use of a metronome during cardiopulmonary resuscitation in the emergency room of a university hospital

2016 ◽  
Vol 24 (0) ◽  
Author(s):  
Renata Maria de Oliveira Botelho ◽  
Cássia Regina Vancini Campanharo ◽  
Maria Carolina Barbosa Teixeira Lopes ◽  
Meiry Fernanda Pinto Okuno ◽  
Aécio Flávio Teixeira de Góis ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Survival Rates ◽  
Spontaneous Circulation ◽  
University Hospital ◽  
Control Group ◽  
Case Group ◽  
Chi Square ◽  
Significant Difference ◽  
Service Data

ABSTRACT Objective: to compare the rate of return of spontaneous circulation (ROSC) and death after cardiac arrest, with and without the use of a metronome during cardiopulmonary resuscitation (CPR). Method: case-control study nested in a cohort study including 285 adults who experienced cardiac arrest and received CPR in an emergency service. Data were collected using In-hospital Utstein Style. The control group (n=60) was selected by matching patients considering their neurological condition before cardiac arrest, the immediate cause, initial arrest rhythm, whether epinephrine was used, and the duration of CPR. The case group (n=51) received conventional CPR guided by a metronome set at 110 beats/min. Chi-square and likelihood ratio were used to compare ROSC rates considering p≤0.05. Results: ROSC occurred in 57.7% of the cases, though 92.8% of these patients died in the following 24 hours. No statistically significant difference was found between groups in regard to ROSC (p=0.2017) or the occurrence of death (p=0.8112). Conclusion: the outcomes of patients after cardiac arrest with and without the use of a metronome during CPR were similar and no differences were found between groups in regard to survival rates and ROSC.

Abstract 217: Increased Oxidation of Amplex Red in Post-Cardiac Arrest Human and Rat Plasma Can Be Utilized as a Potential Marker of Injury Severity

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Muhammad Shoaib ◽  
Ann Iverson ◽  
Tai Yin ◽  
Lance B Becker ◽  
Junhwan KIM
Keyword(s):  
Hydrogen Peroxide ◽  
Cardiac Arrest ◽  
Injury Severity ◽  
Ischemia Reperfusion ◽  
University Hospital ◽  
Ros Generation ◽  
Ischemic Damage ◽  
Sprague Dawley ◽  
Amplex Red ◽  
Potential Marker

Introduction: Cardiac arrest (CA), an unexpected loss of appropriate electrical signaling in the heart, leads to a loss of blood circulation and decreased oxygen perfusion. Ischemia results in the generation of hydrogen peroxide and other reactive oxygen species (ROS), thereby causing damage to tissues. Currently, there are no available biomarkers to elucidate the severity of ischemic damage. Therefore, oxidation of the Amplex Red (AR) assay by ROS into its fluorescent product, resorufin, may be used as a marker to determine injury severity. Methods: Plasma isolated from human CA patients from North Shore University Hospital was obtained to determine ROS generation. A commercially available Amplex Red assay kit was used to measure the amount of resorufin produced after oxidation due to hydrogen peroxide, peroxynitrite, and other ROS. To verify our human findings, we arbitrarily assigned adult male Sprague-Dawley rats into three groups (control, 10 min cardiac arrest, and 20 min cardiac arrest) using our reliable asphyxia-induced cardiac arrest model. Results: Despite human variations, our data on human CA patients showed an increased amount of AR oxidation as a result of ischemia. Our 10 min CA rat experimental model verified that Amplex Red is capable of detecting hydrogen peroxide and peroxynitrite formation after ischemia. Rats with 20 mins of ischemia time also produced resorufin, confirming that ischemia induces AR oxidation. Removing horseradish peroxidase and adding catalase controls for hydrogen peroxide and peroxynitrite, which should decrease AR oxidation; however, we observed an increase in AR oxidation. Therefore, we added phenylmethyl sulfonyl acid (PMSF), an inhibitor of carboxylesterase, an enzyme also capable of oxidizing Amplex Red, which resulted in decreased AR oxidation. Conclusion: By accounting for peroxide and peroxynitrite species, the increase in Amplex Red oxidation in the plasma of cardiac arrest human patients and rats can be attributed to carboxylesterase activity. Our data corroborates the various mechanisms of AR oxidation in the setting of ischemia-reperfusion allowing the Amplex Red assay to be utilized as a potential tool for assessing the degree of ischemic damage resulting from cardiac arrest.

Cardiopulmonary resuscitation in a rat model of chronic myocardial ischemia

2006 ◽  
Vol 101 (4) ◽  
pp. 1091-1096 ◽  
Author(s):  
Xiangshao Fang ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Lei Huang ◽  
Yun-Te Chang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Artery ◽  
Cardiopulmonary Resuscitation ◽  
Myocardial Ischemia ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Chronic Myocardial Ischemia

Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.

scholarly journals Modification of T cells function after restoration of spontaneous circulation in a rat model of cardiac arrest

2019 ◽  
Author(s):  
Chunlin Xing ◽  
Yang Chen ◽  
Xuemei Zhu ◽  
Guoping Lu ◽  
Weiming Chen
Keyword(s):  
T Cells ◽  
Cardiac Arrest ◽  
Rat Model ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Sprague Dawley ◽  
Surface Molecules ◽  
Number Of Patients ◽  
Ifn Γ ◽  
Inhibitory Molecules

AbstractCardiac arrest (CA) is a prominent cause of mortality worldwide. A large number of patients after post-cardiac arrest is often associated with a phase of impaired immunity. Through an asphyxial cardiac arrest rat model, we investigate the peripheral blood T cells subsets and the expressions of surface molecules after restoration of spontaneous circulation (ROSC). Sprague-Dawley rats (weight, 300-400 g) were randomly divided into cardiac arrest (CA) group and sham-operated group. CA group rats were induced by 6 minutes of asphyxia. After successful ROSC, 24 surviving rats in two groups were randomly assigned to be sacrificed (n = 8 per subgroup) at 3, 24 and 72 h. The proportion of T cells and CD4+, CD8+ subsets as well as the expression of surface molecules (CTLA-4, PD-1, CD28) on T cells were identified by flow cytometry. The protein concentrations of cytokines (TNF-α, IL-6, IL-10, IL-4, IFN-γ, IL-17A) in serum were measured by ELISA. Compared with sham-operated control group, CD3+ lymphocytes in CA group were significantly decreased at 24 and 72 h post-ROSC. The expression levels of CD28, PD-1, and CTLA-4 on T cells were markedly increased in CA groups at 24 h post-ROSC. Additionally, the concentrations of IFN-γ were significantly declined, while IL-4 was markedly elevated in the CA group at 24 and 72 h post-ROSC. T cells function is moderately changed after CA, which is associated with decreased percentage of T cells, the upregulation of co-inhibitory molecules, and the shift from T helper (Th) 1 to Th2.

Abstract 11029: Netrin-1 Alleviates Post-Resuscitation Myocardial Dysfunction in a Rat Model of Cardiac Arrest

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Lu Yin ◽  
Shen Zhao ◽  
JoongBum Moon ◽  
Peng Sun ◽  
Jiangang Wang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Saline Group ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Group 2

Introduction: Post-resuscitation myocardial dysfunction has been recognized as one of the major causes of fatal outcomes after initial successful cardiopulmonary resuscitation (CPR). Previous research demonstrated that Netrin-1 improved post ischemic injury cardiac function via preservation of mitochondrial integrity. In the present study, we investigated the role of netrin-1 after cardiac arrest. Hypothesis: We hypothesized that the netrin-1 alleviated post-resuscitation myocardial dysfunction in a rat model of cardiac arrest. Methods: A total of sixteen male Sprague-Dawley rats (450-550 g) were randomized to two groups as follows: (1) Control group (C group); (2) Netrin-1 group (N group). Ventricular fibrillation was induced and untreated for 8 mins followed by 8 mins of CPR. Netrin-1 or saline were given at the onset of precordial compression. Ejection fraction (EF) was measured by echocardiography at baseline, 1,2,3 and 4 hours after ROSC. Results: Eight rats were resuscitated in the netrin-1 group and 7 rats were resuscitated in the saline group. In both groups, EF decreased after resuscitation when compared to the baseline (#p < 0.05). In the netrin-1 group, EF decreased from ( 68.1±3.4)% at baseline to (51.1±5.0)% at 1 hour post-resuscitation. In the saline group, EF decreased from (67.7±2.1)% at baseline to (44.5±5.3)% at 1 hr post-resuscitation. EF was better in the netrin-1 group than in the saline group at 2, 3 and 4 hours post-resuscitation (*p < 0.05) ( Figure 1). Conclusion: Netrin-1 alleviates post-resuscitation myocardial dysfunction in a rat model of cardiac arrest.

scholarly journals Post‐Cardiac Arrest Hydrocortisone Use Ameliorates Cardiac Mitochondrial Injury in a Male Rat Model of Ventricular Fibrillation Cardiac Arrest

2021 ◽  
Author(s):  
Min‐Shan Tsai ◽  
Chien‐Hua Huang ◽  
Chen‐Hsu Wang ◽  
Hsaio‐Ju Cheng ◽  
Shih‐Ni Wu ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Rat Model ◽  
Low Dose ◽  
Myocardial Damage ◽  
Male Rat ◽  
Control Group ◽  
High Dose ◽  
Mitochondrial Injury ◽  
Treatment Groups

Background Steroid use after cardiac arrest has been reported to improve survival and neurological outcome in cardiac arrest survivors. The study aimed to evaluate the effect of post‐arrest hydrocortisone use on myocardial damage and cardiac mitochondrial injury in a rat model of ventricular fibrillation cardiac arrest. Methods and Results Ventricular fibrillation cardiac arrest was induced and left untreated for 5 minutes in adult male Wistar rats. Cardiopulmonary resuscitation and electric shocks were then applied to achieve return of spontaneous circulation (ROSC). Successfully resuscitated animals were randomized into 3 groups: control, low‐dose hydrocortisone (2 mg/kg), and high‐dose hydrocortisone (8 mg/kg). The low‐dose hydrocortisone and high‐dose hydrocortisone (treatment) groups received intravenous hydrocortisone immediately after ROSC and the control group received saline as placebo. Each group consisted of 15 animals. Within 4 hours of ROSC, both treatment groups showed a higher cardiac output than the control group. At the fourth hour following ROSC, histological examination and transmission electron microscopy demonstrated less myocardial damage and mitochondrial injury in the animals treated with hydrocortisone. In the treatment groups, hydrocortisone mitigated the acceleration of Ca 2+ ‐induced mitochondrial swelling and suppression of complex activity observed in the control group. At the 72nd hour after ROSC, a significantly higher proportion of animals treated with hydrocortisone survived and had good neurological recovery compared with those given a placebo. Conclusions Hydrocortisone use after cardiac arrest may mitigate myocardial injury and cardiac mitochondrial damage and thus improve survival, neurological and histological outcomes in a rat model of ventricular fibrillation cardiac arrest.

Abstract 122: The Role of Plasma Lysophosphatidylcholine in Patients With Out-of-Hospital Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Tsukasa Yagi ◽  
Tai Yin ◽  
Koichiro Shinozaki ◽  
Lance B Becker ◽  
Junhwan Kim
Keyword(s):  
Fatty Acids ◽  
Cardiac Arrest ◽  
Brain Damage ◽  
Brain Function ◽  
Saturated Fatty Acids ◽  
Acyl Chain ◽  
University Hospital ◽  
Proper Function ◽  
The Brain ◽  
Hospital Cardiac Arrest

Background: Phosphatidylcholine (PC) is the most abundant class of phospholipid found in plasma. Lysophosphatidylcholine (LPC), PC missing one acyl chain, is believed to be the main carrier of polyunsaturated fatty acids (PUFAs) to the brain. The continuous supply of PUFAs, such as eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA), are important to maintain proper function of the brain. Therefore, alterations in the plasma levels of LPC containing these fatty acids, LPC-EPA, LPC-DHA, and LPC-AA, indicate impaired delivery of fatty acids, which in turn may indicate abnormal brain function. Numerous animal studies have found altered LPC compositions in Alzheimer’s disease, cognitive impairment, brain ischemia, and aging. Moreover, administration of LPC has been shown to improve brain function in these pathological conditions. Since brain damage is the main cause of death in cardiac arrest, altered LPC profiles may be indicative of brain damage and also play a role in the recovery of brain function. The aim of this study was to measure the content of plasma LPC species in out-of-hospital cardiac arrest (OHCA) patients compared to healthy controls. Methods: Blood samples were obtained from 11 OHCA patients, who were admitted to Northshore University Hospital and achieved return of spontaneous circulation. Within 4 h of drawing, plasma was separated from the whole blood using centrifugation and stored at -80°C. Control samples were obtained from 19 healthy volunteers. The contents of LPC species were measured using LC-mass spectrometry. Results: We found the overall content of LPC is significantly lower in OHCA patients. The decrease is found in all species of LPC, including LPC-EPA (patients vs Controls = 0.17 vs 0.55 μmol/L, p=0.003), LPC-DHA (patients vs Controls = 0.47 vs 1.72 μmol/L, p=0.003), and LPC-AA (patients vs Controls = 1.98 vs 5.39 μmol/L, p<0.001). We also found decreased in LPC species containing saturated fatty acids, showing the decrease was not specific to PUFAs. Conclusion: We found OHCA patients have a significantly lower plasma LPC content. Understanding the detailed mechanism for this decrease and the role that LPC plays in the recovery of patients after OHCA requires more investigation.

Abstract 83: Effect of Therapeutic Hypothermia on Oxygenation Index in Rat Model of Cardiac Arrest

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Haifang Yu ◽  
Lu Yin ◽  
Ping Gong ◽  
Jiangang Wang ◽  
Zhengfei Yang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Pulmonary Function ◽  
Therapeutic Hypothermia ◽  
Rat Model ◽  
Mild Hypothermia ◽  
Oxygenation Index ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Sprague Dawley ◽  
Successful Resuscitation

Introduction: Therapeutic hypothermia improves the outcomes of cerebral function after resuscitation from cardiac arrest (CA). The effect of therapeutic hypothermia on post resuscitation pulmonary function, however, is less known. In the present study, we investigated the effect of therapeutic hypothermia on oxygenation index, a sensitive index of pulmonary function,in a rat model of cardiac arrest and resuscitation. Hypothesis: We hypothesize that during therapeutic mild hypothermia in a rat model of cardiac arrest, the pulmonary function following resuscitation is less impaired when compare to normothermia. Methods: Twenty-one male Sprague-Dawley rats were randomized into three groups: 1) control group (control, n=5): the normothermic rats only received anesthesia and the surgical procedure as the other groups without ventricular fibrillation (VF); 2) normothermia group (NT, n=7): the normothermic rats were subjected to induced VF for 8 mins followed by 8 mins of cardiopulmonary resuscitation (CPR); 3) Mild hypothermia group (HT, n=9): the rats were subjected to induced VF for 8 mins followed by 8 mins of CPR. Mild hypothermia of 33±0.5°C was started 5 mins after return of spontaneous circulation (ROSC) and maintained for 8 hrs. The oxygenation indexes were measured at baseline, 2, 4 or 8 hours after ROSC with a conventional blood gas analyzer (PHOX plus L; Nova Biomedical Corporation, Waltham, MA, USA). Results: Compared to the control group, the oxygenation indexes of both the NT and HT groups were significantly decreased at 2 hrs after ROSC. However, more significant reduction in oxygenation index was observed in the NT group (Figure). Conclusions: There is an early pulmonary dysfunction after successful resuscitation from cardiac arrest. Hypothermia reduces the impairment of pulmonary function.

Abstract 329: N-acetylcyteine Alleviate Inflammasome-Induced Myocardial Pyroptosis After Successful Resuscitation in a Rat Model of Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Fenglian He
Keyword(s):  
Cardiac Arrest ◽  
Western Blotting ◽  
Rat Model ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Control Group ◽  
Successful Resuscitation ◽  
Caspase 1

Introduction: Previous studies have demonstrated that pyroptosis is involved in myocardial ischemia/reperfusion injury (MIRI). In addition, N-acetylcyteine (NAC) can attenuate inflammasome-induced pyroptosis during regional MIRI. In the present study, we investigated whether pyroptosis participate in global MIRI after successful resuscitation, and if it does, whether NAC can reduce inflammasome-induced pyroptosis in a rat model of cardiac arrest and resuscitation. Hypothesis: N-acetylcyteine reduces inflammasome-induced myocardial pyroptosis after successful resuscitation in a rat model of cardiac arrest. Methods: Fifteen male rats weighing 450g-550g were randomized into three groups: sham group, control group and NAC group (150 mg/kg). Ventricular fibrillation (VF) was electrically induced and untreated for 8 min. After VF, CPR was initiated for 8 mins and then defibrillation was attempted. Animals in sham group only were underwent the same operation but without inducing CA. The expressions of Nod-like receptor protein3 (NLRP3), adaptor apoptosis-associated speck-like protein (ASC), caspase-1 and gasdermin D (GSDMD) proteins were detected by western blotting at 6h following successful resuscitation. Results: All animals were resuscitated. Significantly higher levels expressions of GSDMD, NLRP3, ASC and caspase-1 were observed in control group and NAC group when compared with sham group. However, the expressions in GSDMD, NLRP3, ASC and caspase-1 were downregulated in NAC group in comparison with the control group. (Figure) Conclusion: N-acetylcyteine attenuate inflammasome-induced myocardial pyroptosis after successful resuscitation in a rat model of cardiac arrest. Figure Expressions of GSDMD, NLRP3, ASC and caspase-1 proteins, and effect of NAC on cardiac pyroptosis after successful resuscitation in a rat model of CA. (A) Representative western blotting images of GSDMD, NLRP3, ASC and caspase1 proteins in the hearts at 6h after successfully resuscitated (B) Quantitative protein analysis of GSDMD, NLRP3, ASC and caspase1 expression in three groups. The columns represent means ± SEM of three independent experiments. * p < .05

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