scholarly journals Sulforaphane Attenuates Isoproterenol-Induced Myocardial Injury in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Lijuan Song ◽  
Mudduluri Srilakshmi ◽  
Yi Wu ◽  
T. S. Mohamed Saleem
Keyword(s):  
Oxidative Stress ◽  
Myocardial Injury ◽  
Antioxidant Properties ◽  
Weight Ratio ◽  
Heart Weight ◽  
Thiobarbituric Acid Reactive Substance ◽  
Mitochondrial Atpase ◽  
Mitochondrial Enzymes ◽  
Cardiac Markers ◽  
Endogenous Antioxidant

The development of isoproterenol- (ISO-) induced oxidative stress in the myocardium results in myocardial necrosis. Sulforaphane (SFN-0.4% of sulforaphane from standardized broccoli sprout extract) possesses chemoprotective, antidiabetic, and antibacterial activities and is also active against cardiovascular-related problems due to its antioxidant properties. This study was designed to investigate the cardioprotective effect of SFN against isoproterenol-induced myocardial injury in mice. Healthy male Swiss albino mice weighing 20–30 g were used in this study. These mice were randomly divided into five groups ( n = 6 ). All the mice in the experimental groups received isoproterenol (5 mg/kg bw, via i.p.) consecutively for 2 days. The mice were treated with SFN (4 mg/kg bw) and α-tocopherol (TCF) (10 mg/kg bw) by oral gavage for 1-7 days as pre- and posttreatment for the prophylactic and treatment groups, respectively. On day 10, the following parameters were studied: heart weight to body weight ratio, antioxidant parameters, and cardiac markers; and mitochondrial enzymes were estimated for cardioprotection. Administration of isoproterenol in mice showed an increased level of serum cardiac markers and heart mitochondrial ATPase enzymes. An increased level of myocardial thiobarbituric acid-reactive substance and decreased levels of endogenous antioxidant enzymes indicated that oxidative stress is induced by isoproterenol in the myocardium. The administration of SFN in mice restored the levels of all biochemical parameters to near-normal levels. Histopathological studies further confirmed the protective effect of sulforaphane. This study concluded that treatment with SFN boosts the endogenous antioxidant activity and prevents isoproterenol-induced myocardial injury.

scholarly journals Alpha-Lipoic Acid Protects Cardiomyocytes against Heat Stroke-Induced Apoptosis and Inflammatory Responses Associated with the Induction of Hsp70 and Activation of Autophagy

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Hsin-Hsueh Shen ◽  
Yu-Shiuan Tseng ◽  
Ni-Chun Kuo ◽  
Ching-Wen Kung ◽  
Sherif Amin ◽  
...  
Keyword(s):  
Lipoic Acid ◽  
Myocardial Injury ◽  
Inflammatory Responses ◽  
Heat Stroke ◽  
Heat Exposure ◽  
Antioxidant Properties ◽  
Mitochondrial Enzymes ◽  
Protective Effects ◽  
Anion Formation ◽  
Anti Inflammatory

Heat stroke (HS) is a life-threatening illness and defined as when body temperature elevates above 40°C accompanied by the systemic inflammatory response syndrome that results in multiple organ dysfunctions. α-Lipoic acid (ALA) acts as a cofactor of mitochondrial enzymes and exerts anti-inflammatory and antioxidant properties in a variety of diseases. This study investigates the beneficial effects of ALA on myocardial injury and organ damage caused by experimental HS and further explores its underlying mechanism. Male Wistar rats were exposed to 42°C until their rectal core temperature reached 42.9°C and ALA was pretreared 40 or 80 mg/kg (i.v.) 1.5 h prior to heat exposure. Results showed that HS-induced lethality and hypothermia were significantly alleviated by ALA treatment that also improved plasma levels of CRE, LDH, and CPK and myocardial injury biomarkers myoglobin and troponin. In addition, ALA reduced cardiac superoxide anion formation and protein expression of cleaved caspase 3 caused by HS. Proinflammatory cytokine TNF-α and NF-κB pathways were significantly reduced by ALA treatment which may be associated with the upregulation of Hsp70. ALA significantly increased the Atg5-12 complex and LC3B II/LC3B I ratio, whereas the p62 and p-mTOR expression was attenuated in HS rats, indicating the activation of autophagy by ALA. In conclusion, ALA ameliorated the deleterious effects of HS by exerting antioxidative and anti-inflammatory capacities. Induction of Hsp70 and activation of autophagy contribute to the protective effects of ALA in HS-induced myocardial injury.

P6284The antioxidant MitoQ protects against intestinal disturbances in the experimental autoimmune model of myocarditis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
I Gallardo ◽  
B Gutierrez ◽  
M Hernandez ◽  
I Cabero ◽  
Y Alvarez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Weight Ratio ◽  
Heart Weight ◽  
Preclinical Model ◽  
Myeloperoxidase Activity ◽  
Gut Health ◽  
Barrier Dysfunction ◽  
Autoimmune Myocarditis ◽  
Fatty Acid Binding ◽  
Experimental Autoimmune

Abstract Purpose Myocarditis and dilated cardiomyopathy represent the acute and chronic phases of an inflammatory disease of the myocardium, for which no standardized treatment is currently available in clinical practice. Myocardial fibrosis an oxidative stress are pathogenic factors associated with these processes. However, new research has found that gut health can be linked to some cardiac conditions. Thus, in this study we investigated whether intestinal disturbances are present in myocarditis, using a murine experimental autoimmune model (EAM) that mimics human myocarditis, as well as the potential beneficial effect of treatment with the mitochondrial antioxidant, MitoQ. Methods and results EAM was induced in BALB/c mice with a myocardiogenic peptide and mice were treated with MitoQ (50 mg/kg/day, i.p). On day 21 (acute phase), we assessed signs of heart injury (e.g. hypertrophy, fibrosis, oxidative stress) and parameters related to gut damage such as accumulation of reactive oxigen species (superoxide anion: O2·−), inflammation (IL-1β, IL-33, TNFα), microbial translocation (sCD14; intestinal fatty acid binding protein, I-FABP) and mucins in serum and/or intestine. MitoQ teatment significantly reduced the high heart weight/body weight ratio (HW/BW) of EAM mice, a characteristic hallmark of cardiac hyperthropy. Histological analysis of hearts showed presence of fibrosis (Sirius Red stain) and high O2·− levels (DHE stain) in EAM mice whereas these effects were not detectable in cardiac tissue from healthy or MitoQ-treated EAM mice. In addition, the enhanced O2·− ions (DHE stain) and mucin loss (Alcian Blu/PAS stain) found in colon, ileum, jejunum and duodenum sections from EAM mice were attenuated by MitoQ treatment. The systemic markers associated to intestinal barrier disruption, sCD14 and I-FABP, were found strongly increased in serum from EAM mice, and MitoQ prevents this rise. The beneficial MitoQ effects were also associated with a decrease in the pro-inflammatory cytokines TNFα, IL-33 and IL-1β, both in serum and colonic tissue of treated-EAM mice, as well as a reduction of the myeloperoxidase activity in colon, compared with untreated EAM mice. Conclusion Our data show that in addition to the heart, the intestinal tissue is also damaged in the preclinical model of experimental autoimmune myocarditis, and that MitoQ treatment could reverse this profile. Since there are systemic markers released from the intestine, therapeutic strategies targeting to prevent the intestinal oxidative stress and its associated gut barrier dysfunction, could contribute to the amelioration of the disease. Acknowledgement/Funding SAF2016-81063; CIBERCV

scholarly journals Antioxidant Roles of Heme Oxygenase, Carbon Monoxide, and Bilirubin in Cerebral Circulation during Seizures

2012 ◽  
Vol 32 (6) ◽  
pp. 1024-1034 ◽  
Author(s):  
Helena Parfenova ◽  
Charles W Leffler ◽  
Shyamali Basuroy ◽  
Jianxiong Liu ◽  
Alexander L Fedinec
Keyword(s):  
Oxidative Stress ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Vascular Dysfunction ◽  
Antioxidant Properties ◽  
Cerebrovascular Function ◽  
Cerebrovascular Dysfunction ◽  
Cobalt Protoporphyrin ◽  
Endogenous Antioxidant ◽  
The Brain

Postictal cerebrovascular dysfunction is an adverse effect of seizures in newborn piglets. The brain heme oxygenase (HO) provides protection against cerebrovascular dysfunction. We investigated the contribution of reactive oxygen species (ROS) to seizure-induced vascular damage and the mechanism of HO vasoprotection. In a bicuculline model of seizures, we addressed the hypotheses: (1) seizures increase brain ROS; (2) ROS contribute to cerebral vascular dysfunction; (3) ROS initiate a vasoprotective mechanisms by activating endogenous HO; and (4) HO products have antioxidant properties. As assessed by dihydroethidium oxidation (ox-DHE), seizures increased ROS in cerebral vessels and cortical astrocytes; ox-DHE elevation was prevented by tiron and apocynin. An HO inhibitor, tin protoporphyrin, potentiated, whereas an HO-1 inducer, cobalt protoporphyrin, blocked seizure-induced increase in DHE oxidation. Heme oxygenase products carbon monoxide (CO) (CORM-A1) and bilirubin attenuated ox-DHE elevation during seizures. Antioxidants tiron and bilirubin prevented the loss of postictal cerebrovascular dilations to bradykinin, glutamate, and sodium nitroprusside. Tiron and apocynin abrogated activation of the brain HO during seizures. Overall, these data suggest that long-term adverse cerebrovascular effects of seizures are attributed to oxidative stress. On the other hand, seizure-induced ROS are required for activation of the endogenous antioxidant HO/CO/bilirubin system that alleviates oxidative stress-induced loss of postictal cerebrovascular function in piglets.

scholarly journals Effects of Ginkgo biloba on Diseases Related to Oxidative Stress

Planta Medica ◽  
2020 ◽  
Vol 86 (06) ◽  
pp. 376-386 ◽  
Author(s):  
Gabriela Achete de Souza ◽  
Sâmylla Vaz de Marqui ◽  
Júlia Novaes Matias ◽  
Elen Landgraf Guiguer ◽  
Sandra Maria Barbalho
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Liver Damage ◽  
Ginkgo Biloba ◽  
Myocardial Injury ◽  
Low Cost ◽  
Antioxidant Properties ◽  
Positive Effects ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract Ginkgo biloba (GB) is one of the most widely used phytotherapeutic products in the world, and its extract has beneficial properties for the treatment of several pathologies, such as diabetic cardiomyopathy, neurodegenerative diseases, cataracts, hearing loss, myocardial lesion, hippocampus neuronal lesions, morphometry testicular changes, and liver damage. This review aims to investigate the effects of GB on diseases related to oxidative stress. Databases such as MEDLINE/PUBMED and EMBASE were consulted, and PRISMA guidelines were used to build the review. This plant has antioxidant properties since it regulates the expression of antioxidant enzymes positively and reduces reactive oxygen and nitrogen species, contributing to the reduction of lipid peroxidation. It also exhibits anti-inflammatory properties, inhibiting the expression of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. In animal models, the use of GB can show positive effects on brain damage, neurodegenerative diseases, myocardial injury, and renal and liver damage. In humans, the positive effects were shown in diabetes, metabolic syndrome, and ischemic colitis. These effects are due to the presence of compounds such as bilobalide, isoramnetina, quercetin, kaempferol, and ginkgolides A, B, and C. For these reasons, GB can be a low-cost alternative to the therapeutic approach of several pathologies since it acts in the prevention, treatment, and inhibition of several complications of common comorbidities.

Genistein prevents isoproterenol-induced cardiac hypertrophy in rats

2012 ◽  
Vol 90 (8) ◽  
pp. 1117-1125 ◽  
Author(s):  
Subir Kumar Maulik ◽  
Pankaj Prabhakar ◽  
Amit Kumar Dinda ◽  
Sandeep Seth
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Body Weight ◽  
Nitric Oxide Synthase ◽  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Heart Weight ◽  
Once Daily ◽  
Oxide Synthase

Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150–200 g, 10–12 weeks old) rats. Isoproterenol (5 mg·(kg body weight)–1) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg–1, subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities.

Abstract 56: Endothelial Adam17 Contributes to Angiotensin Ii-induced Abdominal Aortic Aneurysm in Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Tomonori Kobayashi ◽  
Takehiko Takayanagi ◽  
Tomoki Hashimoto ◽  
Carl P Blobel ◽  
Satoru Eguchi
Keyword(s):  
Oxidative Stress ◽  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Weight Ratio ◽  
Oxidase Inhibitor ◽  
Heart Weight ◽  
Similar Degree ◽  
Matrix Deposition ◽  
Abdominal Aortic

Enhancement of the renin angiotensin II (AngII) system has been implicated in the development of abdominal aortic aneurysm (AAA) in animal models as well as in clinical studies. However, detailed molecular mechanism(s) by which AngII promotes AAA remain uncertain. We have demonstrated the critical roles of a metalloprotease, ADAM17, in AngII signal transduction in cultured vascular cells. Endothelial AT1 receptor has been recently implicated in oxidative stress. Interestingly, others have reported that ADAM17 expression was enhanced in CaCl2-induced AAA in mice and that systemic ADAM17 silencing attenuated AAA formation. However, the cell type that is mediating the deleterious effect of ADMA17 signaling is not well understood. Here we tested our hypothesis that endothelial ADAM17 activation is required for AngII-promoted AAA formation using ADAM17flox/flox mice bred with Tie2 Cre transgenic mice. 8 week old mice were co-infused with AngII 1000 ng/kg/min (4 weeks) and beta-aminopropionitrile, a lysyl oxidase inhibitor, 150 mg/kg/day (2weeks) or control saline (4 weeks) via osmotic mini-pump, and AAA formation was evaluated by the diameters. AAA formation was attenuated in ADAM17flox/flox Tie2 Cre(+/-) mice compared with ADAM17flox/flox Tie2 Cre(-/-) mice (1.50±0.44 mm vs 3.96±0.61 mm). Cardiac hypertrophy evaluated by heart weight body weight ratio was also attenuated in the Tie2 Cre(+/-) mice (0.0063±0.0005 vs 0.0092±0.0013). However, AngII induced hypertension to a similar degree in both mice groups, as assessed by telemetries. The ADAM17 deletion was associated with less oxidative stress as assessed by anti-nitrotyrosine IHC and less extravascular fibrosis/matrix deposition. Also, the aorta was less stained with MMP2 antibody and phospho-JNK antibody. In conclusion, endothelial ADAM17 appears to be a critical metalloprotease contributing to AAA formation and cardiac remodeling but not hypertension induced by AngII. The mechanism by which endothelial ADAM17 promotes AAA seems to involve induction of oxidative stress, JNK activation and subsequent MMP2 induction.

MCI-186 (edaravone), a novel free radical scavenger, protects against acute autoimmune myocarditis in rats

2005 ◽  
Vol 289 (6) ◽  
pp. H2514-H2518 ◽  
Author(s):  
Masaomi Nimata ◽  
Taka-aki Okabe ◽  
Miki Hattori ◽  
Zuyi Yuan ◽  
Keisuke Shioji ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Hydroxyl Radicals ◽  
Radical Scavenging ◽  
Weight Ratio ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Cytotoxic Activities ◽  
Thiobarbituric Acid Reactive Substance ◽  
Autoimmune Myocarditis

In this study, we tested the hypothesis that MCI-186 (3-methyl-1-phenyl-2-pyrazolin-5-one; edaravone), a novel free radical scavenger, protects against acute experimental autoimmune myocarditis (EAM) in rats by the radical scavenging action associated with the suppression of cytotoxic myocardial injury. Recent evidence suggests that oxidative stress may play a role in myocarditis. We administered MCI-186 intraperitoneally at 1, 3, and 10 mg·kg−1·day−1 to rats with EAM for 3 wk. The results were compared with untreated rats with EAM. MCI-186 treatment did not affect hemodynamics. MCI-186 treatment (3 and 10 mg·kg−1·day−1) reduced the severity of myocarditis as assessed by comparing the heart-to-body weight ratio and pathological scores. Myocardial interleukin-1β (IL-1β)-positive cells and myocardial oxidative stress overload with DNA damage in rats with EAM given MCI-186 treatment were significantly less compared with those of the untreated rats with EAM. In addition, MCI-186 treatment decreased not only the myocardial protein carbonyl contents but also the myocardial thiobarbituric acid reactive substance products in rats with EAM. The formation of hydroxyl radicals in MCI-186-treated heart homogenates was decreased compared with untreated heart homogenates. Furthermore, cytotoxic activities of lymphocytes of rats with EAM treated with MCI-186 were significantly lower compared with those of the untreated rats with EAM. Hydroxyl radicals may be involved in the development of myocarditis. MCI-186 protects against acute EAM in rats associated with scavenging hydroxyl free radicals, resulting in the suppression of autoimmune-mediated myocardial damage associated with reduced oxidative stress state.

scholarly journals Assessing the influence of curcumin in sex-specific oxidative stress, survival and behavior in Drosophila melanogaster

2020 ◽  
Vol 223 (22) ◽  
pp. jeb223867
Author(s):  
Abigail R. Esquivel ◽  
Jenna C. Douglas ◽  
Rachel M. Loughran ◽  
Thomas E. Rezendes ◽  
Kaela R. Reed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Properties ◽  
Yellow Pigment ◽  
Specific Effects ◽  
Age Related ◽  
Stress Survival ◽  
Endogenous Antioxidant ◽  
And Behavior

ABSTRACTOxidative stress, which occurs from an imbalance of reactive oxygen and nitrogen species (RONS) and both endogenous and exogenous antioxidants, promotes aging and underlies sex-specific differences in longevity and susceptibility to age-related neurodegeneration. Recent evidence suggests that curcumin, a yellow pigment derived from turmeric and shown to exhibit antioxidant properties as a RONS scavenger, influences the regulation of genetic elements in endogenous antioxidant pathways. To investigate the role of curcumin in sex-specific in vivo responses to oxidative stress, Drosophila were reared on media supplemented with 0.25, 2.5 or 25 mmol l−1 curcuminoids (consisting of curcumin, demethoxycurcumin and bisdemethoxycurcumin) and resistance to oxidative stress and neural parameters were assessed. High levels of curcuminoids exhibited two sex-specific effects: protection from hydrogen peroxide as an oxidative stressor and alterations in turning rate in an open field. Taken together, these results suggest that the influence of curcuminoids as antioxidants probably relies on changes in gene expression and that sexual dimorphism exists in the in vivo response to curcuminoids.

scholarly journals Mesoporous Polydopamine Nanoparticles Attenuate Morphine Tolerance in Neuropathic Pain Rats by Inhibition of Oxidative Stress and Restoration of the Endogenous Antioxidant System

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 195
Author(s):  
Yaswanth Kuthati ◽  
Prabhakar Busa ◽  
Srikrishna Tummala ◽  
Vaikar Navakanth Rao ◽  
Venkata Naga Goutham Davuluri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuropathic Pain ◽  
Pain Management ◽  
Liver Enzymes ◽  
Histopathological Examination ◽  
Drug Loading ◽  
Antioxidant Properties ◽  
Ros Scavenging ◽  
Endogenous Antioxidant

Oxidative stress resulting from reactive oxygen species (ROS) is known to play a key role in numerous neurological disorders, including neuropathic pain. Morphine is one of the commonly used opioids for pain management. However, long-term administration of morphine results in morphine antinociceptive tolerance (MAT) through elevation of ROS and suppression of natural antioxidant defense mechanisms. Recently, mesoporous polydopamine (MPDA) nanoparticles (NPS) have been known to possess strong antioxidant properties. We speculated that morphine delivery through an antioxidant nanocarrier might be a reasonable strategy to alleviate MAT. MPDAs showed a high drug loading efficiency of ∼50%, which was much higher than conventional NPS. Spectral and in vitro studies suggest a superior ROS scavenging ability of NPS. Results from a rat neuropathic pain model demonstrate that MPDA-loaded morphine (MPDA@Mor) is efficient in minimizing MAT with prolonged analgesic effect and suppression of pro-inflammatory cytokines. Additionally, serum levels of liver enzymes and levels of endogenous antioxidants were measured in the liver. Treatment with free morphine resulted in elevated levels of liver enzymes and significantly lowered the activities of endogenous antioxidant enzymes in comparison with the control and MPDA@Mor-treated group. Histopathological examination of the liver revealed that MPDA@Mor can significantly reduce the hepatotoxic effects of morphine. Taken together, our current work will provide an important insight into the development of safe and effective nano-antioxidant platforms for neuropathic pain management.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

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