Protective effect of GSK-3β/Nrf2 mediated by dimethyl fumarate in middle cerebral artery embolization reperfusion rat model

2021 ◽  
Vol 18 ◽  
Author(s):  
Yuan Li ◽  
Lan Chu ◽  
Chunfeng Liu ◽  
Zongyi Zha ◽  
Yuanlu Shu
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Sham Group ◽  
Infarct Volume ◽  
Dimethyl Fumarate ◽  
Control Group ◽  
Related Factor ◽  
Nissl Staining ◽  
Gsk 3Β ◽  
Nrf2 Expression

Aim: This study investigated the protective effect of dimethyl fumarate (DMF) in rats by mediating GSK3-β/Nrf2 using the middle cerebral artery embolization reperfusion (MCAO/R) rat model. Background: After an acute ischemic stroke (AIS), oxidative stress occurs. Dimethyl fumarate (DMF), a nuclear factor-E2-related factor 2 (Nrf2) activator, approved by the US Food and Drug Administration (FDA), was observed to regulate the Nrf2 pathway by acting as an anti-oxidative stress agent; however, whether this agent is involved in inhibiting GSK-3β remains to be established. Methods: DMF model was used to explore the effects of GSK-3β on Nrf2 expression level, Nrf2-ARE binding activity and Nrf2/ARE downstream expression level of anti-oxidant stress protein in Cerebral ischemia-reperfusion injury (CIRI). 60 rats were randomly divided into Sham group, MCAO/R group, solvent control group (DMSO group) and DMF treatment group, with 15 rats in each group. The MCAO/R, DMSO and DMF groups were considered in the MCAO/R model using the modified thread embolization method. In contrast, the Sham group was only anaesthetized and disinfected, and tissue muscle was dissected without inserting suture emboli. DMF group was gavaged with 45mg/kg per day of DMF, DMSO control group was gavaged with DMSO of equal volume, while MCAO/R group was only modeled without any intragastric treatment. The rats were treated seven days after the operation, and a neurological function Longa score was estimated. The rats were sacrificed seven days later, and the infarct volume was assessed by TTC staining. Hematoxylin-eosin (HE) staining was used to observe the pathological changes in rat brain tissue. Nissl staining was used to observe the expression of neurons in the infarcted cortex. Western blotting (WB) was used to observe the protein expression levels of glycogen synthase kinase 3β(GSK-3β), nuclear factor E2-related factor 2 (Nrf2), downstream heme oxygenase 1 (HO1) and NADPH quinone oxidoreductase 1 (NQO1) in four groups. The expression levels of GSK-3β and Nrf2 in the four groups were observed by immunohistochemistry and immunofluorescence. Results: (1) The Longa score of the MCAO/R, DMSO and DMF groups was found to be higher compared to the Sham group, indicating successful operation. The Longa score of the DMF group was lower than that of the other three groups 4-7 days after surgery (P<0.05). (2) HE and Nissl staining showed that the DMF group had lower neuron necrosis and higher gliosis compared to the control groups. (3) TTC staining results showed that the infarct volume of the DMF group was significantly smaller than the MCAO/R and DMSO groups. (4) Protein results showed that the GSK-3β expression in the DMF group was lower than that in all groups, while the expression of Nrf2, HO1 and NQO1 was higher compared to other groups. Conclusion: DMF can reduce neurological deficits and infarct size in the MCAO/R model. The protective effect may be related to decreased GSK-3β expression and increased Nrf2 expression, which may play a role in anti-oxidative stress.

Neuroprotective effect of dimethyl fumarate in stroke: The role of nuclear factor erythroid 2-related factor 2

2019 ◽  
Author(s):  
Anahid Safari ◽  
Hamzeh Badeli-Sarkala2 ◽  
Mohammad Reza Namavar ◽  
Elias Kargar-Abarghouei ◽  
Neda Anssari ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Infarct Volume ◽  
Dimethyl Fumarate ◽  
Treated Group ◽  
Vehicle Group ◽  
Related Factor ◽  
Nuclear Factor ◽  
Neuroprotective Effects ◽  
Total Brain ◽  
Nrf2 Expression

Background: There is evidence that supports the neuroprotective effects of dimethyl fumarate (DMF) in stroke. Nuclear factor erythroid 2-related factor 2 (Nrf2) has both anti-oxidant and anti-inflammatory mechanisms. We investigated the neuroprotective effects of DMF via Nrf2 activation in the cortex, striatum, and diencephalon in a middle cerebral artery occlusion (MCAO) model of stroke. Methods: 22 Sprague-Dawley male rats were randomized into 3 groups. In DMF-treated group (n = 8), rats received 15 mg/kg oral DMF twice daily by gavage from day 0 to 14 after a 60-minute MCAO. The vehicle group (n = 7) underwent MCAO and were given methocel/H2O, using the same method and schedule. In the sham group (n = 7), neck was opened, but neither middle cerebral artery (MCA) was occluded nor any drug was administered. After 14 days, the animals were sacrificed. The infarct volume were assessed by stereology method. Nrf2 expression was evaluated in the cortex, striatum, and diencephalon by immunohistochemistry method. Results: Ratio of infarct to total brain volume was significantly lower in the DMF-treated group (5.76%) in comparison with the vehicle group (22.39%) (P < 0.0001). Nrf2 expression was higher in DMFtreated group in comparison with both the vehicle and sham groups in cortex, striatum, diencephalon, and total brain (P < 0.0001). In the DMF-treated group, significant negative correlation between Nrf2 expression and infarct volume was observed in cortex, striatum, diencephalon, and total brain. Conclusion: DMF induces Nrf2 expression and its neuroprotective effects in different brain anatomical regions.  

scholarly journals Nestin is essential for cellular redox homeostasis and gastric cancer metastasis through the mediation of the Keap1–Nrf2 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Lv ◽  
Meiqiang Xie ◽  
Shufen Zhao ◽  
Wensheng Qiu ◽  
Shasha Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Cancer ◽  
Antioxidant Enzyme ◽  
Cell Lines ◽  
Cancer Metastasis ◽  
Redox Homeostasis ◽  
Migration And Invasion ◽  
Control Group ◽  
Related Factor ◽  
Nrf2 Expression

Abstract Background Gastric cancer (GC) is a common malignancy of the digestive system. Antioxidant activity is regarded as a possible mechanism in ectopic cancer. Hence, oxidative stress regulation is being evaluated for cancer treatment. Previous research has demonstrated that Nestin is associated with antioxidative resistance via its modulation of the Kelch-like ECH-associated protein 1 (Keap1)–nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Methods We determined the role of Nestin-mediated redox homeostasis and tumor phenotypes in GC cells. Results We found that the Nestin expression level was high in GC tissues and cell lines. Nestin knockdown in the GC cell lines SGC-7901 and MKN-45 reduced viability, induced apoptosis, decreased antioxidant enzyme generation, and repressed GC metastasis. Nestin binds to Keap1, resulting in Nrf2 degradation and influencing downstream gene expression. Nestin knockdown resulted in the downregulation of Nrf2 expression in GC cells. The restoration of Nrf2 expression or treatment with the Nrf2 activator sulforaphane counteracted the inhibitory effect of Nestin knockdown on the proliferation, migration, invasion, and antioxidant enzyme production in GC cells. Moreover, xenograft GC tumors exhibited a slower growth rate than those of the control group in vivo. Conclusions Taken together, these findings suggest that the Nestin–Keap1–Nrf2 axis confers oxidative stress resistance and plays an important role in the proliferation, migration, and invasion of GC cells.

scholarly journals Protective Effect of Low Molecular Weight Seleno-Aminopolysaccharide on the Intestinal Mucosal Oxidative Damage

Marine Drugs ◽  
2019 ◽  
Vol 17 (1) ◽  
pp. 64 ◽  
Author(s):  
Zheng-Shun Wen ◽  
Zhen Tang ◽  
Li Ma ◽  
Tian-Long Zhu ◽  
You-Ming Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Weight ◽  
Protective Effect ◽  
Antioxidant Capacity ◽  
Control Group ◽  
Low Molecular Weight ◽  
Related Factor ◽  
Intestinal Damage ◽  
Nrf2 Signaling Pathway ◽  
Weaning Piglets

Low molecular weight seleno-aminopolysaccharide (LSA) is an organic selenium compound comprising selenium and low molecular weight aminopolysaccharide (LA), a low molecular weight natural linear polysaccharide derived from chitosan. LSA has been found to exert strong pharmacological activity. In this study, we aimed to investigate the protective effect of LSA on intestinal mucosal oxidative stress in a weaning piglet model by detecting the growth performance, intestinal mucosal structure, antioxidant indices, and expression level of intracellular transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and its related factors. Our results indicated that LSA significantly increased the average daily gain and feed/gain (p < 0.05), suggesting that LSA can effectively promote the growth of weaning piglets. The results of scanning electron microscope (SEM) microscopy showed that LSA effectively reduced intestinal damage, indicating that LSA improved the intestinal stress response and protected the intestinal structure integrity. In addition, diamine oxidase (DAO) and d-lactic acid (d-LA) levels remarkably decreased in LSA group compared with control group (p < 0.05), suggesting that LSA alleviated the damage and permeability of weaning piglets. LSA significantly increased superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC) levels, but decreased malondialdehyde (MDA) level, indicating that LSA significantly enhanced the antioxidant capacity and reduced oxidative stress in weaning piglets. RT-PCR results showed that LSA significantly increased GSH-Px1, GSH-Px2, SOD-1, SOD-2, CAT, Nrf2, HO-1, and NQO1 gene expression (p < 0.05). Western blot analysis revealed that LSA activated the Nrf2 signaling pathway by downregulating the expression of Keap1 and upregulating the expression of Nrf2 to protect intestinal mucosa against oxidative stress. Collectively, LSA reduced intestinal mucosal damage induced by oxidative stress via Nrf2-Keap1 pathway in weaning stress of infants.

Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Protective Effect ◽  
Infarct Size ◽  
Rat Model ◽  
Left Ventricular ◽  
Related Factor ◽  
Nuclear Factor ◽  
Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

scholarly journals Upregulation of Nrf2 expression by human cytomegalovirus infection protects host cells from oxidative stress

2013 ◽  
Vol 94 (7) ◽  
pp. 1658-1668 ◽  
Author(s):  
Junsub Lee ◽  
Kyungmi Koh ◽  
Young-Eui Kim ◽  
Jin-Hyun Ahn ◽  
Sunyoung Kim
Keyword(s):  
Oxidative Stress ◽  
Human Cytomegalovirus ◽  
Survival Rates ◽  
Buthionine Sulfoximine ◽  
Host Cells ◽  
Related Factor ◽  
Downstream Target ◽  
Human Foreskin Fibroblasts ◽  
Cellular Defence ◽  
Nrf2 Expression

NF-E2 related factor 2 (Nrf2) is a transcription factor that plays a key role(s) in cellular defence against oxidative stress. In this study, we showed that the expression of Nrf2 was upregulated in primary human foreskin fibroblasts (HFFs), following human cytomegalovirus (HCMV/HHV-5) infection. The expression of haem oxygenase-1, a downstream target of Nrf2, was also increased by HCMV infection, and this induction was suppressed in HFFs expressing a small hairpin RNA (shRNA) against Nrf2. The HCMV-mediated increase in Nrf2 expression was abolished when UV-irradiated virus was used or when the activity of casein kinase 2 was inhibited. Host cells infected by HCMV had higher survival rates following oxidative stress induced by buthionine sulfoximine compared with uninfected control cells, but this cell-protective effect was abolished by the use of Nrf2 shRNA. Our results suggest that HCMV-mediated activation of Nrf2 might be beneficial to the virus by increasing the host cell’s ability to cope with oxidative stress resulting from viral infection and/or inflammation.

scholarly journals Protective Effect of Decursin Extracted fromAngelica gigasin Male Infertility via Nrf2/HO-1 Signaling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Woong Jin Bae ◽  
U. Syn Ha ◽  
Jin Bong Choi ◽  
Kang Sup Kim ◽  
Su Jin Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Semen Quality ◽  
Antioxidant Activities ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Testicular Weight ◽  
Unilateral Cryptorchidism

Higher testicular temperature results in altered spermatogenesis due to heat-related oxidative stress. We examined the effects of decursin extracted fromAngelica gigasNakai on antioxidant activityin vitroand in a cryptorchidism-induced infertility rat model. TM3 Leydig cell viability was measured based on oxidative stress according to treatment. Either distilled water or AG 400 mg/kg ofA. gigasextract was administered orally for 4 weeks after unilateral cryptorchidism was induced. After 1, 2, and 4 weeks, six rats from the control group and six rats from treatment group were sacrificed. Testicular weight, semen quality, antioxidant activities, nuclear factor erythroid 2-related factor 2 (Nrf2) protein, and mRNA expression of Nrf2-regulated genes were analyzed. Treatment withA. gigasextract (1) protected TM3 cells against oxidative stress in a dose-dependent manner, (2) improved the mean weight of the cryptorchid testis, (3) maintained sperm counts, motility, and spermatogenic cell density, (4) decreased levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) and increased levels of superoxide dismutase (SOD), (5) significantly increased Nrf2 and heme oxygenase-1 (HO-1), and (6) significantly decreased apoptosis. This study suggests that decursin extracted fromA. gigasis a supplemental agent that can reduce oxidative stress by Nrf2-mediated upregulation of HO-1 in rat experimentally induced unilateral cryptorchidism and may improve cryptorchidism-induced infertility.

scholarly journals Protective Effect of Melatonin Against Radiotherapy-Induced Small Intestinal Oxidative Stress: Biochemical Evaluation

Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 308 ◽  
Author(s):  
Ahmed Eleojo Musa ◽  
Dheyauldeen Shabeeb ◽  
Haider Saadoon Qasim Alhilfi
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Radical Scavenging ◽  
Common Side Effect ◽  
Control Group ◽  
Intestinal Damage ◽  
Pelvic Malignancies ◽  
Group I ◽  
Male Wistar Rats ◽  
Small Intestinal

Background and Objectives: Radiation enteritis is a common side effect after radiotherapy for abdominal and pelvic malignancies. The aim of the present study was to investigate the protective effect of melatonin, known for its free radical scavenging ability, against radiotherapy-induced small intestinal oxidative damage. Materials and Methods: Thirty male Wistar rats were randomly assigned to six groups (5 rats in each) as follows: Group I (control group) rats received neither radiation nor melatonin; group II rats received only 8 Gy single dose of gamma radiation to their abdomen and pelvis regions; group III (administered with only 50 mg/kg melatonin); group IV (administered with only 100 mg/kg melatonin); group V (50 mg/kg melatonin + 8 Gy radiation), group VI (100 mg/kg melatonin + 8 Gy radiation). All rats were sacrificed after 5 days for biochemical assessments of their intestinal tissues. Results: Treatment with melatonin post irradiation significantly reduced malondialdehyde (MDA) levels as well as increased both superoxide dismutase (SOD) and catalase (CAT) activities of the irradiated intestinal tissues. In addition, melatonin administration with different doses pre irradiation led to protection of the tissues. Moreover, the 100 mg/kg dose was more effective compared to 50 mg/kg. Conclusions: The results of our study suggest that melatonin has a potent protective effect against radiotherapy-induced intestinal damage, by decreasing oxidative stress and increasing antioxidant enzymes. We recommend future clinical trials for more insights.

scholarly journals The Protective Effect of Hispidin against Hydrogen Peroxide-Induced Oxidative Stress in ARPE-19 Cells via Nrf2 Signaling Pathway

Biomolecules ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 380 ◽  
Author(s):  
Huang ◽  
Chang ◽  
Chau ◽  
Chiu
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Retinal Pigment ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Glutamate Cysteine Ligase ◽  
Jnk Pathway ◽  
Nrf2 Signaling Pathway

Hispidin, a polyphenol compound isolated from Phellinus linteus, has been reported to possess antioxidant activities. In this study, we aimed to investigate the mechanisms underlying the protective effect of hispidin against hydrogen peroxide (H2O2)-induced oxidative stress on Adult Retinal Pigment Epithelial cell line-19 (ARPE-19) cells. Hispidin was not cytotoxic to ARPE-19 cells at concentrations of less than 50 μM. The levels of intracellular reactive oxygen species (ROS) were analyzed by dichlorofluorescin diacetate (DCFDA) staining. Hispidin significantly restored H2O2-induced cell death and reduced the levels of intracellular ROS. The expression levels of antioxidant enzymes, such as NAD(P)H:Quinine oxidoreductase-1 (NQO-1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and glutamate-cysteine ligase modifier subunit (GCLM) were examined using real-time PCR and Western blotting. Our results showed that hispidin markedly enhanced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), HO-1, NQO-1, GCLM, and GCLC in a dose-dependent manner. Furthermore, knockdown experiments revealed that transfection with Nrf2 siRNA successfully suppresses the hispidin activated Nrf2 signaling in ARPE-19 cells. Moreover, activation of the c-Jun N-terminal kinase (JNK) pathway is involved in mediating the protective effects of hispidin on the ARPE-19 cells. Thus, the present study demonstrated that hispidin provides protection against H2O2-induced damage in ARPE-19 cells via activation of Nrf2 signaling and up-regulation of its downstream targets, including Phase II enzymes, which might be associated with the activation of the JNK pathway.

scholarly journals Protective effect of chlorogenic acid on renal ischemia/reperfusion injury in rats

2020 ◽  
Vol 92 (2) ◽  
Author(s):  
Tuncay Toprak ◽  
Cagri Akin Sekerci ◽  
Hasan Riza Aydın ◽  
Mehmet Akif Ramazanoglu ◽  
Fatma Demet Arslan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Chlorogenic Acid ◽  
Tissue Damage ◽  
Sham Group ◽  
Ischemia Reperfusion ◽  
Statistical Significance ◽  
Histological Evaluation ◽  
Renal Histology ◽  
Biochemical Examination

Objectives: Ischemia/reperfusion (I/R) injury is a common cause of renal injury and to date, many pharmacological agents have been identified to decrease I/R injury. One of the potential compound that can target I/R injury is chlorogenic acid (CGA). It has potent antiinflammatory, antibacterial, anti-oxidant, analgesic and antipyretic activities in in vitro experiments and in vivo animal models. The aim of the study was to investigate the protective characteristic of CGA on renal I/R injury. Material and Methods: 24 rats were randomly allocated to three groups (n = 8): Sham, I/R+CGA and I/R groups. CGA was administered intraperitoneally at a dose of 20 mg/kg, 10 min before reperfusion. I/R injury was achieved by clamping the left renal artery for 45 minutes, followed by reperfusion for 4 hours. The left kidneys of the rats were examined for tissue damage by histopathological and biochemical examination. For histological evaluation, EGTI scoring system was used. For biochemical examination total oxidant status, total antioxidant status and oxidative stress index were used. The power analysis indicated that 8 subjects per group would be required to produce 80% chance of achieving statistical significance at p < 0.05 level. The results are expressed as mean ± SD. Mann- Whitney U was performed for statistical analysis. Results: Histopathological examination of the tissue damage revealed that all kidneys in the sham group were normal. I-R group had significantly higher histopathological scores than other groups. Histopathological improvement was seen after CGA treatment. TAS, TOS and OSI values of I-R group were significantly higher than sham group (0.88 vs 0.76 (p: 0.004), 13.8 vs 7.04 (p: 0.021) and 0.15 vs 0.09 (p: 0.034), respectively). In CGA treated group TAS, TOS and OSI levels were 0.84, 6.47 and 0.07, respectively. CGA treatment resulted in significant improvement in TOS and OSI parameters. Conclusions: CGA treatment provided marked improvement in renal histology and suppressed oxidative stress. Thus, CGA may have a protective effect in renal tissue against I/R injury.

scholarly journals Protective effect of apricot (Prunus armeniacaL.) on hepatic steatosis and damage induced by carbon tetrachloride in Wistar rats

2009 ◽  
Vol 102 (12) ◽  
pp. 1767-1775 ◽  
Author(s):  
Feral Ozturk ◽  
Mehmet Gul ◽  
Burhan Ates ◽  
I. Cetin Ozturk ◽  
Asli Cetin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Hepatic Steatosis ◽  
Wistar Rats ◽  
Liver Steatosis ◽  
Radical Scavenging ◽  
Hepatic Necrosis ◽  
Control Group ◽  
Cytoplasmic Matrix

The present study was planned to investigate the protective effect of 10 % and 20 % apricot-containing feed on carbon tetrachloride (CCl4)-induced hepatic steatosis and damage. Adult male Wistar rats (n42) were divided into six groups of seven each, as follows: control group; CCl4group; CCl4+10 % apricot group; CCl4+20 % apricot group; 10 % apricot group; 20 % apricot group. All apricot groups were fed with 10 % or 20 % apricot-containing feed for 5 months. CCl4injections were applied to the CCl4groups at the dose of 1 mg/kg for 3 d at the end of 5 months. In the CCl4group, vacuolated hepatocytes and hepatic necrosis were seen, especially in the centrilobular area. Hepatocytes showed an oedematous cytoplasmic matrix, large lipid globules and degenerated organelles. The area of liver injury was found significantly decreased with apricot feeding. Malondialdehyde and total glutathione levels and catalase, superoxide dismutase and glutathione peroxidase activities were significantly changed in the CCl4group and indicated increased oxidative stress. Apricot feeding decreased this oxidative stress and ameliorated histological damage. We concluded that apricot feeding had beneficial effects on CCl4-induced liver steatosis and damage probably due to its antioxidant nutrient (β-carotene and vitamin) contents and high radical-scavenging capacity. Dietary intake of apricot can reduce the risk of liver steatosis and damage caused by free radicals.

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