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Objective The aim of this study was to compare the efficacy of multiple antioxidant (Proxeed Plus (PP) with Carnitine, Selenium, Zinc, Coenzyme Q10, Vitamin C, Folic Acid, Vitamin B12) on local random skin flap healing with the hyperbaric oxygen (HBO) therapy. Methods Fourty rats were equally divided into five groups (Control, PP, HBO, HBO + PP, PP + HBO + PP). Local random McFarlane skin flap was applied to all rats. Following the applications, evaluations were made biochemical (TAS, TOS, OSI, IL-1β, IL-6, TNF-α, TGF-β, VEGF) and histopathological parameters. Results Necrosis percentage was found to be lower in the PP + HBO + PP group than all other groups whereas the necrosis percentages of PP and HBO groups were similar. Oxidative stress rates were significantly higher in the control group compared to the other groups whereas it was lower in the PP + HBO + PP group than all other groups. The inflammation parameters were the highest in the control group and the lowest in the PP + HBO + PP group. Growth factors were higher in the PP + HBO + PP group than all other groups. Epithelialization and wound healing were better in the HBO and PP groups than in the control group. The greatest healing, epithelialization and vascularization was seen in the PP + HBO + PP group. The histopathological findings in the PP + HBO + PP group were better in each inner region than in the other groups. Conclusion Biochemical and histopathological parameters have shown that PP reduces ischemia and necrosis and increases oxygenation in flap healing by providing significant improvement thanks to the multiple molecular structures in its content.

Objective:It was aimed to investigate the effect of isotretinoin (ISR), a retinoid derivative of vitamin A, on spermatogenesis via follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone levels.Methods:Twelve male Balb/c mice were divided into two groups: Control and ISR groups. FSH, LH and testosterone levels were biochemically determined by ELISA assay. All statistical analyses were made with SPSS 20.0 (IBM, New York, USA) and graphics were prepared with Graph Pad Prism Version 6.01 (USA). The parametric Student’s t-test was applied for comparison among groups. A p value ≤0.05 was accepted as statistically significant.Results:Mean FSH, LH and testosterone levels were increased in the ISR group when compared to those of control group. The increases in all hormone levels were found statistically significant between the two groups (p

The aim of this study is to show if cyclosporine has an antiallergic role in a rat model of ovalbumin-induced allergic rhinitis. The 54 rats were divided into six equal groups. The first group was a negative control group without induced allergic rhinitis; the second group a positive control with induced allergic rhinitis not receiving treatment. The remaining four groups, after induction of allergic rhinitis, received intranasal cyclosporine treatment in doses of 0.05, 0.1, or 0.2% or nasal steroid treatment. In the biochemical examination, on the surface of the tissue tumor necrosis factor (TNF) interferon (IFN), interleukin (IL)-5, IL-13, as well as IL-2, IL-4, IL-17A, and IgE were studied. Histologically, ciliary loss, increase of goblet cells, vascular congestion, and the degree of eosinophil infiltration were rated. In all treatment groups, on average, a significant reduction in all histological and biochemical values was found compared to the positive control group. Comparing each of the three cyclosporine-using groups with the group of nasal corticosteroid did not show any significant difference in the average scores. Cyclosporine nasal drops are effective to be used in an animal model of experimental allergic rhinitis without systemic effects.

Epithelial components of the organs of the digestive system are derived from the endoderm, whereas connective tissue and muscle components are derived from the mesoderm. At the 3rd-4th week of development, as a result of cephalocaudal and lateral foldings of the embryo, a portion of the endoderm-lined yolk sac cavity is incorporated in the embryo to form the primitive gut. Primitive gut is composed of four main regions: pharyngeal gut, foregut, midgut, and hindgut. The esophagus and stomach are derived from the foregut. The development of the esophagus is characterized by lengthening, widening, thickening, and histological changes. The development of the stomach is characterized by widening, thickening, and histological changes as well as positional changes. In the present study, we tried to review the morphological and functional development of the esophagus and stomach with the aid of pictures obtained from various stages of prenatal and postnatal development of the organs of rats. Previous reviews lack information on both histological and functional development of the organs.

The parenchyma of the liver and pancreas is derived from the endoderm, whereas the stroma is derived from the mesoderm. Both of them are derived from the endoderm of the foregut as the esophagus, stomach, and a part of duodenum. At the 3rd-4th of development, the liver, gallbladder and bile ducts become diverticulum hepaticum that is derived from the caudal portion of the foregut. There were inductive effects of septum transversum and cardiac mesoderm for the development of liver diverticulum. The pancreas arise from the endoderm of the foregut. The pancreas is derived from the fusion of the ventral and dorsal pancreas bulbs, which arise from the endoderm of the duodenum. The inductive effects of the notochord and dorsal aorta play a role in the development of the pancreas. In this manuscript, we attempted to review the morphological and functional development of the liver and pancreas with the aid of pictures obtained from various stages of prenatal and postnatal development in the organs of rats.

This experimental study was designed to investigate the effects of 10weeks genistein administration on oxidative stress and inflammation in serum and liver of rats fed with fructose.6-8weeks old, 40 male Sprague-Dawley rats were included. Group 1 (control) was fed with standard chow food and 100μl/kg/day/rat dimethyl sulfoxide (DMSO) administered subcutaneously; group 2 (genistein) with standard chow food and 0.25mg/kg/day/rat genistein; group 3 (fructose) with standard chow food and drinking water 20% fructose, group 4 (fructose+genistein) with standard chow food, drinking water with 20% fructose and 0.25mg/kg/day/rat genistein. TNF-α, IL-6, visfatin as inflammatory markers and 8-isoprostane as a oxidative stress marker were measured by ELISA, glucose, triglyceride, total cholesterol, LDL-cholesterol and HDL-cholesterol by enzymatic colorimetric method, AST and ALT by kinetic UV method.Significantly high 8-isoprostane levels in serum (p0.001) and liver (p0.05) in group 3 compared to control group indicate that presence of oxidative stress. Significantly high TNF-α and IL-6 levels in serum (p0.05) and liver (p0.01) and visfatin levels in serum (p0.001) of group 3 indicate inflammation accompanying insulin resistance and oxidative stress. Genistein administration to fructose group causes a significant decrease in HOMA-IR (p0.001) and LDLC (p0.05) level. Significantly lower serum 8-isoprostane (p0.01) level indicates the antioxidant effect of genistein and significantly lower liver TNF-α (p0.01), serum, liver IL-6(p0.01) and serum visfatin (p0.01) levels reflect the antiinflammatory effects of genistein.Genistein administration to rats fed with fructose causes an ameliorating effect on HOMA-IR values and lipid status markers in addition to its antioxidant and antiinflammatory effects.

Lipopolysaccharide (LPS)-induced endotoxemia can cause serious organ damage such as acute lung injury and death by triggering the secretion of proinflammatory cytokines and acute-phase reactants. The goal of this study was to evaluate the effects of β-glucan on inflammatory mediator levels and histopathological changes in LPS-induced endotoxemia.Forty-seven male Wistar albino rats were randomly allocated into four groups as follows: control group, LPS group (10 mg/kg LPS), LPS + β-glucan group (100 mg/kg β-glucan before LPS administration), and β-glucan group. Twelve hours after LPS administration, lung and serum samples were collected. Concentrations of IL-6, IL-8, C-reactive protein (CRP), and procalcitonin were measured in the serum at hours 0 (basal) and 12. The severity of lung damage was assessed by an appropriate histopathological scoring system.Serum levels of CRP in the LPS group at 12 h were significantly higher than in the other groups, whereas serum IL-6 levels in the LPS and LPS + β-glucan groups at 12 h were significantly decreased. The mean histopathological damage score of the LPS group was slightly higher than that of the LPS + β-glucan group. Moreover, mortality rate was significantly decreased in the LPS + β-glucan group versus the LPS group.β-glucan reduces endotoxemia-induced mortality and might be protective against endotoxemia-induced lung damage.

OBJECTIVES We aim to evaluate the effect of ischemic preconditioning (IPreC) on testicular tissue after transient middle cerebral artery occlusion (MCAo) in Streptozotocin-induced diabetic (STZ) and non-diabetic rats. METHODS Testis injury and alterations of testosterone levels were evaluated histologically.. Testicular damage was detected by using hematoxylin- eosin and periodic acid- schiff staining and apoptosis was identified by terminal-deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL). RESULTS Total mean serum testosterone levels decreased in all diabetic groups (p < 0.05) although remote ischemia and IPreC did not have any effect. Serious testicular tubular damage was observed in both, diabetic and ischemic groups (p 0.05). Otherwise, remote IPreC induced MNAC instead of any changes in histopathological architecture. Moreover, remote IPreC reduced the tubular degeneration against synergistic damage of both ischemia and diabetes (p < 0.05). CONCLUSIONS It can be suggested that remote ischemic preconditioning prevents testicular damage by improving histopathological alterations and inducing apoptosis, probably temporarily, after focal transient middle cerebral artery occlusion in both, diabetic and non-diabetic rats. This is the first report demonstrating protective effects of ischemic preconditioning on remote testis injury after transient middle cerebral artery occlusion in diabetic rats (Fig. 6, Ref. 23).

Background Non-alcoholic steatohepatitis, a cause of cirrhosis, is characterized by fatty infiltration of the liver, inflammation, hepatocellular damage and fibrosis. The aim of the present study was to investigate the effects of melatonin and quercetin on CCl4-induced steatosis characterized by fatty infiltration of the liver, inflammation, hepatocellular damage and fibrosis. Methods Rats were divided into 5 groups: Ethanol, Olive oil, CCl4, CCl4+Melatonin (CCl4+Mel), CCl4+Quercetin. Rats were sacrificed and livers were removed for being evaluated by histopathological, immunohistochemical and biochemical methods. Results In CCI4 group, vacuolization, vascular congestion, haemorrhage, necrosis, and inflammatory infiltration were identified. The mean tissue MDA level was increased, whereas GSH level and SOD and CAT activities were decreased in comparison with ethanol and olive oil groups. MDA levels were decreased in CCI4+Quercetin and CCI4+Mel groups versus CCI4 group. CAT activity of CCI4+Mel group was higher than that of CCI4 and CCI4+Quercetin groups. The mean tissue GSH level of CCI4+Mel group versus CCI4 group was significantly increased. Conclusions By the means of histopathological examination, we suggest that both agents are beneficial against necrotic and apoptotic cell death during steatosis. Thus, melatonin and quercetin might be beneficial in the improvement of hepatic steatosis by supporting conventional therapy in humans (Tab. 1, Fig. 5, Ref. 53).

Epithelial components of the organs of the digestive system are derived from endoderm whereas connective tissue and muscle components are derived from mesoderm. At the 3-4th of development, as a result of cephalocaudal and lateral foldings of the embryo, a portion of the endoderm-lined yolc sac cavity is incorporated in the embryo to from the primitive gut. Primitive gut is composed of four main regions which are pharyngeal gut, foregut, midgut, and hindgut; respectively. Intestines are derived from foregut, midgut and hindgut. The development of the intestines is characterised by lengthening, widening, thickening, histological and positional changes. In this manuscript we tried to review the morphological and functional development of the small and large intestines with the aid of pictures obtained from various stages of prenatal and postnatal development the intestines of rats. Previous reviews lack of information on both histological and functional development of the small and large intestines.

AIM Current stroke therapies include lipid-lowering drugs, which reduce inflammation and serve to stabilize the atherosclerotic plaque to demonstrate better outcome and neuroprotection. Peroxisome proliferator activated receptors (PPAR) ? regulates lipid homeostasis and is a target of fibrates, which have a neuroprotective function by various mechanisms. In this study, we aimed to evaluate the role of the PPAR? agonist, fenofibrate, in the modulation of cleaved caspase-3 immunoreactivity and at the final infarct volume in an experimental ischemia/reperfusion rat model by induced transient proximal middle cerebral artery occlusion. MATERIAL AND METHODS A total of 65 male Sprague Dawley rats were allocated into 4 groups; sham (n =5), experiment 1 (n=20), experiment 2 (n=20), experiment 3 (n=20). All experiment groups were divided to 3 subgroups in order to evaluate the final infarct volume at 24th hour (n=5) and the immunoreactivity of cleaved caspase -3 at different time periods [at first hour (n=5), at 6th hour (n=5), at 24th hour (n=5)] after transient middle cerebral artery occlusion (MCAo). At the study, the experiment groups (Experiment 1 and Experiment 2) were received the fenofibrate-diet during 14 days before ischemia procedure. All animals were sacrificed at 24th hours after MCAo. Infarction volumes were calculated from 2,3,5,triphenyltetrozolium chloride (TTC)- stained brain sections. RESULTS We found that fenofibrate-therapy reduced significantly more body weight than the other experiment groups (p < 0.05). At the time intervals, a decrease of immunoreactivity of cleaved caspase-3 was significantly observed with fenofibrate therapy after MCAo (p < 0.05). Chronic fenofibrate treatment before cerebral ischemia significantly reduced the infarction size after MCAo compared with the other groups (respectively; p = 0.011 and p < 0.000). CONCLUSION Fenofibrate treatment has neuroprotective effects on middle cerebral artery infarcts.

The role of oxygen radicals are known for the pathogenesis of kidney damage. The aim of the present study was to investigate the antioxidative effects of melatonin, quercetin, and resveratrol on streptozotocin (STZ)-induced diabetic nephropathy in rats. A total of 35 male Wistar rats were divided into 5 groups as follows: control, diabetes mellitus (DM), DM + melatonin, DM + quercetin, and DM + resveratrol. All the injections started on the same day of single-dose STZ injection and continued for 30 days. At the end of this period, kidneys were removed and processed for routine histological procedures. Biochemical parameters and morphological changes were examined. In DM group, blood glucose levels were significantly increased, whereas body weights were decreased compared with the control group. Significant increases in blood urea nitrogen and tissue malondialdehyde (MDA) levels and decreases in superoxide dismutase and catalase activities were detected in DM group. Administration of melatonin, quercetin, and resveratrol significantly reduced these values. Melatonin was more efficient in reducing MDA levels than other antioxidants ( p < 0.05). STZ-induced histopathological alterations including epithelial desquamation, swelling, intracytoplasmic vacuolization, brush border loss and peritubular infiltration. Additionally, basement membrane thickening and sclerotic changes were observed in glomerulus. Transforming growth factor-β1 positive cells were also increased. Melatonin, quercetin, and resveratrol significantly reduced these histopathological changes. Our results indicate that melatonin, quercetin, and resveratrol might be helpful in reducing diabetes-induced renal damage

Context: Oxidative damage due to oxidative stress is the failure of the cell’s defense against the deleterious effects of harmful agents by means of its numerous autoprotective mechanisms. Oxidative stress is a key impairment induced by various conditions, including atherosclerosis, hypertension, ischemia-reperfusion, hepatitis, pancreatitis, cancer, and neurodegenerative diseases. Evidence Acquisition: Oxidative stress is a common pathogenetic mechanism contributing to the initiation and progression of hepatic damage in cases of inflammatory liver disorders, including acute and chronic hepatitis. Antioxidant administration is a good therapeutic strategy for the treatment of hepatitis. Results: Our comprehensive review of the literature revealed that contradictory results have been obtained with many antioxidants and antioxidant agents. Conclusion: Since clinical studies to date have generally involved testing of the effects of antioxidant mixtures containing more than 2 antioxidants and also have been limited because of toxic effects of high doses of some antioxidants, antioxidant therapy for acute and chronic hepatitis needs further study.

Age-related myocardial dysfunction has important implications with impaired redox homeostasis. Current study focused on investigation of redox homeostasis and histopathological changes in the myocardium of mimetically (MA), naturally aged (NA), and young control (YC) rats. Chronic D-galactose administration to young male Wistar rats (5 months old) was used to set up experimental aging models. We investigated 16 different oxidative damage biomarkers which have evaluated redox homeostasis of cellular macromolecules such as protein, lipid, and DNA. As a protein oxidation biomarker, advanced oxidation end products, protein carbonyl groups, protein-bound advanced glycation end products, dityrosine, kynurenine, and N-formylkynurenine concentrations in MA and NA rats were found to be significantly higher compared to those in YC rats. On the other hand, the levels of protein thiol groups were not significantly different between groups, whereas lipid peroxidation biomarkers such as conjugated diens, lipid hydroperoxides, and malondialdehyde in MA and NA rats were found to be significantly higher in comparison to those in YCs. For the assessment of oxidative DNA damage, we analyzed eight hydroxy-5'-deoxyguanosine concentrations of MA and NA groups which were higher than YCs. As an antioxidant status in the MA and NA groups, Cu-Zn superoxide dismutase, ferric reducing antioxidant power, and total thiol levels were lower than those in the YCs. Only nonprotein thiol levels were not significantly different. We also observed similar histopathological changes in MA and NA rats. We concluded that the mimetic aging model could be considered as a reliable experimental model for myocardial senescence. Türkiye Bilimsel Ve Teknolojik Araştırma Kurumu ( Tübitak ) İstanbul Üniversitesi

ulkay, muzaffer basak/0000-0002-0928-0462; Kaplan, Suleyman/0000-0003-1477-5002; WOS: 000327321900019 PubMed: 23735011 Objective: Non-steroidal anti-inflammatory drugs (NSAIDs) can have adverse effects for in both mother and fetus following administration during the prenatal period. If given during pregnancy, diclofenac sodium (DS), an NSAID, is given during the pregnancy, may also affect the development of the central nervous system (CNS) or related structures. Methods: Pregnant rats were separated into pure control (PG), saline (SG) and diclofenac groups (DG). A daily dose of 1 mg/kg of DS and 1 mL/kg saline was injected intraperitoneally to the DG and SG groups, respectively, from the 5th gestation day for a 15 day of period; the PG group received no treatment. After spontaneous delivery, female offspring were obtained from all groups. After the 20th week of postnatal life, the animals (n = 6 for each group) were perfused and the right optic nerves were resected. Sections were subjected to stereological and histological analysis. Results: There were no significant differences (p > 0.05) between PG, SG and DG groups with respect to myelin thickness, axonal cross-sectional area, axon numerical density, total section area of optic nerve and axon number. Conclusions: Histological and stereological results indicated that treatment with DS or saline produced undesirable effects on female rat optic nerve development and myelinization with respect to morphology.

Although the liver has a high regenerative capacity, as a result of massive hepatocyte death, liver failure occurs. In addition to liver failure, for acute, chronic and hereditary diseases of the liver, cell transplantation therapies can stimulate regeneration or at least ensure sufficient function until liver transplantation can be performed. The lack of donor organs and the risks of rejection have prompted extensive experimental and clinical research in the field of cellular transplantation. Transplantation of cell lineages involved in liver regeneration, including mature hepatocytes, fetal hepatocytes, fetal liver progenitor cells, fetal stem cells, hepatic progenitor cells, hepatic stem cells, mesenchymal stem cells, hematopoietic stem cells, and peripheral blood and umbilical cord blood stem cells, have been found to be beneficial in the treatment of liver failure. In this article, the results of experimental and clinical cell transplantation trials for liver failure are reviewed, with an emphasis on regeneration. © 2013 Baishideng. All rights reserved. Key words: Liver regeneration; Liver failure; Stem cell Core tip: Although the liver has a high regenerative capacity, as a result of massive hepatocyte death, liver failure occurs. In recent years, there has been extensive experimental and clinical research in the field of cellular transplantation. Transplantation of cell lineages involved in liver regeneration, including mature and fetal hepatocytes, fetal liver progenitor and stem cells, hepatic progenitor and stem cells, mesenchymal stem cells, hematopoietic stem cells, and peripheral blood and umbilical cord blood stem cells, have been found to be beneficial for treating of liver failure. Herein, I review the results of experimental and clinical cell transplantation trials for liver failure.

Oxidative stress has been shown to play an important role in the pathogenesis of acute pancreatitis (AP). Antioxidants, alone or in combination with conventional therapy, should improve oxidative-stress-induced organ damage and therefore accelerate the rate of recovery. In recent years, substantial amounts of data about the efficiency of antioxidants against oxidative damage have been obtained from experiments with rodents. Some of these antioxidants have been found beneficial in the treatment of AP in humans; however, at present there is insufficient clinical data to support the benefits of antioxidants, alone or in combination with conventional therapy, in the management of AP in humans. Conflicting results obtained from experimental animals and humans may represent distinct pathophysiological mechanisms mediating tissue injury in different species. Further detailed studies should be done to clarify the exact mechanisms of tissue injury in human AP. Herein I tried to review the existing experimental and clinical studies on AP in order to determine the efficiency of antioxidants. The use of antioxidant enriched nutrition is a potential direction of clinical research in AP given the lack of clues about the efficiency and safety of antioxidant usage in patients with AP.

Microscopic features and antioxidant status of kidneys of young, old, and caffeic acid phenethyl ester (CAPE) and melatonin administered old Sprague Dawley rats were evaluated. Aging-related tubular and glomerular changes were evident. The most prominent tubular alterations were massive vacuole formation, mitochondrial degeneration, and lysosome accumulation. Mean tissue malondialdehyde (MDA) level was increased, mean tissue superoxide dismutase (SOD), catalase (CAT) (p < .001), and glutathione peroxidase (GPx) activities (p < .05), and total glutathione (GSH) level were decreased in old animals. Melatonin significantly reduced tissue MDA levels (p < .005), but increased tissue SOD (p < .001), CAT, and GPx activities (p < .05), and GSH levels (p < .005) in old animals. CAPE also significantly reduced tissue MDA levels (p < .005), but increased tissue SOD (p < .05), CAT (p < .005), GPx activities, and GSH levels (p < .001) in old rats. Mean tissue MDA levels of melatonin and CAPE-administered rats were even lower than those of young rats (p < .05). In conclusion, tubular and glomerular structures and tissue antioxidant enzyme activities were very well preserved in CAPE and melatonin-administered rats.

The liver continuously produces free radicals and reactive oxygen species (ROS) as part of metabolic process. These free radicals are neutralized by an elaborate antioxidant defense system consisting of enzymes and numerous nonenzymatic antioxidants like flavonoids. In this study, we have evaluated effects of melatonin and caffeic acid phenethyl ester (CAPE) to young and aged rat liver. Aging-related hepatic changes examined by light and electron microscopy and biochemical methods. Melatonin and CAPE decreased tissue malondialdehyde (MDA) levels in aged rats. Melatonin elevated tissue glutathione peroxidase (GSH-Px) activity and tGSH level, whereas CAPE elevated tissue catalase activity in aged rats. This study demonstrates that both melatonin and CAPE are beneficial in delaying age-related hepatocellular changes. Melatonin and CAPE supplementation in older ages may support liver to protect itself from various damaging agents including infectious agents and toxins.

Recently the authors have reported the potent beneficial effect of caffeic acid phenethyl ester (CAPE) on cholestatic oxidative liver injury induced by acute bile ligation in Swiss albino rats. Herein, they report the ultrastructural hepatocellular alterations induced by acute bile duct ligation and the effect of CAPE administration on these alterations. Bile duct ligation resulted in many degenerative changes, such as vacuolization, mitochondrial degeneration, endoplasmic reticulum dilatation, and lysosome accumulation within the cytoplasm of hepatocytes. Mitochondrial degeneration was also observed within the cytoplasm of the cells of biliary ductular epithelium. CAPE potentially protected the hepatocytes from the cholestasis-induced cellular injury.

Caffeic acid phenethyl ester (CAPE) has been subjected to considerable investigations that have revealed its antioxidant and anti-inflammatory activities in different conditions. But there is not a previous investigation about its effect on cholestatic liver injury. The aim of this study was to investigate the effect of CAPE in rat liver against cholestatic liver injury induced by bile duct ligation.Swiss-albino rats were recruited in the study as follows; Group 1 rats subjected to simple laparotomy known as the sham group; Group 2 rats subjected to bile duct ligation (BDL); Group 3 bile duct ligated rats treated with CAPE. The third group received CAPE (10 micromol/kg) intraperitoneally daily throughout 14 d.Data showed a decrease in gamma glutamyl transferase (GGT), aspartate aminotransferase (AST), and alanine aminotransferase levels (ALT) of the CAPE treated rats, compared with BDL group (P0.001, P0.01, and P0.02, respectively). In the CAPE treated rats, tissue levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were significantly lower than that of the BDL group (P0.001). The levels of glutathione (GSH) in CAPE treated rats were significantly higher than that of BDL group (P0.001). In CAPE treated group, the levels of interleukin-1alpha (IL-1alpha) and interleukin-6 (IL-6) were significantly lower than that of BDL group (P0.03, P0.02, respectively). Administration of CAPE in the rats with biliary obstruction resulted in inhibition of necro-inflammation.These results suggest that treatment of CAPE maintains antioxidant defenses, reduces oxidative liver injury, cytokine damage, and necro-inflammation in bile duct ligated rats. Thus, CAPE seems to be a promising agent for the attenuation of cholestatic liver injury.