scholarly journals Adalimumab Ameliorates Abdominal Aorta Cross Clamping Which Induced Liver Injury in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Erkan Cure ◽  
Medine Cumhur Cure ◽  
Levent Tumkaya ◽  
Yildiray Kalkan ◽  
Ibrahim Aydin ◽  
...  
Keyword(s):  
Liver Injury ◽  
Abdominal Aorta ◽  
Liver Tissue ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels

The aim of this study was to investigate the possible protective effects of adalimumab (ADA) on cell damage in rat liver tissue during ischemia/reperfusion (I/R) injury of infrarenal abdominal aorta. Thirty male Wistar-albino rats were divided into three groups: control, I/R, and I/R+ADA, each group containing 10 animals. Laparotomy without I/R injury was performed in the control group animals. Laparotomy in the I/R group was followed by two hours of infrarenal abdominal aortic cross ligation and then two hours of reperfusion. ADA (50 mg/kg) was administered intraperitoneally as a single dose, to the I/R+ADA group, five days before I/R. The tumor necrosis factor-alpha (TNF-α) (pg/mg protein) and nitric oxide (NO) (µmol/g protein) levels in the I/R group (430.8 ± 70.1, 8.0 ± 1.1, resp.) were significantly higher than those in the I/R+ADA group (338.0 ± 71.6,P=0.006; 6.3 ± 1.2,P=0.008) and the control group (345.5 ± 53.3,P=0.008; 6.5 ± 1.5,P=0.010, resp.). I/R causes severe histopathological injury to the liver tissue, but ADA leads to much less histopathological changes. ADA treatment significantly decreased the severity of liver I/R injury. ADA pretreatment may have protective effects on experimental liver injury.

scholarly journals The efficacy of dexmedetomidine on lung injury induced by renal ischemia/reperfusion indiabetic rats

2020 ◽  
Vol 24 (3) ◽  
Author(s):  
Seyfi Kartal ◽  
Gülay Kip ◽  
Ayşegül Küçük ◽  
Ali Atan ◽  
Özlem Erdem ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Diabetic Control Group ◽  
Wistar Albino Rats

Ischemia-reperfusion injury is a complex, which causes cell damage. In this study, we aimed to investigate the protective effects of dexmedetomidine on lung in the renal IR model in diabetic rats. After approval of the ethics committee, diabetes was induced by streptozocin (55 mg/kg) and then 24 Wistar Albino rats were randomly divided into 4 groups. Diabetic control group (group DC), diabetic dexmedetomidine (group DD), diabetic ischemia-reperfusion (group DIR), diabetic ischemia-reperfusion - dexmedetomidine (group DIR-D).

scholarly journals Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Weitao Ji ◽  
Hongyun Shi ◽  
Hailin Shen ◽  
Jing Kong ◽  
Jiayi Song ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Acute Liver Injury ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Klf4 Expression ◽  
Mrna And Protein Expression

Krüppel-like factor 4 (KLF4) is a key transcription factor that regulates genes involved in the proliferation or differentiation in different tissues. Apelin plays roles in cardiovascular functions, metabolic disease, and homeostatic disorder. However, the biological function of apelin in liver disease is still ongoing. In this study, we investigated the mechanism of KLF4-mediated protection against acute liver injury via the inhibition of the apelin signaling pathway. Mice were intraperitoneally injected with carbon tetrachloride (CCl4; 0.2 mL dissolved in 100 mL olive oil, 10 mL/kg) to establish an acute liver injury model. A KLF4 expression plasmid was injected through the tail vein 48 h before CCl4 treatment. In cultured LX-2 cells, pAd-KLF4 or siRNA KLF4 was overexpressed or knockdown, and the mRNA and protein levels of apelin were determined. The results showed that the apelin serum level in the CCl4-injected group was higher than that of control group, and the expression of apelin in the liver tissues was elevated while KLF4 expression was decreased in the CCl4-injected group compared to the KLF4-plasmid-injected group. HE staining revealed serious hepatocellular steatosis in the CCl4-injected mice, and KLF4 alleviated this steatosis in the mice injected with KLF4 plasmid. In vitro experiments showed that tumor necrosis factor-alpha (TNF-α) could downregulate the transcription and translation levels of apelin in LX-2 cells and also upregulate KLF4 mRNA and protein expression. RT-PCR and Western blotting showed that the overexpression of KLF4 markedly decreased basal apelin expression, but knockdown of KLF4 restored apelin expression in TNF-α-treated LX-2 cells. These in vivo and in vitro experiments suggest that KLF4 plays a key role in inhibiting hepatocellular steatosis in acute liver injury, and that its mechanism might be the inhibition of the apelin signaling pathway.

scholarly journals Aster glehniExtract Containing Caffeoylquinic Compounds Protects Human Keratinocytes through the TRPV4-PPARδ-AMPK Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-13
Author(s):  
Yong-Jik Lee ◽  
Yoo-Na Jang ◽  
Yoon-Mi Han ◽  
Hyun-Min Kim ◽  
Changbae Jin ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Sodium Dodecyl ◽  
Skin Barrier ◽  
Human Keratinocytes ◽  
Control Group ◽  
Hacat Cells ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Ampk Pathway

Aster glehni(AG) has been used in cooking and as a medicine to treat various diseases for over hundreds of years in Korea. To speculate the protective effects of AG on skin barrier, we estimated the protein levels of biomarkers related to skin barrier protection in human keratinocytes, HaCaT cells treated with sodium dodecyl sulfate (SDS), or 2,4-dinitrochlorobenzene (DNCB). The protein levels for keratin, involucrin, defensin, tumor necrosis factor alpha (TNFα), peroxisome proliferator-activated receptor delta (PPARδ), 5′ adenosine monophosphate-activated protein kinase (AMPK), serine palmitoyltransferase long chain base subunit 2 (SPTLC2), and transient receptor potential cation channel subfamily V member 4 (TRPV4) were evaluated using western blotting or immunocytochemistry in HaCaT cells. AG extract increased the protein levels of PPARδ, phosphorylated AMPK, SPTLC2, keratin, involucrin, and defensin compared to the SDS or DNCB control group. However, TNFαexpression increased by SDS or DNCB was decreased with AG extract. The order of action of each regulatory biomarker in AG pathway was identified TRPV4→PPARδ→AMPK from antagonist and siRNA treatment studies. AG can ameliorate the injury of keratinocytes caused by SDS or DNCB through the sequential regulation of TRPV4→PPARδ→AMPK pathway.

scholarly journals Melatonin and Glycine Reduce Uterus Ischemia/Reperfusion Injury in a Rat Model of Warm Ischemia

2021 ◽  
Vol 22 (16) ◽  
pp. 8373
Author(s):  
Viktorija Zitkute ◽  
Mindaugas Kvietkauskas ◽  
Vygante Maskoliunaite ◽  
Bettina Leber ◽  
Diana Ramasauskaite ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Combined Treatment ◽  
Warm Ischemia ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley

Ischemia/reperfusion injury (IRI) remains a significant problem to be solved in uterus transplantation (UTx). Melatonin and glycine have been shown to possess direct cytoprotective activities, mainly due to their antioxidative and anti-inflammatory properties. The aim of this study was to investigate the protective effects of melatonin and glycine and their combination on IRI in a rat model of warm ischemia. In this study, Sprague-Dawley rats were assigned to eight groups, including sham and IRI (n = 80). Melatonin and glycine alone or their combination were administered prior to 1 h of uterus ischemia followed by 1 h of reperfusion. Melatonin (50 mg/kg) was administered via gavage 2 h before IRI and glycine in an enriched diet for 5 days prior to intervention. Uterus IRI was estimated by histology, including immunohistochemistry, and biochemical tissue analyses. Histology revealed that uterus IRI was significantly attenuated by pretreatment with melatonin (p = 0.019) and glycine (p = 0.044) alone as well as their combination (p = 0.003). Uterus IRI led to increased myeloperoxidase expression, which was significantly reduced by melatonin (p = 0.004), glycine (p < 0.001) or their combination (p < 0.001). The decline in superoxide dismutase activity was significantly reduced in the melatonin (p = 0.027), glycine (p = 0.038) and combined treatment groups (p = 0.015) when compared to the IRI control group. In conclusion, melatonin, glycine and their combination significantly reduced oxidative stress-induced cell damage after IRI in a small animal warm ischemia model, and, therefore, clinical studies are required to evaluate the protective effects of these well-characterized substances in uterus IRI.

scholarly journals Protective effects of pentoxifylline in small intestine after ischemia–reperfusion

2018 ◽  
Vol 46 (10) ◽  
pp. 4140-4156 ◽  
Author(s):  
Seracettin Eğin ◽  
Mehmet İlhan ◽  
Süleyman Bademler ◽  
Berk Gökçek ◽  
Semih Hot ◽  
...  
Keyword(s):  
Small Intestine ◽  
Histopathological Examination ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Albino Rats ◽  
Ischemic Damage ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Molecular Responses

Objective This study was performed to determine the healing effects of pentoxifylline on molecular responses and protection against severe ischemic damage in the small intestine. Methods Thirty-six Wistar albino rats were divided into six groups. The superior mesenteric artery was clamped for 120 minutes, and reperfusion was performed for 60 minutes. Saline (0.4 mL), pentoxifylline (1 mg/kg), and pentoxifylline (10 mg/kg) were intraperitoneally administered to the rats in the C1, P1, and P3 groups, respectively, 60 minutes before ischemia and to the rats in the C2, P2, and P4 groups, respectively, during reperfusion onset. Malondialdehyde, myeloperoxidase, tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 in serum and tissue were measured by enzyme-linked immunosorbent assay. Intestinal ischemic injury was histopathologically evaluated by the Chiu score and immunohistochemical staining. Results All serum and tissue molecular responses were significantly blunted in the pentoxifylline-treated groups compared with the controls. Significant improvement in ischemic damage was demonstrated in the pentoxifylline-treated groups by histological grading and immunohistochemical scoring. Conclusions The protective effects of pentoxifylline were confirmed by molecular responses and histopathological examination.

scholarly journals Pistacia Terebinthus Coffee Protects against Thioacetamide-Induced Liver Injury in Rats

2015 ◽  
Vol 58 (2) ◽  
pp. 56-61 ◽  
Author(s):  
Ibrahim Halil Bahçecıoğlu ◽  
Murat Ispiroglu ◽  
Mehmet Tuzcu ◽  
Cemal Orhan ◽  
Mustafa Ulas ◽  
...  
Keyword(s):  
Liver Injury ◽  
Transforming Growth Factor Beta ◽  
Unsaturated Fatty Acids ◽  
Transforming Growth Factor ◽  
Tap Water ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Pistacia Terebinthus

Aim/background: Pistacia terebinthus is used as a coffee substitute in the East and Southern Anatolia regions of Turkey. It contains unsaturated fatty acids, tocopherols, polyphenols and carotenoids. P. terebinthus has anti-inflammatory and potential antioxidant activity. In this study we evaluated the protective effects of P. terebinthus coffee (PTC) on thioacetamide (TAA)-induced liver injury in rats. Materials and methods: Twenty-eight male Sprague-Dawley rats were equally randomized into four groups. Chronic liver injury was induced with TAA (100 mg/kg i.p. three times weekly). The first group of rats served as control and received only tap water (G1), and the remaining groups of rats received PTC, p.o (G2); TAA (G3); TAA plus PTC, p.o (G4), respectively. Results: After 8 weeks, PTC intake significantly reduced fibrosis/inflammation scores (p < 0.05) in the livers of TAA-treated group. Compared to control group, PTC intake reduced transforming growth factor beta (TGF-β) concentrations in the liver (p < 0.05). Compared to the TAA group, TGF-β, nuclear factor kappa B (NF)-κB (p < 0.05), tumor necrosis factor alpha (TNF-α) concentrations in the liver tissue were reduced by PTC intake. Discussion and conclusion: PTC intake provided beneficial effects against TAA-induced liver injury in rats. PTC probably suppresses the proinflammatory cytokines through NF-κB signaling pathway.

scholarly journals Evaluation of protective effects of melatonin on free radical metabolism in rat kidney during ischemia-reperfusion

2019 ◽  
pp. 20-29
Author(s):  
M. Nisari ◽  
A. Yay ◽  
T. Ertekin ◽  
M. Nisari ◽  
Ö. Al ◽  
...  
Keyword(s):  
Tap Water ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Sod Activity ◽  
Renal Pedicle ◽  
Group I

The purpose of this research was to investigate the possible protective effect of melatonin, as a potent antioxidant on I/R-induced renal injury in rats. Methods. We used 28 female Wistar albino rats weight 200-250g. The rats were randomly divided into 4 groups. Control Group (C): They were fed with only standard rat diet and tap water without drug injections or ischemia-reperfusion. Melatonin Group (M): 25 mg/kg melatonin was administered i.p 30 min.  Ischemia/Reperfusion Group (I/R): Rats were subjected to 45 min of renal pedicle occlusion followed by 24 hours reperfusion. Melatonin+ischemia/reperfusion Group (M+I/R): Melatonin (25 mg/kg) was administered 30 min prior to ischemia and immediately before the reperfusion period. Rats were subjected to 45 min of renal pedicle occlusion followed by 24 hours reperfusion. Results. While MDA levels increased in the I/R group, SOD and GST activities were seen to be significantly increased. Although the increase of the SOD activity was observed in the M+I/R group, no meaningful difference was found. MDA levels were significantly decreased in M+I/R group compared to the control group, CAT and GST activities were significantly increased. Conclusions. Our results show that the treatment with M may prevent kidney damage due to ischemia result in increasing oxidant stress peroxidation damages further. Melatonin or its metabolites are capable of neutralizing free radicals and non-radical oxygen-based reactants. This study suggests that melatonin may be an effective antioxidant agent.

Withdrawn: Hepatoprotective effects of Tribulus terrestris L. (Zygophyllales: Zygophyllaceae) hydro-alcholic extract on non-alcoholic fatty liver-induced rats

2016 ◽  
Vol 3 (5) ◽  
pp. 143
Author(s):  
Fatemeh Almasi ◽  
Mozafar Khazaei ◽  
Shima Chehrei ◽  
Ali Ghanbari
Keyword(s):  
Fatty Liver ◽  
Liver Tissue ◽  
Serum Lipid ◽  
Histopathological Examination ◽  
Serum Levels ◽  
Lipid Profiles ◽  
Control Group ◽  
Tribulus Terrestris ◽  
Protective Effects ◽  
Alcoholic Fatty Liver

Non-alcoholic fatty liver induces many complications to the liver tissue and also serum related parameters. Medicinal plants are the safe therapeutic strategy for the treatment of diseases. In this regards, the present study was conducted to evaluate the effect of Tribulus terrestris L. (Zygophyllales: Zygophyllaceae) extract on non-alcoholic fatty liver in rats. In this experimental study, thirty male Wistar rats were divided into five groups (n = 6). Animals in experimental groups were received high fructose diet (70%) (HDF) daily alone or in combined with daily intraperitoneal injection of 500, 700 and 1,000 mg/kg extract of T. terrestris. Control group of rats was feed with standard chow. The serum levels of biomarkers of liver and serum lipid profiles were assessed, also histopathological examination of liver tissue done. Data were analyzed using One-way ANOVA method followed by Tukey’s post-hoc multiple comparison test and P < 0.05 was considered statistically significant. There were significant improvements for biomarkers of liver tissue (P < 0.05) and serum lipid profiles (P < 0.01) in the HFD-fed rats that were treated with T. terrestris extract compare to HFD-fed group. In addition, accumulation of lipids in hepatocytes was significantly reduced in the HFD-fed + extract administrated groups in comparison to HFD-fed rats (P < 0.01). T. terrestris extract has protective effects against non-alcoholic fatty liver by changing biomarkers of liver tissue, serum lipid profiles and histopathological anomalies of liver tissue, to normal range.

Effect of Chinese Herbal Monomer Hairy Calycosin on Nonalcoholic Fatty Liver Rats and its Mechanism

2019 ◽  
Vol 22 (3) ◽  
pp. 194-200 ◽  
Author(s):  
Xiang Liu ◽  
Zhi-Hong Xie ◽  
Chen-Yuan Liu ◽  
Ying Zhang
Keyword(s):  
Fatty Liver ◽  
Liver Tissue ◽  
Liver Homogenate ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Alcoholic Fatty Liver ◽  
Nonalcoholic Fatty Liver ◽  
Chinese Herbal ◽  
Tnf Α ◽  
Model Control

Background: Chinese herbal monomer hairy Calycosin is a flavonoid extracted from Radix astragali. Aims and Scope: The aim of the research was to investigate the effect and mechanism of Hairy Calycosin on Non-Alcoholic Fatty Liver Dieases (NAFLD) in rats. Materials and Methods: 60 rats were randomly divided into 6 groups, then NAFLD rat models were prepared and treated with different doses of Hairy Calycosin (0.5, 1.0, 2.0 mg/kg) or Kathyle relatively. Results: Both 1.0 mg/kg and 2.0 mg/kg Hairy Calycosin treatment could significantly increase the serum Superoxide Dismutase (SOD) content of the model rats and reduce the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), Free Fatty Acid (FFA), IL-6, tumor necrosis factor-alpha (TNF-α) and liver homogenate malondialdehyde (MDA), while 2.0 mg/kg Hairy Calycosin can down-regulate liver tissue cytochrome p450 2E1 (CYP2E1). In the electron microscope, compared with the model control group, the mitochondrial swelling in the hepatocytes of Hairy Calycosin (1.0, 2.0 mg/kg) treatment group was significantly reduced, the ridge on the inner membrane of mitochondria increased, and the lipid droplets became much smaller. Conclusion: Hairy Calycosin can effectively control the lipid peroxidation in liver tissues of rats with NAFLD, and reduce the levels of serum TNF-α, IL-6, MDA and FFA, effectively improve the steatosis and inflammation of liver tissue, and down-regulate the expression of CYP2E1, inhibit apoptosis of hepatocytes.

scholarly journals Late Protective Effect of Netrin-1 in the Murine Acetaminophen Hepatotoxicity Model

2020 ◽  
Vol 175 (2) ◽  
pp. 168-181 ◽  
Author(s):  
Luqi Duan ◽  
Benjamin L Woolbright ◽  
Hartmut Jaeschke ◽  
Anup Ramachandran
Keyword(s):  
Liver Injury ◽  
Alanine Aminotransferase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Clinical Problem ◽  
The United States ◽  
Therapeutic Window ◽  
Protective Effects ◽  
Apap Overdose ◽  
Important Clinical Problem

Abstract Acetaminophen (APAP) overdose-induced acute liver failure is an important clinical problem in the United States and the current antidote N-acetylcysteine, has a short early therapeutic window. Since most patients present late to the clinic, there is need for novel late-acting therapeutic options. Though the neuronal guidance cue netrin-1, has been shown to promote hepatic repair and regeneration during liver ischemia/reperfusion injury, its effect in APAP-induced hepatotoxicity is unknown. In the quest for a late-acting therapeutic intervention in APAP-induced liver injury, we examined the role of netrin-1 in a mouse model of APAP overdose. Male C57BL/6J mice were cotreated with exogenous netrin-1 or vehicle control, along with 300 mg/kg APAP and euthanized at 6, 12, and 24 h. Significant elevations in alanine aminotransferase indicative of liver injury were seen in control mice at 6 h and this was not affected by netrin-1 administration. Also, netrin-1 treatment did not influence mitochondrial translocation of phospho-JNK, or peroxynitrite formation indicating that there was no interference with APAP-induced injury processes. Interestingly however, netrin-1 administration attenuated liver injury at 24 h, as seen by alanine aminotransferase levels and histology, at which time significant elevations in the netrin-1 receptor, adenosine A2B receptor (A2BAR) as well as macrophage infiltration was evident. Removal of resident macrophages with clodronate liposomes or treatment with the A2BAR antagonist PSB1115 blocked the protective effects of netrin-1. Thus, our data indicate a previously unrecognized role for netrin-1 in attenuation of APAP hepatotoxicity by enhancing recovery and regeneration, which is mediated through the A2BAR and involves resident liver macrophages.

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