scholarly journals Expression Pattern of MicroRNA-21 during the Liver Ischemia/Reperfusion

2021 ◽  
Author(s):  
Alireza Salah ◽  
Mohammad Hossein Karimi ◽  
Javad Sajedianfard ◽  
Saeed Nazifi ◽  
Ramin Yaghobi
Keyword(s):  
Expression Pattern ◽  
Liver Damage ◽  
Liver Tissue ◽  
Fas Ligand ◽  
Ischemia Reperfusion ◽  
Inflammatory Phase ◽  
Total Antioxidant ◽  
Programmed Cell Death 4 ◽  
Intracellular Antigen ◽  
Injury Recovery

Ischemia/reperfusion (I/R) injury in cadaveric liver transplantation is not avoidable. Liver I/R injury is an important phenomenon in hepatic damage. MicroRNA-21 (miR-21) plays an important role in I/R injury. The present study aimed to determine the expression pattern of miR-21 in liver I/R injury/recovery and its correlation with the immunologic transmission signals pathways in several days post-reperfusion. In an animal model for I/R in the liver, 40 male Balb/c mice were divided into 3 groups. The animals were monitored for 3 and 24 hours, and also for 4, 7, 14, and 28 days postreperfusion. Liver tissue damage was assessed by histopathology. The plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total antioxidant capacity (TAC) levels were measured with enzymatic assays. MiR-21, programmed cell death 4 (PDCD4) mRNA, T-cell-restricted intracellular antigen 1 (TIA1) mRNA, and fas ligand (FASL) mRNA expression levels were measured; using reverse transcription-polymerase chain reaction (RT-PCR) at different times after the reperfusion in liver tissue and blood. Histopathology and plasma ALT, AST, ALP, and TAC levels confirmed liver damage induced by I/R injury. MiR-21 increased by twofold in the liver tissue and on the inflammatory phase after 24 hours of reperfusion; it then continued to decrease up to day 7 post-reperfusion. Afterward, it continued to rise slightly up to day 14 post-reperfusion. This trend was in parallel with the recovery of the liver damage. MiR-21 expression level in the liver and blood is a predictor of the extent of I/R injury.

Flaxseed Protects Against the Inflammatory Phase of Lung Ischemia Reperfusion Injury in a Murine Model

2010 ◽  
Vol 158 (2) ◽  
pp. 358
Author(s):  
S.S. Razi ◽  
G. Schwartz ◽  
D. Boone ◽  
X. Li ◽  
S. Belsley ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Murine Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inflammatory Phase

Abstract 028: CCN1 Enables Fas Ligand-Induced Apoptosis by Elevating Fas Expression in Primary Cardiomyocytes or by Increasing Cytoplasmic Smac in Cardiomyoblast H9c2 Cells

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Bor-Chyuan Su ◽  
Fan-E Mo
Keyword(s):  
Cell Surface ◽  
Fas Ligand ◽  
Ischemia Reperfusion ◽  
Surface Display ◽  
Critical Role ◽  
Mitogen Activated Protein Kinase ◽  
Neonatal Rat ◽  
Ros Generation ◽  
H9c2 Cells ◽  
Induced Apoptosis

Fas/Fas ligand (FasL) is implicated in cardiac ischemia/reperfusion injury. However, cardiomyocytes in culture are resistant to FasL-induced apoptosis, suggesting that additional factor(s) are required for FasL-induced apoptosis. Matricellular protein CCN1 has been demonstrated to promote cytotoxicity of FasL in human skin fibroblasts. CCN1 is induced in a variety of cardiac pathologies. We assessed the hypothesis that CCN1 may be involved in the regulation of FasL-induced apoptosis in cardiomyocytes. We found that either FasL or CCN1 did not induce cell death in neonatal rat ventricular cardiomyocytes (NRVM). Interestingly, the combination of FasL+CCN1 generated 2-fold induction of apoptosis (vs. control p<0.001). An integrin-α 6 β 1 -binding defective mutant CCN1, CCN1-DM failed to exert synergy with FasL to induce apoptosis, indicating a critical role of α 6 β 1 . The engagement between CCN1 and α 6 β 1 instigated the elevation of cellular reactive oxygen species (ROS), the activation of mitogen activated protein kinase p38, and followed by the induction of cell surface display of Fas, thereby sensitizing NRVM to FasL-induced apoptosis. Pretreatment of the p38 inhibitor SB202190 abolished the CCN1-induced cell-surface Fas expression and the apoptosis induced by FasL+CCN1. In addition, we tested the interaction between CCN1 and FasL on the cardiomyoblast H9c2 cells. We found that FasL or CCN1 alone did not cause apoptosis in H9c2, and required the combination of FasL+CCN1 to induced apoptosis (vs. control p<0.001) in H9c2 cells, reminiscent of the observation in NRVM. Mechanistically, CCN1 acted through binding to integrin α 6 β 1 , ROS generation, and p38 activation, however, did not increase the expression of cell surface Fas for its synergy with FasL in H9c2 cells. Instead, CCN1 induced Bax translocation to mitochondria, which in turn led to the release of Smac from mitochondria to cytosol. The cytosolic Smac functions to neutralize XIAP. Smac is critical for CCN1 action, because the knockdown of Smac blunted the apoptotic activities of CCN1. In conclusion, CCN1 may play a detrimental role in a stressed heart to both the differentiated cardiomyocytes and the proliferative cardioblasts through distinct signaling mechanisms.

A peculiar malignant liver adenoma

1910 ◽  
Vol 10 (5-6) ◽  
pp. 159-160
Author(s):  
F. Ya. Chistovich
Keyword(s):  
Portal Vein ◽  
Liver Damage ◽  
Liver Tissue ◽  
Liver Adenoma ◽  
Blood Clots ◽  
Septic Peritonitis ◽  
Malignant Liver ◽  
Lobular Structure ◽  
Cerebral Convolutions ◽  
As If

In October 1909, the speaker met at an autopsy a completely peculiar liver damage in a 21-year-old child, more than 3 years of diarrhea and a significant increase in the spleen (with ascites); the last one was removed to him, and the patient died from septic peritonitis. The liver was smooth, 1270 gm. vѣsom and extremely soft; in the portal vein and she herself turned out to be clogged with blood clots, red in the liver, and whitish in the drink itself. Liver tissue appeared to be red and och. soft, in some places whitish-yellowish color; areas of the last days formed nodes in the forms of cerebral convolutions, enveloping the rays of the Glisson capsule with large veins; the convolutions seemed striated, as if folded from the tubes, vertical to the axis of the crossbeam of the Glisson capsule. Such whitish areas were scattered everywhere and in the red parenchyma, not sharply delimited * from it and without lobular structure.

scholarly journals Remote post-conditioning and allopurinol reduce ischemia-reperfusion injury in an infra-renal ischemia model

2018 ◽  
Vol 12 (12) ◽  
pp. 341-349 ◽  
Author(s):  
Rafael Inácio Brandão ◽  
Ricardo Zanetti Gomes ◽  
Luana Lopes ◽  
Filipe Silva Linhares ◽  
José Carlos Rebuglio Vellosa ◽  
...  
Keyword(s):  
Histological Analysis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Protective Effects ◽  
Positive Effects ◽  
Additional Protection ◽  
Total Antioxidant ◽  
Lactate Levels ◽  
Harmful Effects

Background: The aim of this study was to evaluate the effects of the antioxidant allopurinol and ischemic post-conditioning on the deleterious effects of ischemia followed by reperfusion (I/R) in a standardized model of ischemia involving infra-renal aortic occlusion in rats. Methods: The animals were randomly divided into five groups: (A) animals not subjected to ischemia; (B) animals subjected to 2 h of ischemia and reperfusion only once; (C) animals given an allopurinol dose by gavage, then subjected to 2 h of ischemia and reperfusion only once; (D) animals subjected to 2 h of ischemia and post-conditioning and (E) animals that received allopurinol, then subjected to 2 h of ischemia and post-conditioning. The blood samples and small intestine segments were harvested for analysis after 3 days. Results: The protective effects of the use of allopurinol and ischemic post-conditioning were observed by measuring aspartate aminotransferase, alanine aminotransferase and lactate levels. The benefits of post-conditioning were evident from the total antioxidant capacity and creatinine levels, but these could not ascertain any positive effects of allopurinol. The histological analysis of mesentery revealed that both methods were effective in minimizing the harmful effects of the ischemia and reperfusion process. Conclusion: Individual protocols significantly reduced I/R systemic injuries, but no additional protection was observed when the two strategies were combined.

Protective Effects of Hypericum perforatum and Quercetin in a Rat Model of Ischemia/Reperfusion Injury of Testes

2017 ◽  
Vol 28 (01) ◽  
pp. 096-100
Author(s):  
Leyla Tekin ◽  
Mehmet Erdemli ◽  
Nazile Erturk ◽  
Zeynep Aksungur ◽  
Serdar Aktas ◽  
...  
Keyword(s):  
Antioxidant Status ◽  
Hypericum Perforatum ◽  
Ischemia Reperfusion Injury ◽  
Histopathological Examination ◽  
Ischemia Reperfusion ◽  
Total Antioxidant Status ◽  
Albino Rats ◽  
Protective Effects ◽  
Total Antioxidant ◽  
Markers Of Oxidative Stress

Purpose This study aimed to compare the protective effects of Hypericum perforatum (Hp) and quercetin, a flavonoid, against ischemia/reperfusion (I/R) injury in rat testes. Materials and Methods This study included 28 male Wistar albino rats that were divided into four groups. Except for the sham group, torsion was created by rotating both testes at an angle of 720 degrees clockwise for 2 hours. The Hp and quercetin groups received 25 mg/kg Hp and quercetin intraperitoneally 30 minutes before detorsion, respectively. Orchiectomy was performed for the measurement of markers of oxidative stress and histopathological examination. Results In the Hp and quercetin groups, malondialdehyde (MDA) and nitric oxide (NO) levels and total oxidant capacity were significantly lower, the glutathione level and total antioxidant status were significantly higher, and Johnsen's testis biopsy scores were significantly higher than in the torsion/detorsion group (p ˂ 0.001). The markers of oxidative injury were significantly lower (p ˂ 0.001) and total antioxidant status was significantly higher (p ˂ 0.001), except for glutathione (p = 0.62) in the Hp group than in the quercetin group. Johnsen's score between Hp and quercetin groups was not significantly different (p = 0.80). Conclusion Both Hp and quercetin have protective effects against I/R injury of the testes, but the protective effect of Hp was found to be stronger than that of quercetin.

scholarly journals The role of nitrosative and oxidative stress in rainbow trout (Oncorhynchus mykiss) liver tissue applied mercury chloride (HgCl2)

2021 ◽  
Vol 38 (3) ◽  
pp. 269-273
Author(s):  
Mehmet Reşit Taysı ◽  
Muammer Kırıcı ◽  
Mahinur Kırıcı ◽  
Hasan Ulusal ◽  
Bünyamin Söğüt ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Liver Tissue ◽  
Stress Index ◽  
Mercury Chloride ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Total Antioxidant ◽  
Ld50 Value

The aim of this study was to determine oxidative stress caused by mercury chloride (HgCl2) in rainbow trout (Oncorhynchus mykiss) liver tissue. For this purpose, the LD50 value of HgCl2 on rainbow trout was determined as 551 μg/L. In the study, 40 fish in four groups were exposed to 25% and 50% (138 and 276 µg/L) of the two subletal doses of HgCl2 for 2 and 7 days, with 10 fish (n=10) in each group. To determine oxidative stress; peroxynitrite (ONOO−), total oxidant level (TOS), total antioxidant level (TAS), oxidative stress index (OSI) and malondialdehyde (MDA) were analyzed. In the study, it was observed that the differences between the groups in terms of ONOO−, TOS, TAS and OSI levels in the liver tissues was significant (P<0.05), however, this difference was not significant (P>0.05) in terms of MDA values. As a result, it can be concluded that HgCl2 increases ONOO−, TOS, TAS, OSI and MDA levels in liver tissue and even small doses of mercury are toxic to fish.

Dexmedetomidine Suppressing Apoptosis to Release Rats’ Liver Ischemia-Reperfusion Injury

2021 ◽  
Vol 11 (8) ◽  
pp. 1536-1542
Author(s):  
Zhao Hai-Fan ◽  
Li Chong ◽  
Hu Zhi-Duo ◽  
Chen Hong ◽  
Jiang Tao ◽  
...  
Keyword(s):  
Western Blot ◽  
Liver Tissue ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological State ◽  
Inhibitory Effects ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

Purpose: Explore the dexmedetomidine’s therapeutic impact on hepatic ischemia-reperfusion (I/R) injury and the related principle. Methods: The work established the rats’ liver I/R model. Liver tissues’ pathological state from each rat was evaluated by HE staining. ELISA was utilized to confirm the activity of MDA and SOD in the liver tissue, AST in the serum, and the ALT’s concentration. The apoptotic state of liver tissue was detected by TUNEL assay. Bcl-2, Caspase-3, HO-1, and BAX’s expressions of each rat’s liver tissue had been confirmed through immunohistochemistry and western blot. Results: Rats’ liver injury from I/R group and DEX+A group was rat’s liver tissue had been confirmed through immunohistochemistry and western blot. severer than that from Sham group in terms of HE staining and ELISA. The injured tissue has been improved by the introduction of Dexmedetomidine. The TUNEL, Immunohistochemistry and Western Blot results indicated that the high apoptotic rate in I/R model was inhibited using Dexmedetomidine. However, the inhibitory effects were reversed by the co-administration of Atipamezole. Conclusion: Dexmedetomidine suppressed apoptosis to alleviate rats’ hepatic ischemia-reperfusion injuries.

Protocol for the pig liver ischemia/reperfusion injury

2020 ◽  
Author(s):  
Eric Felli ◽  
Mahdi Al-Taher ◽  
Emanuele Felli ◽  
Lorenzo Cinelli ◽  
Michele Diana
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Liver Damage ◽  
Porcine Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Loss ◽  
Vascular Complication ◽  
Liver Ischemia ◽  
Pig Liver

Abstract Liver ischemia/reperfusion injury (IRI) is a dreadful vascular complication, which leads to liver damage. It is often associated with graft loss in liver transplantation and with a higher morbidity and mortality. IRI can have different causes, such as inflow clumping during surgical procedures in hepatic resection, liver transplantation, trauma, as well as during the stenosis of the vasculature caused by cancer. Here, we show a detailed IRI protocol in a porcine model.

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