The histopathological effects of levosimendan on liver injury induced by myocardial ischemia and reperfusion

Oktar, Gürsel Levent; Amac, N Demir; Elmas, Çiğdem; Arslan, M; Goktas, Guleser; İriz, Erkan; Erer, Dilek; Zor, Mustafa Hakan; Tatar, Tolga

doi:10.4149/bll_2015_047

Cited by 5 publications

(8 citation statements)

References 31 publications

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“…Histopathological examination was performed as described previously to observe the pathological changes in the liver tissues and determine the extent of liver fibrosis [ 30 – 32 ]. Samples of liver tissue were fixed in 10% buffered formalin, routinely embedded in paraffin, cut into 4 mm thick sections, and stained with hematoxylin and eosin (HE) and Masson trichrome staining for examination by light microscopy.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-195 Activates Hepatic Stellate Cells In Vitro by Targeting Smad7

et al. 2017

BioMed Research International

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Background and Aim Aberrant activation of the TGF-β1/Smad pathway contributes to the activation of hepatic stellate cells (HSCs). MicroRNA-195 has been shown to regulate the activation of HSCs. The aim of this study was to investigate the role of miRNA-195 in HSCs activation. Methods A liver fibrotic rat model induced by diethylnitrosamine was established. Dual luciferase reporter assays were performed to verify that Smad7 was the target of miRNA-195. The expression levels of miR-195, Smad7, and α-SMA in HSC-T6 transfected, respectively, with miR-195 mimic, inhibitor, or control were measured by qRT-PCR. The protein expression of Smad7 was detected by Western blot analysis. Results Enhanced miR-195 and decreased Smad7 were observed in diethylnitrosamine-induced liver fibrotic rats (P < 0.05). Dual luciferase reporter assays showed that the miR-195 mimic significantly suppressed the luciferase activity of a reporter plasmid carrying the binding site of miR-195 on the 3′UTR of Smad7 (P < 0.05). The miR-195 mimics activated HSCs, further elevated miR-195 and α-SMA (P < 0.01), and reduced the Smad7 level (P < 0.05). The miR-195 inhibitors blocked the activation of HSCs, reduced the expression of miR-195 and α-SMA (P < 0.01), and upregulated the expression of Smad7 (P < 0.05). Conclusion Collectively, we demonstrated that miRNA-195 activated HSCs by targeting Smad7.

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Section: Methodsmentioning

confidence: 99%

MicroRNA-195 Activates Hepatic Stellate Cells In Vitro by Targeting Smad7

et al. 2017

BioMed Research International

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“…Finally, they concluded that levosimendan significantly ameliorates damage in a liver IRI model, especially when given before induction of ischemia. [14] In our present study, the infusion of levosimendan was maintained during the reperfusion. In the levosimendan groups, both serum AST and ALT levels and histopathological injury score were significantly decreased.…”

Section: Discussionmentioning

confidence: 86%

“…In their experimental study, Oktar et al [14] used levosimendan in liver injury induced by myocardial ischemia and reperfu- sion. They used a cycle of 60 minutes of ischemia and 60 minutes of reperfusion for rat liver and used levosimendan at a dose of 100 mcg/kg.…”

Section: Discussionmentioning

confidence: 99%

A combination of Levosimendan and N-Acetylcysteine shows significant favorable efficacy on experimental liver ischemia/reperfusion injury

Suakıtıcı

Güven²,

Tanoğlu³

et al. 2020

Ulus Travma Acil Cerrahi Derg

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BACKGROUND: Ischemia-reperfusion injury (IRI) is cellular damage that emerges from re-oxygenation of a hypoxic organ. In the present study, we aimed to examine the effects of a combination of levosimendan, an inotropic agent, and N-Acetylcysteine, the precursor of antioxidants and glutathione, in an experimental liver IRI model. METHODS:In this study, 38 rats were randomly divided into five groups. Before the ischemia, study arms were given physiological saline solution, N-Acetylcysteine (NAS), levosimendan or a combination of NAS+levosimendan in a predetermined amount and duration, and the infusion was continued until the end of this study. The hepatic pedicle was occluded using an atraumatic vein clamp, and 60 minutes of ischemia was achieved. The clamp was then opened and 60 minutes of reperfusion was ensured. Liver tissue samples were obtained after sacrifice, and tissue malondialdehyde (MDA) and myeloperoxidase (MPO) levels were determined. Serum Tumor Necrosis Factor (TNF)-α, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and MPO levels of blood samples were also measured. RESULTS:Among the histopathological changes in the liver tissue after IRI, differences between groups were statistically significant in the injury scoring system based on congestion, vacuolization and necrosis levels. Histopathological injury score, plasma MPO, AST, ALT, tissue MPO and tissue MDA values were statistically significantly lower in the treatment groups, prominently in the levosimendan and NAS combination group concerning liver histopathological damage. CONCLUSION:The use of a levosimendan plus NAS combination in liver IRI markedly suppressed inflammation and oxidative stress and significantly reduced liver ischemia-reperfusion injury and can be recommended for decreasing IRI instead of single agent use of levosimendan or NAS.

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“…However, there is a limited number of clinical and experimental studies on distal organ I-R-related liver injury. In literature, there two studies that have reported the histopathological and biochemical effects of distal organ ischemia reperfusion on liver [ 17 ] . Based on similar studies, we planned to use I-R duration as 60 minutes of ischemia and 120 minutes of reperfusion [ 14 , 16 ] .…”

Section: Discussionmentioning

confidence: 99%

Avoiding Liver Injury with Papaverine and Ascorbic Acid Due to Infrarenal Cross-Clamping: an Experimental Study

Hüseyın

Güçlü

Yüksel

et al. 2017

Braz J Cardiovasc Surg

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ObjectiveIschemia-reperfusion injury after acute ischemia treatment is a serious condition with high mortality and morbidity. Ischemia-reperfusion injury may result in organ failure particularly in kidney, lung, liver, and heart. In our study, we investigated the effects of papaverine and vitamin C on ischemia-reperfusion injury developed in the rat liver after occlusion-reperfusion of rat aorta.Methods32 Sprague-Dawley female rats were randomized into four groups (n=8). Ischemia was induced with infrarenal aortic cross-clamping for 60 minutes; then the clamp was removed and reperfusion was allowed for 120 minutes. While the control group and the ischemia-reperfusion group did not receive any supplementary agent, two other groups received vitamin C and papaverine hydrochloride (papaverine HCL). Liver tissues were evaluated under the light microscope. Histopathological examination was assessed by Suzuki's criteria and results were compared between groups.ResultsIn ischemia-reperfusion group, severe congestion, severe cytoplasmic vacuolization, and parenchymal necrosis over 60% (score 4) were observed. In vitamin C group, mild congestion, mild cytoplasmic vacuolization and parenchymal necrosis below 30% (score 2) were found. In papaverine group, moderate congestion, moderate cytoplasmic vacuolization and parenchymal necrosis below 60% (score 3) were observed.ConclusionAn ischemia of 60 minutes induced on lower extremities causes damaging effects on hepatic tissue. Vitamin C and papaverine are helpful in reducing liver injury after acute ischemia reperfusion and may partially avoid related negative conditions.

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The histopathological effects of levosimendan on liver injury induced by myocardial ischemia and reperfusion

Cited by 5 publications

References 31 publications

MicroRNA-195 Activates Hepatic Stellate Cells In Vitro by Targeting Smad7

MicroRNA-195 Activates Hepatic Stellate Cells In Vitro by Targeting Smad7

A combination of Levosimendan and N-Acetylcysteine shows significant favorable efficacy on experimental liver ischemia/reperfusion injury

Avoiding Liver Injury with Papaverine and Ascorbic Acid Due to Infrarenal Cross-Clamping: an Experimental Study

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