Perindopril Ameliorates Hepatic Ischemia Reperfusion Injury <i>Via</i> Regulation of NF‐κB‐p65/TLR‐4, JAK1/STAT‐3, Nrf‐2, and PI3K/Akt/mTOR Signaling Pathways

Kamel, Esam O.; Hassanein, Emad H.M.; Ahmed, Marwa A.; Ali, Fares E.M.

doi:10.1002/ar.24292

Cited by 31 publications

(21 citation statements)

References 61 publications

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“…It has been proposed that oxidative stress is a crucial contributor of I/R‐induced neuronal injury (Kamel, Hassanein, Ahmed, & Ali, 2019). Therefore, the level of oxidation‐related markers was measured.…”

Section: Resultsmentioning

confidence: 99%

Xanthoangelol alleviates cerebral ischemia reperfusion injury in rats

Meng

Gao

Huang

2020

The Anatomical Record

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Ischemia/reperfusion (I/R) injury accounts to be a prime cause of neurological deficit following stroke. This study aimed to explore the neuro‐protective effects of Xanthoangelol (XAG) on I/R‐induced injury in both in vivo and in vitro models. Our data demonstrated that XAG can shrink infarct size and brain edema in middle cerebral artery occlusion (MCAO) model. In addition, XAG was capable of alleviating the neurological deficit in rats that have undergone MCAO procedure. Meanwhile, antiapoptotic activities of XAG against I/R‐induced neuronal injury were evidenced and further illustrated that XAG elicits antiapoptotic activities by suppressing excessive oxidative stress via nuclear factor erythroid‐2‐related factor 2 activation. Overall, our study revealed that XAG displayed the potential to be utilized as a neuroprotective agent against I/R‐induced neurological injury.

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Section: Resultsmentioning

confidence: 99%

Xanthoangelol alleviates cerebral ischemia reperfusion injury in rats

Meng

Gao

Huang

2020

The Anatomical Record

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“…Hepatic IR resulted in hepatic injury as proved by increased level of liver enzymes. Hepatic IR causes the disruption of the membrane stability of hepatocytes due to necrosis, cellular damage, and structural changes with release of large quantities of liver enzymes [37][38][39].…”

Section: Discussionmentioning

confidence: 99%

“…Other studies demonstrated that IR results in increased gene expression of both nuclear factor kappa B (NF-kβ) and Toll-like receptor 4 (a protein involved in both innate and adaptive immune system response), which constantly increased TNF-α leading to liver damage [38,49].…”

Section: Discussionmentioning

confidence: 99%

Hepatic ischemia reperfusion injury: effect of moderate intensity exercise and oxytocin compared to l-arginine in a rat model

ELKady

El-Kafoury

Saad

et al. 2021

Egypt Liver Journal

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Background Hepatic ischemia reperfusion (IR) injury is considered as a main cause of liver damage and dysfunction. The l-arginine/nitric oxide pathway seems to be relevant during this process of IR. Although acute intense exercise challenges the liver with increased reactive oxygen species (ROS), regular training improves hepatic antioxidant status. Also, oxytocin (Oxy), besides its classical functions, it exhibits a potent antistress, anti-inflammatory, and antioxidant effects. This study was designed to evaluate the hepatic functional and structural changes induced by hepatic IR injury in rats and to probe the effect and potential mechanism of moderate intensity exercise training and/or Oxy, in comparison to a nitric oxide donor, l-arginine, against liver IR-induced damage. Results Compared to the sham-operated control group, the hepatic IR group displayed a significant increase in serum levels of ALT and AST, plasma levels of MDA and TNF-α, and significant decrease in plasma TAC and nitrite levels together with the worsening of liver histological picture. L-Arg, Oxy, moderate intensity exercise, and the combination of both Oxy and moderate intensity exercises ameliorated these deleterious effects that were evident by the significant decrease in serum levels of ALT and AST, significant elevation in TAC and nitrite, and significant decline in lipid peroxidation (MDA) and TNF-α, besides regression of histopathological score regarding hepatocyte necrosis, vacuolization, and nuclear pyknosis. Both the moderate intensity exercise-trained group and Oxy-treated group showed a significant decline in TNF-α and nitrite levels as compared to l-Arg-treated group. The Oxy-treated group showed statistical insignificant changes in serum levels of ALT, AST, and plasma levels of nitrite, MDA, TAC, and TNF-α as compared to moderate intensity exercise-trained group. Conclusion The combination of both moderate intensity exercise and Oxy displayed more pronounced hepatoprotection on comparison with l-Arg which could be attributed to their more prominent antioxidant and anti-inflammatory effects but not due to their NO-enhancing effect.

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“…In the present study, the liver biochemical indicator levels revealed considerable liver cell injury. AST, ALT, and ALP are biomarkers of liver function [31]. ALT is mainly distributed in hepatocyte cytoplasm, and elevated ALT levels indicate damage of hepatocyte membrane.…”

Section: Discussionmentioning

confidence: 99%

Screening of the Hepatotoxic Components in Fructus Gardeniae and Their Effects on Rat Liver BRL-3A Cells

Lan

et al. 2019

Molecules

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Fructus Gardeniae (FG) is a common Chinese medicine and food. However, the toxicity of FG has drawn increasing concern, especially its hepatotoxicity. The purpose of this study was to screen the hepatotoxic components of FG and evaluate their effects on rat liver BRL-3A cells. The chemical composition of FG was determined by HPLC-ESI-MS. CCK-8 assay was used to evaluate the cytotoxicity of ten chemical components from FG, and then the toxic components with significant inhibitory activity were selected for further study. The results showed that geniposide, genipin, genipin-1-gentiobioside, gardenoside, and shanzhiside all suppress cells viability. Apoptosis assays further indicated that geniposide and its metabolite genipin are the main hepatotoxic components of FG. Pretreatment of cells with geniposide or genipin increased the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). The activities of superoxide dismutase (SOD) and glutathione (GSH) were decreased, while the malondialdehyde (MDA) level was increased. The cell contents of tumor necrosis factor (TNF-α), interleukin-6 (IL-6), and nitric oxide (NO) were also increased. Molecular docking simulations were used to investigate the mechanism of FG-induced hepatotoxicity, revealing that geniposide and genipin bind strongly to the pro-inflammatory factor TNFR1 receptor of the NF-κB and MAPK signaling pathways. The obtained results strongly indicate that the hepatotoxicity of FG is caused by iridoids compounds. Genipin had the most significant hepatotoxic effect. These toxic substances destroy the cell antioxidant defense system, increasing inflammatory injury to the liver cells and leading to apoptosis and even necrosis. Thus, this study lays a foundation for toxicology research into FG and its rational application.

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Perindopril Ameliorates Hepatic Ischemia Reperfusion Injury Via Regulation of NF‐κB‐p65/TLR‐4, JAK1/STAT‐3, Nrf‐2, and PI3K/Akt/mTOR Signaling Pathways

Cited by 31 publications

References 61 publications

Xanthoangelol alleviates cerebral ischemia reperfusion injury in rats

Xanthoangelol alleviates cerebral ischemia reperfusion injury in rats

Hepatic ischemia reperfusion injury: effect of moderate intensity exercise and oxytocin compared to l-arginine in a rat model

Screening of the Hepatotoxic Components in Fructus Gardeniae and Their Effects on Rat Liver BRL-3A Cells

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