scholarly journals Chicoric acid ameliorate inflammation and oxidative stress in Lipopolysaccharide and d ‐galactosamine induced acute liver injury

2020 ◽  
Vol 24 (5) ◽  
pp. 3022-3033 ◽  
Author(s):  
Zheng Li ◽  
Haihua Feng ◽  
Lu Han ◽  
Lu Ding ◽  
Bingyu Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Chicoric Acid ◽  
And Oxidative Stress

scholarly journals Boldine Supplementation Regulates Mitochondrial Function and Oxidative Stress in a Rat Model of Hepatotoxicity

2019 ◽  
Vol 25 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Reza Heidari ◽  
Mohammad Reza Arabnezhad ◽  
Mohammad Mehdi Ommati ◽  
Negar Azarpira ◽  
Elham Ghodsimanesh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Liver Tissue ◽  
Acute Liver Injury ◽  
Experimental Models ◽  
Clinical Value ◽  
Protective Properties ◽  
Markers Of Oxidative Stress ◽  
Dehydrogenases Activity ◽  
And Oxidative Stress

Background: The xenobiotics-induced liver injury is a clinical complication. Hence, finding new hepatoprotective strategies has clinical value. Oxidative stress and its subsequent complications are major mechanisms involved in xenobiotics-induced hepatotoxicity. Boldine is one of the most potent antioxidant molecules widely investigated for its protective properties in different experimental models. In the current study, the hepatoprotective properties of boldine and its potential mechanisms of hepatoprotection have been investigated. Methods: Rats received thioacetamide (TAA; 200 mg/kg, i.p) as a model of acute liver injury. Boldine (5, 10, 1nd 20 mg/kg; 24 hours intervals; oral) was administered as the hepatoprotective agent. Results: Liver injury was evident in TAA-treated animals (48 hours after TAA exposure) as a severe increase in serum level of liver injury biomarkers and histopathological alterations. Moreover, markers of oxidative stress were increased in liver tissue of TAA-treated rats. Assessment of mitochondrial indices of functionality revealed a significant decrease in mitochondrial dehydrogenases activity, the collapse of mitochondrial membrane potential, mitochondrial swelling and depletion of ATP content. It was found that boldine supplementation mitigated liver tissue markers of oxidative stress and improved mitochondrial indices of functionality in TAA-treated animals. Conclusion: The hepatoprotective properties of boldine might primarily rely on antioxidant and mitochondria protecting effects of this alkaloid.

scholarly journals Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. S. Bruells ◽  
P. Duschner ◽  
G. Marx ◽  
G. Gayan-Ramirez ◽  
N. Frank ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Liver Injury ◽  
Liver Damage ◽  
Acute Liver Injury ◽  
Serum Levels ◽  
Acute Liver Damage ◽  
Markers Of Inflammation ◽  
Amino Phenol ◽  
And Oxidative Stress

AbstractN-acetyl-para-amino phenol (APAP, usually named paracetamol), which is commonly used for its analgesic and antipyretic properties may lead to hepatotoxicity and acute liver damage in case of overdoses. Released cytokines and oxidative stress following acute liver damage may affect other organs’ function notably the diaphragm, which is particularly sensitive to oxidative stress and circulating cytokines. We addressed this issue in a mouse model of acute liver injury induced by administration of APAP. C57BL/6J mice (each n = 8) were treated with N-acetyl-para-amino phenol (APAP) to induce acute drug caused liver injury and sacrificed 12 or 24 h afterwards. An untreated group served as controls. Key markers of inflammation, proteolysis, autophagy and oxidative stress were measured in diaphragm samples. In APAP treated animals, liver damage was proven by the enhanced serum levels of alanine aminotransferase and aspartate aminotransferase. In the diaphragm, besides a significant increase in IL 6 and lipid peroxidation, no changes were observed in key markers of the proteolytic, and autophagy signaling pathways, other inflammatory markers and fiber dimensions. The first 24 h of acute liver damage did not impair diaphragm atrophic pathways although it slightly enhanced IL-6 and lipid peroxidation. Whether longer exposure might affect the diaphragm needs to be addressed in future experiments.

Cytoprotective potential of tiron and methyl palmitate against acetaminophen-induced acute liver injury

2016 ◽  
Vol 94 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Amal M. Shoeib ◽  
Eman Said ◽  
Elsayed M. Ammar
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Inflammatory Response ◽  
Biochemical Markers ◽  
Methyl Palmitate ◽  
Inflammatory Cytokine ◽  
Acute Liver Injury ◽  
Histopathological Examination ◽  
Hepatoprotective Effects ◽  
And Oxidative Stress

Acute liver injury is a debilitating disorder associated with loss of synthetic and detoxifying functions of the liver. This investigation was designed to assess cytoprotective efficacy of daily oral tiron (300 mg/kg) and daily oral methyl palmitate (300 mg/kg) against acetaminophen-induced acute liver injury. Rats were orally pretreated with either tiron or methyl palmitate at doses (300 mg/kg) for 7 days prior to oral acetaminophen (3 g/kg). Biochemical assay of markers of hepatotoxicity indices and oxidative stress was undertaken. Expression of inflammatory cytokine IL-6 was also evaluated. Histopathological examination of liver specimens was carried out as well. Both methyl palmitate and tiron significantly reversed the acetaminophen-induced elevation of biochemical markers (ALT, AST, and ALP) with restoration of SOD levels. Serum albumin levels and GSH liver contents increased, but in a nonsignificant manner. Moreover, methyl palmitate and tiron significantly decreased the level of serum LDH and serum IL-6 levels. Histopathology revealed that tiron markedly reduced the extent of acetaminophen-induced necrosis and methyl palmitate moderately decreased the necrosis in liver tissue. Methyl palmitate (300 mg/kg) and tiron (300 mg/kg) demonstrated promising hepatoprotective effects against acetaminophen-induced acute liver injury via modulation of inflammatory response and alleviation of the oxidative stress, allowing the preservation of hepatic functions.

Sinomenine attenuates alcohol-induced acute liver injury via inhibiting oxidative stress, inflammation and apoptosis in mice

2021 ◽  
pp. 112759
Author(s):  
Hui Fan ◽  
Tingting Tu ◽  
Xiao Zhang ◽  
Qiankun Yang ◽  
Jinxin Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Acute Liver Injury
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