scholarly journals Sulforaphane protects against sodium valproate–induced acute liver injury

2017 ◽  
Vol 95 (4) ◽  
pp. 420-426 ◽  
Author(s):  
Entsar A. Nazmy ◽  
Omar A. El-Khouly ◽  
Hoda Atef ◽  
Eman Said
Keyword(s):  
Liver Injury ◽  
Sodium Valproate ◽  
Acute Liver Injury ◽  
Heme Oxygenase 1 ◽  
Albumin Concentration ◽  
Drug Induced ◽  
Biochemical Alterations ◽  
Factor Α ◽  
Cruciferous Plants ◽  
Necrosis Factor

Drug-induced hepatotoxicity is one of the most commonly encountered obstacles in the field of medical practice. Sodium valproate (VPA) is among many drugs with reported hepatotoxic effects. Sulforaphane (SFN) is a thiol compound found in wide abundance in cruciferous plants that has numerous reported therapeutic efficacies. The current investigation sheds light on the potential hepatoprotective effect of SFN against VPA-induced liver injury in rats. Twice daily VPA (700 mg/kg, i.p.) for 7 days induced significant biochemical alterations and hepatic histopathological damage. SFN (0.5 mg/kg, orally) for 7 days significantly boosted liver function biomarkers; it reduced serum alanine transaminase, aspartate aminotransferase, and alkaline phosphatase, and restored serum albumin concentration in a significant manner. Meanwhile, SFN significantly mitigated VPA-induced histopathological alterations. To highlight the mechanisms implicated in the observed hepatoprotective action, hepatic malondialdehyde and tumour necrosis factor α content significantly declined with concomitant increase in hepatic heme oxygenase-1 content and glutathione concentration with SFN treatment. In conclusion, SFN can significantly ameliorate VPA-induced hepatotoxicity and liver injury primarily by direct association between antioxidant and anti-inflammatory properties.

Expression of Tumor Necrosis Factor-α and Transforming Growth Factor-β1 in Acute Liver Injury

1989 ◽  
Vol 1 (3) ◽  
pp. 219-226 ◽  
Author(s):  
Mark J. Czaja ◽  
Kathleen C. Flanders ◽  
Luis Biempica ◽  
Charna Klein ◽  
Mark A. Zern ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Acute Liver Injury ◽  
Transforming Growth Factor Β1 ◽  
Factor Α ◽  
Necrosis Factor

Effects of OPC-6535 on lipopolysaccharide-induced acute liver injury in the rat: Involvement of superoxide and tumor necrosis factor-α from hepatic macrophages

Surgery ◽  
2003 ◽  
Vol 134 (5) ◽  
pp. 818-826 ◽  
Author(s):  
Tadashi Hasegawa ◽  
Kazushi Sakurai ◽  
Yasuhiro Kambayashi ◽  
Abby R Saniabadi ◽  
Hisashi Nagamoto ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Acute Liver Injury ◽  
Hepatic Macrophages ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Effectiveness of Probiotics and Prebiotics Against Acute Liver Injury: A Meta-Analysis

2021 ◽  
Vol 8 ◽  
Author(s):  
Sheng Xu ◽  
Min Zhao ◽  
Qinjian Wang ◽  
Zhihua Xu ◽  
Binhui Pan ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Meta Analysis ◽  
Clinical Syndrome ◽  
Cochrane Library ◽  
Search Terms ◽  
Junction Protein ◽  
Life Threatening ◽  
Factor Α ◽  
Necrosis Factor

Background and Aims: Acute liver injury (ALI) is a clinical syndrome characterized by rapid loss of liver function, which may progress to life-threatening liver failure. We conducted this meta-analysis to examine the evidence on the effects of probiotics or prebiotics on ALI.Methods and Results: Several databases, including PubMed, EMBASE, and Cochrane Library, were scrutinized from the inception through February 2021 by combining key search terms, yielding 26 eligible studies, which concluded that modulation of gut microbiota significantly decreased aspartate transaminase [standardized mean difference (SMD): −1.51, 95% confidence interval (CI): −2.03 to −1.00], alanine aminotransferase (SMD: −1.42, 95% CI: −1.85 to −0.98), and bilirubin (SMD: −0.91, 95% CI: −1.33 to −0.49). In addition, administration of probiotics or prebiotics also promoted proliferation of Bifidobacterium (SMD: 1.21, 95% CI: −0.18 to 2.60) and inhibited Enterococcus (SMD: −1.00, 95% CI: −1.39 to −0.61), contributing to lower levels of endotoxin (SMD: −2.14, 95% CI: −2.91 to −1.37). Tight junction protein ZO-1 (SMD: 1.95, 95% CI: 0.14 to 3.76) was upregulated after intervention, thereby reducing bacterial translocation to the liver [odds ratio (OR) = 0.23, 95% CI: 0.13–0.44] and mesenteric lymph node (OR = 0.14, 95% CI: 0.08 to 0.26), with decreased tumor necrosis factor-α (SMD: −2.84, 95% CI: −3.76 to −1.93) and interleukin-6 (SMD: −2.62, 95% CI: −4.14 to −1.10). Oxidative stress was also relieved by reducing malondialdehyde (SMD: −1.83, 95% CI: −2.55 to −1.10) while elevating superoxide dismutase (SMD: 1.78, 95% CI: 1.00–2.55) and glutathione (SMD: 1.83, 95% CI: 0.76–2.91).Conclusion: Our findings suggest that probiotics and prebiotics could be a promising therapeutic strategy in ALI and possess a potential for clinical applications.Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=255888, CRD42021255888.

scholarly journals Hepatoprotective Effects of Heracleum candicans Against Carbon Tetrachloride-Induced Acute Liver Injury in Rats

Dose-Response ◽  
2021 ◽  
Vol 19 (3) ◽  
pp. 155932582110295
Author(s):  
Jie Li ◽  
Dan Song ◽  
Bintao Zhang ◽  
Jinwei Guo ◽  
Wenping Li ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Neutrophil Infiltration ◽  
Antioxidant Enzyme Activity ◽  
Necrosis Factor Alpha ◽  
Heracleum Candicans ◽  
The Face ◽  
Factor Alpha ◽  
Necrosis Factor

Purpose: To determine the hepatoprotective mechanisms of Heracleum candicans in rats with acute liver injury induced by carbon tetrachloride (CCl4). Methods: Rats were intragastrically administered H candicans twice a day for 14 consecutive days and were intraperitoneally challenged with CCl4. Alanine aminotransferase and aspartate aminotransferase were measured to indicate liver injury. Malondialdehyde antioxidant enzyme activity and tumor necrosis factor-alpha and interleukin 6 secretion were measured as liver injury indicators. Histopathological tests were conducted to determine whether H candicans ameliorated liver injury. Results: CCl4-induced liver injury led to significant increases in liver injury biochemical indicators transaminase and malondialdehyde activities. H candicans pretreatments inhibited these increases. Pathological sections in pretreated samples exhibited reduced vacuole formation, neutrophil infiltration, and necrosis. Conclusion: H candicans increases the antioxidant capacity of the liver and maintains hepatocyte function in the face of CCl4-induced injury.

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