scholarly journals Swertianlarin, an Herbal Agent Derived fromSwertia mussotiiFranch, Attenuates Liver Injury, Inflammation, and Cholestasis in Common Bile Duct-Ligated Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Liangjun Zhang ◽  
Ying Cheng ◽  
Xiaohuang Du ◽  
Sheng Chen ◽  
Xinchan Feng ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Bile Salt ◽  
Deoxycholic Acid ◽  
Necrosis Factor Alpha ◽  
Liver Histopathology ◽  
Duct Ligation ◽  
Chinese Traditional Herb ◽  
Factor Alpha ◽  
Necrosis Factor

Swertianlarin is an herbal agent abundantly distributed inSwertia mussotiiFranch, a Chinese traditional herb used for treatment of jaundice. To study the therapeutic effect of swertianlarin on cholestasis, liver injury, serum proinflammatory cytokines, and bile salt concentrations were measured by comparing rats treated with swertianlarin 100 mg/kg/d or saline for 3, 7, or 14 days after bile duct ligation (BDL). Serum alanine aminotransferase (ATL) and aspartate aminotransferase (AST) levels were significantly decreased in BDL rats treated with swertianlarin for 14 days (P<0.05). The reduced liver injury in BDL rats by swertianlarin treatment for 14 days was further confirmed by liver histopathology. Levels of serum tumor necrosis factor alpha (TNFα) were decreased by swertianlarin in BDL rats for 3 and 7 days (P<0.05). Moreover, reductions in serum interleukins IL-1βand IL-6 levels were also observed in BDL rats treated with swertianlarin (P<0.05). In addition, most of serum toxic bile salt concentrations (e.g., chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA)) in cholestatic rats were decreased by swertianlarin (P<0.05). In conclusion, the data suggest that swertianlarin derived fromSwertia mussotiiFranch attenuates liver injury, inflammation, and cholestasis in bile duct-ligated rats.

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.

The Possible Protective Effect of Selenium on Liver Dysfunction in a Rat Model of Extrahepatic Cholestasis

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Fatma M Lebda ◽  
Sahar M El Agaty ◽  
Noha A Nassef ◽  
Marina A Aziz
Keyword(s):  
Bile Duct ◽  
Transforming Growth Factor ◽  
Group Versus ◽  
Serum Levels ◽  
Selenium Supplementation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Tgf Β1 ◽  
Necrosis Factor

Abstract Background Oxidative stress and inflammation are primarily implicated in the development and progression of liver injury during cholestasis. Selenium, a known essential antioxidant trace element, was found to provide a remarkable antioxidant and anti-inflammatory effects on various diseases. Aim This study was planned to evaluate the possible protective effect of selenium supplementation in a rat model of chronic cholestasis. Design Experimental study. Methods This study was carried out on adult male rats allocated randomly into sham, bile duct ligated (BDL), and BDL-selenium treated (BDL-Se) groups. Sodium selenite was given by gavage daily, in a dose of 100 µg/kg for 6 weeks, starting 2 weeks before the BDL. Results BDL group presented a significant increase in serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and liver levels of malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and transforming growth factor beta 1(TGF-β1), associated with a significant decrease in serum levels of total proteins (TP) compared to sham group . Selenium supplementation significantly lowered serum levels of AST, ALT, ALP, and liver levels of MDA, TNF-α, and TGF-β1 along with a significant increase in serum TP in BDL-Se group versus BDL rats. Histological analysis of liver showed a significant attenuation of the inflammatory score and a significant decrease in the percentage area of collagen deposition in BDL-Se group versus BDL rats. Conclusion Selenium supplementation reduces liver injury and improves liver functions in experimental cholestasis probably by its antioxidant and anti-inflammatory activities, which further alleviate the liver fibrosis. Abbreviations BDL: bile duct ligated group, BDL-Se: bile duct ligated-selenium group, MDA: malondialdehyde, TNF-α: tumour necrosis factor-alpha, TGF-β1: transforming growth factor- beta1, ROS: reactive oxygen species, mRNA: messenger RNA, IL-6: interleukin-6, BW: body weight, AST: aspartate aminotransferase, ALT: alanine aminotransferase, ALP: alkaline phosphatase, TP: total proteins, CCl4: carbon tetrachloride, GPx: glutathione peroxidase enzyme, SOD: superoxide dismutase, IL-1: interleukin-1.

Tumor necrosis factor-alpha stimulates adrenal glucocorticoid secretion in cholestatic rats

1996 ◽  
Vol 270 (6) ◽  
pp. G987-G991 ◽  
Author(s):  
M. G. Swain ◽  
M. Maric
Keyword(s):  
Bile Duct ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Corticosterone Secretion ◽  
Factor Alpha ◽  
Adrenal Corticosterone ◽  
Necrosis Factor

Tumor necrosis factor-alpha (TNF-alpha ) is capable of activating the hypothalamic-pituitary-adrenal (HPA) axis. We have recently documented altered activation of this axis by endotoxin and interleukin-1 in cholestatic rats. Therefore, in this study, we examined TNF-alpha-induced activation of the HPA axis, in rats with cholestasis due to bile duct resection, with the use of sham-resected rats as controls. Administration of TNF-alpha to bile duct- and sham-resected rats in vivo resulted in a similar increase in plasma adrenocorticotropic hormone levels in both groups of animals but significantly higher corticosterone levels in cholestatic rats, suggesting a direct steroidogenic effect of TNF-alpha in cholestatic rats. This suggestion was confirmed in further experiments by the demonstration of TNF-alpha-induced corticosterone secretion in hypophysectomized cholestatic but not control rats. Furthermore, a direct stimulatory effect of TNF-alpha on adrenal corticosterone secretion in vitro was noted only for cholestatic rats, possibly via augmented adrenal prostaglandin E2 (PGE2) production. These results indicate that TNF-alpha has a direct stimulatory effect on adrenal corticosterone secretion in cholestatic rats, possibly due to augmented adrenal PGE2 release.

Tumor necrosis factor–alpha decreases hepatocyte bile salt uptake and mediates endotoxin-induced cholestasis

Hepatology ◽  
1995 ◽  
Vol 22 (4) ◽  
pp. 1273-1278 ◽  
Author(s):  
James F. Whiting ◽  
Richard M. Green ◽  
Adam B. Rosenbluth ◽  
John L. Gollan
Keyword(s):  
Tumor Necrosis Factor ◽  
Bile Salt ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Salt Uptake ◽  
Factor Alpha ◽  
Necrosis Factor
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