The hydroalcoholic extract of watercress attenuates protein oxidation, oxidative stress, and liver damage after bile duct ligation in rats

Herbal medicines harbor essential therapeutic agents for the treatment of cholestasis. In this study, we have assessed the anticholestatic potential of Stachys pilifera Benth’s (SPB’s) hydroalcoholic extract encapsulated into liposomes using bile duct ligation- (BDL-) induced hepatic cholestasis in rats. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), malondialdehyde (MDA), total thiol (T-SH) content, protein carbonyl (PCO), total bilirubin (TBIL), albumin (ALB), and nitric oxide (NO) metabolite levels were measured in either liver tissue or plasma to assess liver damage. Moreover, expression of proinflammatory cytokines (IL-1β and TNF-α) and liver fibrosis markers (TGF-β and SM-α) which are driving forces of many liver disorders was also determined. The activity of AST, ALT, and ALP was significantly enhanced in the BDL group in comparison to the control group; however, treatment with liposomal (SPB) hydroalcoholic extract significantly reduced AST and ALT’s activity. Increases in MDA, TBIL, and NO levels and T-SH content due to BDL were restored to control levels by liposomal (SPB) hydroalcoholic extract treatment. Similarly, hepatic and plasma oxidative marker MDA levels, significantly enhanced by BDL, were significantly decreased by liposomal (SPB) hydroalcoholic extract treatment. Moreover, histopathological findings further demonstrated a significant decrease in hepatic damage in the liposomal (SPB) hydroalcoholic extract-treated BDL group. In addition, liposomal (SPB) hydroalcoholic extract treatment decreased the liver expression of inflammatory cytokines (IL-1β, TNF-α) and liver fibrosis markers (TGF-β and SM-α). Since liposomal (SPB) hydroalcoholic extract treatment alleviated the BDL-induced injury of the liver and improved the hepatic structure and function more efficiently in comparison to free SPB hydroalcoholic extract, probable liposomal (SPB) hydroalcoholic extract exhibits required potential therapeutic value in protecting the liver against BDL-caused oxidative injury.

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Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats

Research in Pharmaceutical Sciences ◽

10.4103/1735-5362.253359 ◽

2019 ◽

Vol 14 (2) ◽

pp. 122 ◽

Cited By ~ 13

Author(s):

Heibatollah Sadeghi ◽

Fatemeh Jahanbazi ◽

Hossein Sadeghi ◽

Navid Omidifar ◽

Behnam Alipoor ◽

...

Keyword(s):

Oxidative Stress ◽

Bile Duct ◽

Liver Damage ◽

Bile Duct Ligation ◽

Duct Ligation

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THE HYDROALCOHOLIC EXTRACT OF ROSMARINUS OFFICINALIS ATTENUATES LIVER DAMAGE AFTER BILE-DUCT LIGATION IN RATS

The Journal of Animal and Plant Sciences - February ◽

10.36899/japs.2021.2.0232 ◽

2020 ◽

Vol 31 (2) ◽

Keyword(s):

Bile Duct ◽

Liver Damage ◽

Bile Duct Ligation ◽

Rosmarinus Officinalis ◽

Hydroalcoholic Extract ◽

Duct Ligation

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Dose-related effects of dexamethasone on liver damage due to bile duct ligation in rats

World Journal of Gastroenterology ◽

10.3748/wjg.v12.i33.5379 ◽

2006 ◽

Vol 12 (33) ◽

pp. 5379 ◽

Cited By ~ 10

Author(s):

Halil Eken

Keyword(s):

Bile Duct ◽

Liver Damage ◽

Bile Duct Ligation ◽

Duct Ligation

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Cell-specific regulatory effects of CXCR2 on cholestatic liver injury

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00080.2019 ◽

2019 ◽

Vol 317 (6) ◽

pp. G773-G783 ◽

Cited By ~ 2

Author(s):

Takanori Konishi ◽

Rebecca M. Schuster ◽

Holly S. Goetzman ◽

Charles C. Caldwell ◽

Alex B. Lentsch

Keyword(s):

Bile Duct ◽

Liver Injury ◽

Liver Damage ◽

Chemokine Receptor ◽

Therapeutic Target ◽

Bile Duct Ligation ◽

Wild Type ◽

Neutrophil Accumulation ◽

Duct Ligation ◽

Cholestatic Liver Injury

The CXC chemokine receptor 2 (CXCR2) is critical for neutrophil recruitment and hepatocellular viability but has not been studied in the context of cholestatic liver injury following bile duct ligation (BDL). The present study sought to elucidate the cell-specific roles of CXCR2 on acute liver injury after BDL. Wild-type and CXCR2−/− mice were subjected BDL. CXCR2 chimeric mice were created to assess the cell-specific role of CXCR2 on liver injury after BDL. SB225002, a selective CXCR2 antagonist, was administrated intraperitoneally after BDL to investigate the potential of pharmacological inhibition. CXCR2−/− mice had significantly less liver injury than wild-type mice at 3 and 14 days after BDL. There was no difference in biliary fibrosis among groups. The chemokines CXCL1 and CXCL2 were induced around areas of necrosis and biliary structures, respectively, both areas where neutrophils accumulated after BDL. CXCR2−/− mice showed significantly less neutrophil accumulation in those injured areas. CXCR2Liver+/Myeloid+ and CXCR2Liver−/Myeloid− mice recapitulated the wild-type and CXCR2-knockout phenotypes, respectively. CXCR2Liver+/Myeloid+ mice suffered higher liver injury than CXCR2Liver+/Myeloid− and CXCR2Liver−/Myeloid+; however, only those chimeras with knockout of myeloid CXCR2 (CXCR2Liver+/Myeloid− and CXCR2Liver−/Myeloid−) showed reduction of neutrophil accumulation around areas of necrosis. Daily administration of SB225002 starting after 3 days of BDL reduced established liver injury at 6 days. In conclusion, neutrophil CXCR2 guides the cell to the site of injury, while CXCR2 on liver cells affects liver damage independent of neutrophil accumulation. CXCR2 appears to be a viable therapeutic target for cholestatic liver injury. NEW & NOTEWORTHY This study is the first to reveal cell-specific roles of the chemokine receptor CXCR2 in cholestatic liver injury caused by bile duct ligation. CXCR2 on neutrophils facilitates neutrophil recruitment to the liver, while CXCR2 on liver cells contributes to liver damage independent of neutrophils. CXCR2 may represent a viable therapeutic target for cholestatic liver injury.

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CIRRHOSIS INDUCES APOPTOSIS IN RENAL TISSUE THROUGH INTRACELLULAR OXIDATIVE STRESS

Arquivos de Gastroenterologia ◽

10.1590/s0004-28032015000100014 ◽

2015 ◽

Vol 52 (1) ◽

pp. 65-71 ◽

Cited By ~ 5

Author(s):

Keli Cristina Simões da SILVEIRA ◽

Cassiana Macagnan VIAU ◽

Josiane Raskopf COLARES ◽

Jenifer SAFFI ◽

Norma Possa MARRONI ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

Membrane Potential ◽

Bile Duct ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Bile Duct Ligation ◽

Decompensated Cirrhosis ◽

Biliary Cirrhosis ◽

Duct Ligation

Background Renal failure is a frequent and serious complication in patients with decompensated cirrhosis. Objectives We aimed to evaluate the renal oxidative stress, cell damage and impaired cell function in animal model of cirrhosis. Methods Secondary biliary cirrhosis was induced in rats by ligation of the common bile duct. We measured TBARS, ROS and mitochondrial membrane potential in kidney as markers of oxidative stress, and activities of the antioxidant enzymes. Relative cell viability was determined by trypan blue dye-exclusion assay. Annexin V-PE was used with a vital dye, 7-AAD, to distinguish apoptotic from necrotic cells and comet assay was used for determined DNA integrity in single cells. Results In bile duct ligation animals there was significant increase in the kidney lipoperoxidation and an increase of the level of intracellular ROS. There was too an increase in the activity of all antioxidant enzymes evaluated in the kidney. The percentage viability was above 90% in the control group and in bile duct ligation was 64.66% and the dominant cell death type was apoptosis. DNA damage was observed in the bile duct ligation. There was a decreased in the mitochondrial membrane potential from 71.40% ± 6.35% to 34.48% ± 11.40% in bile duct ligation. Conclusions These results indicate that intracellular increase of ROS cause damage in the DNA and apoptosis getting worse the renal function in cirrhosis.

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