Inhibitory effect of MIL glycoprotein on expression of pro-inflammatory mediators in carbon tetrachloride-induced mice liver damage

2010 ◽  
Vol 30 (8) ◽  
pp. 754-760 ◽  
Author(s):  
Phil-Sun Oh ◽  
Jin Lee ◽  
Kye-Taek Lim
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage ◽  
Inflammatory Mediators ◽  
Inhibitory Effect ◽  
Mice Liver

Hepatoprotective Efficacy of Sharbat-e-Deenar Against Carbon Tetrachloride−Induced Liver Damage

2012 ◽  
Vol 31 (2) ◽  
pp. 131-141 ◽  
Author(s):  
Arvind Kumar Shakya ◽  
Monika Saxena ◽  
Neetu Sharma ◽  
Sadhana Shrivastava ◽  
Sangeeta Shukla
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage

EFFECT OF MMSC AND HSC ON REPARATIVE REGENERATION OF THE LIVER UNDER CONDITIONS OF ITS TOXIC DAMAGE

2020 ◽  
Vol 17 (3) ◽  
pp. 243-248
Author(s):  
I.Yu. Maklakova ◽  
◽  
V.V. Bazarniy ◽  
D.Yu. Grebnev ◽  
◽  
...  
Keyword(s):  
Dna Repair ◽  
Carbon Tetrachloride ◽  
Mitotic Activity ◽  
Liver Damage ◽  
Inflammatory Activity ◽  
Control Group ◽  
Nacl Solution ◽  
Repair Enzymes ◽  
Toxic Liver Damage ◽  
Hsc Transplantation

The aim of this study was to study the effect of combined MMSC and HSC transplantation on liver regeneration under conditions of toxic carbon tetrachloride damage. Materials and methods. The study was performed on white male mice with toxic liver damage by intraperitoneal administration of carbon tetrachloride at a dose of 50 µl per mouse once. An hour after modeling liver damage, placental MMSCs and HSCs were administered intravenously at a dose of 4 million cells/kg and 330 thousand cells/kg, respectively, suspended in 0.2 ml of 0.9% NaCl solution. Control group animals were given 0.9% NaCl solution-0.2 ml intravenously. On days 1, 3, and 7 after cell transplantation, changes in inflammatory activity in the liver were evaluated, and mitotic and apoptotic indices were determined. On the 7th day after the introduction of cells, the activity of DNA repair enzymes of the PARP family was analyzed. Results. Combined MMSC and HSC transplantation leads to a decrease in the index of inflammatory activity in the liver due to a decrease in necrosis, hepatocyte dystrophy, and a decrease in infiltration. As a result of the study, an increase in the activity of PARP repair enzymes was found, which led to a decrease in programmed cell death. Also, cotransplantation of MMSCs and HSCs was accompanied by increased mitotic activity of hepatocytes. Conclusion. Cotransplantation of MMSCs and HSCs under conditions of toxic liver damage reduces the inflammatory response, stimulates the mitotic activity of hepatocytes, and increases the activity of enzymes of the DNA repair system. Activation of the liver's reparative system, in turn, reduces the programmed death of hepatocytes.

Hepatoprotective activity ofTrichilia rokaon carbon tetrachloride-induced liver damage in rats

2001 ◽  
Vol 53 (11) ◽  
pp. 1569-1574 ◽  
Author(s):  
M. P. Germanò ◽  
V. D'Angelo ◽  
R. Sanogo ◽  
A. Morabito ◽  
S. Pergolizzi ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage ◽  
Hepatoprotective Activity

Morin protects acute liver damage by carbon tetrachloride (CCl4) in rat

2008 ◽  
Vol 31 (9) ◽  
pp. 1160-1165 ◽  
Author(s):  
Hee Seung Lee ◽  
Kyung-Hee Jung ◽  
Sang-Won Hong ◽  
In-Suh Park ◽  
Chongmu Lee ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage ◽  
Acute Liver Damage

scholarly journals Adenosine pretreatment attenuates angiotensin II-mediated p38 MAPK activation in a protein kinase A dependent manner

2010 ◽  
Vol 4 (5) ◽  
pp. 721-729
Author(s):  
Hamid Yaghooti ◽  
Mohsen Firoozrai ◽  
Soudabeh Fallah ◽  
Mohammad Reza Khorramizadeh
Keyword(s):  
Angiotensin Ii ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
P38 Mapk ◽  
Inflammatory Mediators ◽  
Endothelial Permeability ◽  
Renin Angiotensin System ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Kinase A

Abstract Background: Adenosine is known as a protective and anti-inflammatory nucleoside. Angiotensin II is the main hormone of the renin-angiotensin system. It is associated with endothelial permeability, recruitment, and activation of the immune cells through induction of inflammatory mediators. Matrix metalloproteinase-9 (MMP-9) plays an important role in inflammatory processes mediated by macrophages. Objectives: Investigate whether adenosine pretreatment modulates angiotensin II-induced MMP-9 expression and activation of signaling molecules. Methods: Human monocytic U-937 cells were treated with either adenosine or angiotensin II alone or angiotensin II following a pretreatment with adenosine. Supernatants were analyzed for MMP-9 activity by zymography method. MMP-9 gene expression was analyzed using real-time PCR. Activation of inflammatory mediators IκB-α, NF-κB, JNK, p38 MAPK, and STAT3 were analyzed by a multi-target ELISA kit. Association of Protein kinase A (PKA) in adenosine effects was studied by pre-incubation with H89, a selective PKA inhibitor. Results: Treatment of the cells with angiotensin II significantly increased MMP-9 production (p <0.05). Adenosine pretreatment did not attenuate this angiotensin II effect. Angiotensin II treatment induced NF-κB, JNK and p38 activation. Pretreatment with adenosine prior to angiotensin II stimulation showed a 40% inhibitory effect on p38 induction (p <0.05). This effect was reversed by PKA inhibition. Conclusion: The present data confirmed that monocytic MMP-9 was a target gene for angiotensin II. Adenosine pretreatment did not inhibit MMP-9 increase in response to angiotensin II. However, it showed a potential inhibitory effect on angiotensin II inflammatory signaling.

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