Planta Med 2019; 85(18): 1518
DOI: 10.1055/s-0039-3399973
Main Congress Poster
Poster Session 2
© Georg Thieme Verlag KG Stuttgart · New York

Branched-chain amino acids (BCAAs) promotes liver regeneration by decreasing SOCS3 expression to enhance IL-6/STAT3 proliferative signals

E Ceyhan
1  Department of Biology, Faculty of Science, Eskisehir Osmangazi University,, 26480 Eskisehir, Turkey
,
BD Ozen
1  Department of Biology, Faculty of Science, Eskisehir Osmangazi University,, 26480 Eskisehir, Turkey
,
A Ozen
1  Department of Biology, Faculty of Science, Eskisehir Osmangazi University,, 26480 Eskisehir, Turkey
,
B Berber
2  Eskisehir Technical University,, Department of Biology, Faculty of Science, 26210 Eskisehir, Turkey
,
L Rasulzade
1  Department of Biology, Faculty of Science, Eskisehir Osmangazi University,, 26480 Eskisehir, Turkey
,
M Uyanoglu
1  Department of Biology, Faculty of Science, Eskisehir Osmangazi University,, 26480 Eskisehir, Turkey
› Author Affiliations
Further Information

Publication History

Publication Date:
20 December 2019 (online)

 
 

Liver regeneration is one of the primary clinical importance in the setting of liver injury, resection, and transplantation [1],[2]. Although some amino acids are recognized to have favorable effects on the liver regeneration after partial hepatectomy (PH), molecular mechanisms underlying these effects are barely known [3].

We aimed to investigate the effects of valine, glutamine, and leucine amino acids on PH-induced NF-κB signal pathway.

Expressions of 8 genes involving in the NF-κB signal pathway was examined by an RT-PCR method in the liver tissue specimen. In our study, the effect of Leucine amino acid, a kind of Branched Chain Amino Acid (BCAA) on liver regeneration after PH in rats, was determined by RT-PCR, Western blot, and PCNA. Results showed that significantly decreased BCAA-induced upregulation of STAT-3, SOCS3, and NF-κB. However, IL-6 levels significantly increased in all groups.

In summary, demonstrating that BCAA enhances IL-6 proliferative signals in hepatocytes through down-regulation of SOCS3 while decreasing IL-6 levels and reducing its pro-inflammatory signals, all of which optimize liver regeneration. SOCS3 plays a dual role in modulating the rate of hepatocyte proliferation. In particular, this is the first demonstration of an endogenous mechanism to limit hepatocyte proliferation after injury.

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