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Cyclosporin a inhibits albumin synthesis in Huh7 cells.

AbstractBACKGROUND/AIMS:
Hypoalbuminemia occurs frequently in renal transplant recipients immediately after renal transplantation. We studied the regulation of hepatic albumin synthesis by cyclosporin A (CsA) in Huh7 cells.
METHODS:
Huh7 cells were incubated with various concentrations of CsA for 4, 8, 16, and 24 hours. Albumin was measured in Huh7 cell-conditioned medium by sandwich enzyme-linked immunosorbent assay and Western blot. Albumin mRNA expression was analyzed by Northern blotting in CsA-treated cells.
RESULTS:
CsA (10(-7)-10(-4) M) inhibited albumin synthesis in Huh7 cells in a dose- dependent manner. A Western blot analysis for albumin in the conditioned medium released from CsA-treated (10(-7)-10(-5) M) cells also showed significant inhibition of albumin synthesis in a dose-dependent manner. Vehicle (olive oil) did not affect albumin synthesis. In contrast, a Northern blot analysis revealed no inhibition of albumin mRNA expression by CsA at any time point from 1-24 hours, indicating that the inhibition of albumin synthesis occurred at the translational level.
CONCLUSIONS:
Our results suggest that inhibition of hepatic albumin synthesis by high dose CsA contributes to the hypoalbuminemia in renal transplant recipients.
AuthorsYoun Joo Jeon, Yong Soo Kim
JournalThe Korean journal of internal medicine (Korean J Intern Med) Vol. 26 Issue 3 Pg. 314-9 (Sep 2011) ISSN: 2005-6648 [Electronic] Korea (South)
PMID22016592 (Publication Type: Journal Article)
Chemical References
  • Culture Media, Conditioned
  • Immunosuppressive Agents
  • RNA, Messenger
  • Serum Albumin
  • Cyclosporine
Topics
  • Blotting, Northern
  • Blotting, Western
  • Carcinoma, Hepatocellular (genetics, metabolism)
  • Cell Line, Tumor
  • Cell Survival (drug effects)
  • Culture Media, Conditioned (metabolism)
  • Cyclosporine (pharmacology, toxicity)
  • Dose-Response Relationship, Drug
  • Enzyme-Linked Immunosorbent Assay
  • Gene Expression Regulation, Neoplastic (drug effects)
  • Humans
  • Hypoalbuminemia (chemically induced, metabolism)
  • Immunosuppressive Agents (pharmacology, toxicity)
  • Liver Neoplasms (genetics, metabolism)
  • RNA, Messenger (metabolism)
  • Serum Albumin (genetics, metabolism)
  • Time Factors

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