Interferon Signal Transduction of Biphenyl Dimethyl Dicarboxylate/Amantadine and Anti-HBV Activity in HepG2 2.2.15

Joo Seong-Soo; Won Tae-Joon; Kim Min-Jung; Hwang Kwang-Woo; Lee Do-Ik

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자료유형: 학술저널

저자정보: Joo Seong-Soo (Department of Immunology, College of Pharmacy, Chung-Ang University) Won Tae-Joon (Department of Immunology, College of Pharmacy, Chung-Ang University) Kim Min-Jung (Department of Immunology, College of Pharmacy, Chung-Ang University) Hwang Kwang-Woo (Department of Immunology, College of Pharmacy, Chung-Ang University) Lee Do-Ik (Department of Immunology, College of Pharmacy, Chung-Ang University)

저널정보: 대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제29권 제5호

발행연도: 2006.1

수록면: 405 - 411 (7page)

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Biphenyl dimethyl dicarboxylate (DDB) is a hepatoprotectant, which is used as an adjuvant agent in a treatment for chronic hepatitis. Amantadine is an antiviral agent, which is utilized primarily in the treatment of influenza, but also, occasionally in the treatment of hepatitis C. In a previous study, we reported that DDB, coupled with amantadine, would exert an anti-HBV effect, via the induction of interferon-inducible gene expression in the HepG2 2.2.15 cell line. The primary objective of the present study was to determine whether or not DDB and/or amantadine exhibit anti-HBV properties, and what mechanisms of action might be involved in such properties. In our study, we were able to determine that DDB stimulates Jak/Stat signaling, and induces the expression of interferon alpha $(IFN-\alpha)$ stimulated genes, most notably 6-16 and ISG12. In addition, the antiviral effectors induced by $IFN-\alpha$, PKR, OAS, and MxA, were regulated in the presence of DDB at its optimal concentration $(250{\mu}g/mL)$, to a degree commensurate with the degree of induction associated with the $IFN-\alpha$ treated group. Finally, we determined that the replication of pregenomic RNA and HBeAg was inhibited by DDB treatment, and this inhibition was maximized when coupled with the administration of amantadine $(25{\mu}g/mL)$. In conclusion, the results of this study demonstrated clearly that DDB, as well as the combination of DDB/amantadine, directly inhibited $IFN-\alpha$ signaling-mediated replication of HBV in infected hepatocytes, and thus may represent a novel treatment for chronic hepatitis B, which would be characterized principally by its improved safety over other treatment strategies.

#DDB #Amantadine #Chronic hepatitis B #Interferon alpha #Jak/Stat #6-16 #ISG12

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