Antiviral Agents ; pharmacology ; Humans ; Interferons ; pharmacology ; Pharmacology, Clinical

Antiviral Agents ; pharmacology ; Hepatitis B virus ; drug effects ; Interferons ; pharmacology

Drug Resistance, Viral ; Endopeptidases ; Hepatitis B virus ; drug effects ; Hepatitis B, Chronic ; virology ; Humans ; Interferons ; pharmacology

OBJECTIVETo study the expression of gene associated with retinoid-interferon-induced mortality-19(GRIM-19) in preimplantation embryo of mice and explore its role in embryonic development.

METHODSThe protein and mRNA expressions of GRIM-19 in 2-cell, 4-cell, 8-cell, morula, and blastocyst phases of mice preimplantation embryo were detected by Western blot analysis and Real-time polymerase chain reaction (PCR).

RESULTSGRIM-19 was continuously expressed in every stage of preimplantation embryo of mice. Western blot analysis and Real-time PCR demonstrated a gradual increase of GRIM-19 expression from 2-cell, which reached a peak in 8-cell phase and then decreased progressively.

CONCLUSIONSThe expression of GRIM-19 in mouse preimplantation embryos changes as at different developmental phases. GRIM-19 may play an important role during embryonic development.

Animals ; Blastocyst ; drug effects ; metabolism ; Female ; Interferons ; pharmacology ; Mice ; NADH, NADPH Oxidoreductases ; genetics ; metabolism ; Pregnancy ; RNA, Messenger ; genetics ; Tretinoin ; pharmacology

Hepatitis B virus (HBV) infection is one of the most serious public health problems. HBV infection could lead to hepatitis B, and even further develop into hepatic cirrhosis and hepatocellular carcinoma. Interferon lambda (IFN-λ) is a member of the interferon (IFN) family and an important cytokine for antiviral defense. There are four members in IFN-λ family, including IFN-λ1, IFN-λ2, IFN-λ3, and IFN-λ4. The genetic polymorphisms in the IFN-λ genes are associated with HBV replication and treatment response of HBV patients. In this review, we summarized the roles of genetic polymorphisms of the IFN-λ genes played in HBV infection, disease progression and treatment, with the aim to better understand their function. This review could serve as a reference for the HBV prevention and treatment of HBV patients, as well as for future clinical usage.
Antiviral Agents/pharmacology* ; Hepatitis B/genetics* ; Hepatitis B virus/genetics* ; Humans ; Interferons/pharmacology* ; Liver Neoplasms ; Polymorphism, Genetic ; Virus Replication/genetics*

No abstract available.
Cytokines/pharmacology* ; Gene Expression Regulation ; Genes, MHC Class I* ; Histocompatibility Antigens Class I/biosynthesis* ; Interferons/pharmacology ; Lymphotoxin/pharmacology ; Models, Genetic ; Signal Transduction ; Tumor Necrosis Factor/pharmacology

Amino Acid Sequence ; Hepatitis C, Chronic ; drug therapy ; Humans ; Interferons ; pharmacology ; therapeutic use ; Viral Nonstructural Proteins ; chemistry ; drug effects ; genetics

Adult ; Blood Donors ; Hepacivirus ; drug effects ; genetics ; Hepatitis C, Chronic ; virology ; Humans ; Interferons ; pharmacology ; Middle Aged ; Viral Load

OBJECTIVE: To study the effect of 5-aminoimidazole-4-formamide ribonucleotide (AICAR) combined with interferon (IFN-α-2b) on the proliferation and apoptosis of chronic myeloid leukemia K562 cells, and explore its possible mechanism. METHODS: CCK-8 method was used to detect the inhibition of cell proliferation. Wright Giemsa method was used to stain and cell morphology was observed by light microscopy. FITC Annexin V/PI double staining method was used to analyze the change of apoptosis rate. Immunocytochemistry method was used to detect the expression of wild-type P53 protein. RESULTS: Different concentration of AICAR was inhibitory effect on K562 cells at different time point of action for 24 h, 48 h, and 72 h, and the inhibition was time and dose-dependent (r=0.71, r=0.84). The combination of AICAR and IFN-α-2b could effectively inhibit the proliferation and promote apoptosis of K562 cells. The inhibition rate of K562 cells was (45.26±2.54)%, and the early apoptosis rate was (33.72±0.23)%, which was statistically significantly different from the control group, AICAR or IFN-ɑ-2b alone (P<0.05). The combination of two drugs promoted the expression of wild-type p53 protein. CONCLUSION AICAR and/or IFN-ɑ-2b can inhibit the cell proliferation and promote the apoptosis of K562 cells. The combination of two drugs shows synergistic antitumor effect, and its mechanism may be related to the promotion of high expression of wild-type p53 protein.
Apoptosis ; Cell Proliferation ; Formamides ; Humans ; Imidazoles ; Interferons ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Ribonucleotides/pharmacology*

In addition to immune regulation, interferon could suppress hepatitis B virus (HBV) replication through direct antiviral effect. After binding with the receptors on cell membrane, interferon directly inhibits HBV at different steps in HBV replication cycle by activating cell signaling cascades such as JAK-STAT pathway, interferon regulatory factor (IRFs) signaling pathway, and so on, followed by inducing a series of cytokines which are involved in regulation of the function of HBV enhancer I / X promoter (Ehn I / Xp). Also, interferon could induce the host cells to produce anti-viral proteins. This review describes the direct antiviral mechanism of interferon on HBV.
Animals ; Antiviral Agents ; pharmacology ; Hepatitis B virus ; drug effects ; physiology ; Humans ; Interferons ; classification ; pharmacology ; Signal Transduction ; drug effects ; Virus Replication ; drug effects