Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice.

Background: Complement activation is recognized as an important factor in the progression of liver damage caused by acetaminophen (APAP). However, the role of the complement inhibitor C2-FH in APAP-induced liver injury remains unclear.

Aim: To explore C2-FH in protecting against APAP-induced liver injury by inhibiting complement activation.

Early Application of Auxiliary Partial Orthotopic Liver Transplantation in Murine Model of Wilson Disease.

Background: Liver transplantation (LT) is the only option of treatment for Wilson disease (WD) when chelation therapy fails, but it is limited due to the shortage of donor. Auxiliary partial orthotopic LT (APOLT) has been performed successfully in end-stage WD patients, which expands the donor pool.

Methods: Atp7bmice were used as experimental model of WD.

Involvement of c-Jun N-terminal kinase in reversal of multidrug resistance of human leukemia cells in hypoxia by 5-bromotetrandrine.

5-Bromotetrandrine (BrTet), a candidate multidrug resistance (MDR) modulator, is a potential compound for use in cancer therapy when combined with anticancer agents such as daunorubicin (DNR) and paclitaxel. The purposeof this study was to investigate the mechanism of reversal of P-glycoprotein (P-gp)-mediated MDR by BrTet and the involvement of the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway in both adriamycin-sensitive K562 and adriamycin-resistant K562 (KA) leukemia cells in hypoxia. The combination of BrTet and DNR decreased both phosphorylated JNK1/2 and MDR1/P-gp levels under hypoxic conditions.

Chronic activation of neutral ceramidase protects beta-cells against cytokine-induced apoptosis.

Aim: To investigate the activity and expression of neutral ceramidase (N-CDase) in the insulin-secreting cell line INS-1 and its role in the cellular response to cytokines.

Methods: HPLC, Western blotting, and quantitative real-time PCR were performed to detect the activity and expression of N-CDase in INS-1 cells treated with a cytokine mixture (5 ng/mL interleukin-1beta, 10 ng/mL TNF-alpha, and 50 ng/mL interferon-gamma). The expression and activity of N-CDase in the INS-1 cells were specifically inhibited using N-CDase-siRNA transfection.

[Preparation and characterization of monoclonal antibodies against AR protein].

Aim: To prepare monoclonal antibodies (mAbs) against aldose reductase (AR) and compare with anti-aldose reductase-like protein (ARL-1) mAb.

Methods: The AR gene was gained by RT-PCR and inserted into pGEX-4T-1 (His)(6)C. Recombinant protein GST-AR was used to immunize BALB/c mouse.

[Expression analysis of mouse homologous proteins with human aldose reductase like-1].

Objective: To detect expression of mouse ARL-1 homologous proteins in mouse tissues, and analyze homology, genetic distance and phylogenetic relationship between human aldose reductase like-1 (ARL-1) and mouse homologous proteins.

Methods: Homology of mouse ARL-1 homologous proteins with human ARL-1 was analyzed by software Clustal X 1.8 using GenBank and Swiss-Prot database; genetic distance and phylogenetic relationship between mouse ARL-1 homologous proteins and human ARL-1 were analyzed by software Mega 2.

Preparation and characterization of polyclonal antibodies against ARL-1 protein.

Aim: To prepare and characterize polyclonal antibodies against aldose reductase-like (ARL-1) protein.

Methods: ARL-1 gene was inserted into the E. coli expression vector pGEX-4T-1(His)(6)C and vector pQE-30.