Serum GP73 were increased in patients with fatty liver disease / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To explore the levels of serum GP73 in patients with fatty liver disease.</p><p><b>METHODS</b>The sera GP73 were determined by ELISA in 178 patients with fatty liver disease and 100 healthy controls.</p><p><b>RESULTS</b>Serum GP73 levels were significantly increased in patients with various fatty liver diseases(70.62 +/- 60.60 ng/ml), compared with those of control population (35.61 +/- 12.22 ng/ml). In patients with alcoholic fatty liver disease, acute liver injury, chronic hepatitis B, and non-alcoholic fatty liver disease, their serum GP73 concentration were 81.86 +/- 47.82 ng/ml, 82.77 +/- 77.73 ng/ml, 63.84 +/- 50.62 ng/ml, and 65.75 +/- 62.20 ng/ml, respectively. But no significant difference was found between these groups (P > 0.05). In 68 patients with F > or = 1.0 (71.46 +/- 66.48 ng/ml), 75 patients with F> or = 2.0 (69.58 +/- 62.31 ng/ml), and 34 patients with F3-F4 (71.65 +/- 43.89 ng/ml), there were also no marked differences was observed between these fatty groups (F = 0.02, P = 0.98).</p><p><b>CONCLUSION</b>Serum GP73 levels were increased in patients with different liver diseases, but its concentrations were seems not related with degree of fatty injury.</p>

Role of C6ORF120, an N-glycosylated protein, is implicated in apoptosis of CD4⁺ T lymphocytes / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Although CD4(+) T cell apoptosis and CD8(+) T cell responses have been extensively studied during HIV infection, how apoptosis signals being initiated in CD4(+) T cells still need to be elucidated. The present study was designed to characterize the function-unknown gene, C6orf120, and elucidates its primary role in tunicamycin-induced CD4(+) T apoptosis.</p><p><b>METHODS</b>The C6orf120 coding sequence was amplified from peripheral blood mononuclear cells (PBMCs) total RNA of AIDS patients. The DNA fragment was inserted into the pET-32a expression system, transformed into Escherichia coli, and preparation of C6ORF120 recombinant protein. The magnetic cell separation technology was used to prepare primary CD4(+) T cells and CD8(+) T cells. The primary T cells were cultured at 1 × 10(6) cells/ml, treated with 0, 0.1, 1, 10, 100, and 200 ng/ml of C6orf120 recombinant protein for 48 hours, then harvested for cell cycle and apoptosis analysis. Tunicamycin (0.5 µmol/L) was used to induce endoplasmic reticulum stress in Jurkat cells. The biomarker 78 KDa glucose-regulated protein (GRp78) and growth arrest and DNA damage (GADD) were used to evaluate endoplasmic reticulum stress of Jurkat cells.</p><p><b>RESULTS</b>We prepared C6ORF120 recombinant protein and its polyclonal antibody. Immunohistochemical analysis showed that C6orf120 mainly expressed in hepatocytes and cells in germinal center of lymph node. At concentration of 0.1, 1, 10, 100, and 200 ng/ml, C6orf120 recombinant protein could induce apoptosis of Jurkat cells and primary CD4(+) T cells, and promoting G2 phase of its cell cycle. Western blotting analysis showed that C6ORF120 recombinant protein increased the expression of GRp78 and GADD in Jurkat cells in vitro.</p><p><b>CONCLUSION</b>Our results suggested that C6ORF120 could induce apoptosis of CD4(+) T cells, at least in part, mediated with endoplasmic reticulum stress.</p>

Study on pharmacokinetics of emodin in Rhizoma Polygontum Cuspidatum and its compound / 中国中药杂志

<p><b>OBJECTIVE</b>To study the difference in the pharmacokinetics of emodin in Zhiganning capsules and Rhizoma Polygontum Cuspidatum by nonaqueous RP-HPLC.</p><p><b>METHOD</b>The rats were orally administered with the extraction of Rhizoma Polygontum Cuspidatum and Zhiganning capsules. After hydrolysis and extraction, the content of emodin in the plasma is determined by Nonaqueous RP-HPLC.</p><p><b>RESULT</b>The concentration-time profiles of emodin fit two-compartment model. The pharmacokinetics parameters including, t1/2alpha, AUC(0-infinity), CL(s) and C(max) of emodin in the group of Rhizoma Polygontum Cuspidatum were significantly different from these in the group of its compounds.</p><p><b>CONCLUSION</b>There is a significant difference in pharmacokinetics of emodin between zhiganning capsules and the extraction of Rhizoma Polygontum Cuspidatum.</p>