Thrombomodulin (TM) is expressed on the surface of monocytes and is a key regulator of actual immune capacity. Propofol is an anesthetic agent that exerts anti-inflammatory effects. The objective of this study was to determine whether propofol could modulate TM in TNF-α-stimulated monocytes. THP-1 cells and male New Zealand rabbits were used in this study. The results showed that TNF-α decreases the TM expression by mediating posttranscriptional modification, and this inhibition may be repressed by treatment with propofol. Immunofluorescence, immunoprecipitation, and pull-down assays were used to demonstrate that Rac1-dependent nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, Cdc42, and p38 mitogen-activated protein kinase activation, as well as tristetraprolin (TTP) expression, all contributed to the downregulation of TM in TNF-α-treated cells. Propofol reversed the effects of TNF-α on TM downregulation. Propofol mediated the expression of intracellular TTP and the distribution of cytosolic human antigen R (HuR) and changed their interactions with the 3′-untranslated region of TM mRNA regulating by Cdc42 and Rac1. In addition, the animal study showed that propofol regulates TM, TTP, and HuR expression on monocytes in TNF-α-treated rabbits. In conclusion, the inhibition of TM expression in TNF-α-treated monocytes was mediated by the activation of NADPH oxidase and the expression of TTP. Propofol may inhibit the downregulation of TM by mediating NADPH oxidase and TTP inactivation and through the activation of HuR in vitro and in vivo. Utilizing TTP and HuR to control TM expression may be a promising approach for controlling systemic inflammation, and propofol may possess potential implications for the clinical immunity of monocytes after anesthesia or surgery.

Carcinogens, such as arecoline, play a crucial role in cancer progression and continuous gene mutations by generating reactive oxygen species (ROS). Antioxidants can reduce ROS levels and potentially prevent cancer progression but may paradoxically enhance the survival of cancer cells. This study investigated whether epigallocatechin-3-gallate (EGCG), an antioxidant from green tea, could resolve this paradox. Prostate cancer cells (PC-3 cell line) were cultured and treated with arecoline combined with NAC (N-acetylcysteine) or EGCG; the combined effects on intracellular ROS levels and cell viability were examined using the MTT and DCFDA assays, respectively. In addition, apoptosis, cell cycle, and protein expression were investigated using flow cytometry and western blot analysis. Our results showed that EGCG, similar to NAC (N-acetylcysteine), reduced the intracellular ROS levels, which were elevated by arecoline. Moreover, EGCG not only caused cell cycle arrest but also facilitated cell apoptosis in arecoline-treated cells in a synergistic manner. These were evidenced by elevated levels of cyclin B1 and p27, and increased fragmentation of procaspase-3, PARP, and DNA. Our findings highlight the potential use of EGCG for cancer prevention and therapy.

Dry weight evaluation is generally made from clinical observation of body weight (BW) changes, edema, blood pressure, and chest radiograph. In fact, 25–50% of patients on chronic hemodialysis had an incorrectly determined dry weight. To predict dry weight, twenty stable patients on regular hemodialysis were enrolled to investigate the correlation among dry weight, hematocrit, blood volume (BV), and vasoactive hormones including plasma renin activity (PRA), aldosterone (PA), and cyclic 3',5'-guanosine monophosphate (cGMP) values. BV was estimated by an infrared light reflection method. PRA, PA, and plasma cGMP were determined by commercial radioimmunoassay kits. The results showed significantly decreasing plasma cGMP values toward the end of hemodialysis compared with before hemodialysis (15.76 ± 3.56 pmol/ml vs 33.57 ± 3.98 pmol/ml; p < 0.05). A significant correlation exists between changes in plasma cGMP values and BV (p < 0.05). In addition, no significant correlation exists between changes in plasma cGMP and BW. A good correlation was found between changes in BV and hematocrit throughout dialysis (r = −0.774; p < 0.001). PRA and PA values predict neither BV nor BW changes. All patients were treated to attain a further ultrafiltration of 0.5 to 1.0 L after reaching dry weight, and we found that the critical point in blood pressure drop occurred when BV decreased by 8% or when plasma cGMP values decreased by 50% from their initial values. Continuous BV monitoring with infrared light reflection and detecting of cGMP throughout hemodialysis could help predict dry weight and avoid dialysis hypotension.