In this study, the effects of an ethanolic extract of Aurantiochytrium mangrovei 18W-13a strain (AM18W-13a) on lipopolysaccharide (LPS)-induced inflammatory responses in RAW264 murine macrophages were studied. Pre-treatment with the AM18W-13a extract significantly suppressed the LPS-induced production of nitric oxide and pro-inflammatory cytokines. RAW264 cells treated with the AM18W-13a extract for 1 and 24 h were subjected to DNA microarray analyses for detecting the differentially expressed genes. The treatment of RAW264 cells with the AM18W-13a extract for 24 h significantly suppressed the expression of several genes associated with inflammation or chemotaxis. Furthermore, treatment with the AM18W-13a extract for 1 h suppressed the expression of Pde4b, but induced the expression of Egr2 and Egr3 in RAW264 cells. Additionally, the AM18W-13a extract significantly enhanced the expression of certain anti-inflammatory mediators. This study is the first report of the anti-inflammatory effects of the AM18W-13a extract and its mechanism of action in LPS-stimulated murine macrophages.

We compared the effect of propofol with that of sevoflurane anesthesia on uric acid (UA) excretion in ASA physical status I and II patients with normal renal function. A propofol group (n = 11) received propofol-nitrous oxide-fentanyl after induction of anesthesia by propofol, while a sevoflurane group (n = 12) received sevoflurane-nitrous oxide-fentanyl after induction of anesthesia by thiamylal. UA, creatinine (Cr), and urea nitrogen concentrations in serum and urine were measured before induction of anesthesia, 1, 2, and 3 h after induction, and on Postoperative Day 1. N-acetyl-beta-D-glucosaminidase, beta2-microglobulin concentrations, and pH in urine were also examined. Plasma clearance of UA (CUA) and Cr (CCr) were calculated. The hourly concentration and excretion of urine UA were significantly higher than those of the sevoflurane group (P < 0.01). Significant correlations were noted between the hourly urine volume and UA concentration (r = 0.58, P < 0.01 for the propofol group; r = 0.51, P < 0.01 for the sevoflurane group). The CUA of the propofol group was significantly higher than that of the sevoflurane group (22.9 +/- 10.6 vs 5.9 +/- 3.4 mL/min, mean +/- SD, P < 0.05). There were no significant differences in other renal variables between the two groups. The present study demonstrated that the UA excretion increased during propofol anesthesia, while it remained stable during sevoflurane anesthesia.

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