Objective To explore the effects of lipoxinA4 on expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in rat primary lung fibroblast cells (LF) after lipopolysaccharide (LPS) challenge.Methods Primary lung fibroblast cells were incubated with various concentrations (0.1,1,10 μg/mL) of LPS for different lengths of time (3,6,9 h).Then primary lung fibroblast cells were still incubated in DMEM medium containing LPS in the presence or absence of lipoxinA4.After incubation,the supematant of medium was collected and the level of PGE2 was detected by using ELISA.The cells were harvested,and COX-2 protein was analyzed by Western blot.Results The model of acute inflammation in fibroblasts was well established by administering 1 μg/mL LPS in fibroblasts for 6 hours.Induction of COX-2 protein by LPS was inhibited by lipoxinA4.The levels of PGE2 in control group,LPS group and LPS + LipoxinA4 group were 55.84 pg/mL,411.73 pg/mL and 307.07 pg/mL,respectively,and there was a significantdifference between LPS group and LPS + LipoxinA4 group (P ＜0.01).Conclusion LipoxinA4 down-regulates the expression of the COX-2 induced by LPS in primary lung fibroblast cells and consequently inhibits the production of PGE2 in a dose dependent manner.

AIM: To investigate how brain-dead state affects the heart structure and function and the effect of PKC-? in BA-Ma mini pigs.METHODS: Ten Ba-Ma mini pigs were randomized into 2 groups: brain-dead group(n=5),and control group(n=5).The brain-dead model was made by increasing intracranial pressure,while the control group was maintained anesthesia for 24 h.The concentrations of cTnT,TNF-?,IL-1? and IL-6 in serum were determined at 6,12 and 24 h after brain death.At 24 h,heart tissues were observed by HE staining and electron microscope.The expression of PKC-? was detected by immunohistochemistry and RT-PCR.RESULTS:(1) Histological changes of myocardium: flaky bleeding under endocardium and dissolution of myocardium were found in optical microscope.In electron microscope dropsical mitochondria and confluent muscle fiber were found.(2) Changes of serum cTnT: serum cTnT for brain-dead group began to increase gradually since 6 h,and were significantly higher at each time point than those in control group(P

PURPOSE: Kallikrein (KLK) proteases are hormone-like signaling molecules with critical functions in different cancers. This study investigated the expression of KLK6 in gastric cancer and its potential role in the growth, migration, and invasion of gastric cancer cells. MATERIALS AND METHODS: In this study, we compared protein levels of KLK6, vascular endothelial growth factor (VEGF), and matrix metallopeptidase (MMP) 9 in normal gastric epithelial and gastric cancer cell lines by western blot. Fluorescence-activated cell sorting was employed to sort 2 clones of SGC-7901 cells with distinct KLK6 expression, namely, KLK6-high (KLK6high) and KLK6-low (KLK6low), which were then expanded. Lastly, immunohistochemical analysis was performed to investigate KLK6 expression in gastric cancer patients. RESULTS: The expression levels of KLK6, VEGF, and MMP 9, were significantly higher in the gastric cancer cell lines SGC-7901, BGC-823, MKN-28, and MGC-803 than in the normal gastric epithelial cell line GES-1. Compared to KLK6low cells, KLK6high cells showed enhanced viability, colony-forming ability, migration, and invasion potential in vitro. Importantly, immunohistochemical analysis of a human gastric cancer tissue cohort revealed that the staining for KLK6, VEGF, and MMP9 was markedly stronger in the cancerous tissues than in the adjacent normal tissues. KLK6 expression also correlated with that of VEGF and MMP9 expression, as well as several key clinicopathological parameters. CONCLUSIONS: Together, these results suggest an important role for KLK6 in human gastric cancer progression.
Blotting, Western ; Cell Line ; Clone Cells ; Cohort Studies ; Epithelial Cells ; Flow Cytometry ; Humans ; In Vitro Techniques ; Kallikreins ; Peptide Hydrolases ; Stomach Neoplasms* ; Vascular Endothelial Growth Factor A