[Proventive and Therapentic Effects of Endothelial Progenitor Cells on Monocrotaline-Induced Hepatic Vein Occlusion Disease].

OBJECTIVE: To investigate the preventive and therapeutic effects of endothelial progenitor cells on monocrotaline-induced hepatic vein occlusion disease in mice. METHODS: C57BL/6 mice were randomly divided into 3 groups: saline group (n=15), monocrotaline group (n=15), and endothelial progenitor cell infusion group (n=15). Liver function (TBIL, ALT, AST), liver index, and serum levels of TNF-α and IL-6 were measured on the 8th day after intragastric administration. Hepatic sinusoidal endothelial cells, hepatic central venous endothelial cells and hepatocytes were observed by both HE and immunohistochemical staining. Hepatic fibrosis was observed by Masson's trichrome staining. RESULTS: By the light microscopy, the liver of the monocrotaline group showed moderate to the severe injuries of hepatic sinusoidal and central venous endothelial cells, and hepatic venous congestion. Masson staining showed moderate to severe hepatic fibrosis of central vein and hepatic sinus. In the endothelial progenitor cell group, hepatic sinusoidal and central venous endothelial cell injuries, and the fibrosis of central hepatic vein and hepatic sinus were mild to moderate. Hepatic venous congestion was reduced in comparison with that in the mice of the monocrotaline group. Compared with the endothelial progenitor cell group, the liver index was higher, the liver function was more abnormal, and the serum expression levels of TNF-α and IL-6 were higher in the monocrotaline group. CONCLUSION: The monocrotaline-induced damage of hepatic sinusoidal and central venous endothelial cells is an linitiating factor for hepatic vein occlusive disease. Infusion of endothelial progenitor cells can play a role in preventing and treating hepatic vein occlusion.

Lactoferrin protects against lipopolysaccharide-induced acute lung injury in mice.

Lactoferrin (LF) plays various anti-inflammatory roles in inflammation experimentally induced by lipopolysaccharides (LPS). But the protective effects of LF on LPS-induced acute lung injury (ALI) have not been elucidated. In this study, we aimed to study the effects of LF on ALI caused by LPS in mice. At 1h before or after LPS injection, an intraperitoneal injection of LF (5mg/body) was administered. Lung specimens and the bronchoalveolar lavage fluid (BALF) were isolated for histopathological examinations and biochemical analyses 12h after LPS exposure. We found that both prophylactic and therapeutic administration of LF significantly decreased the W/D ratio of the lung and protein concentration in the BALF. LF significantly reduced the pulmonary myeloperoxidase activity and the number of total cells in the BALF 12h after LPS challenge. LF treatment markedly attenuated lung edema, alveolar hemorrhage and inflammatory cells infiltration. Moreover, LF also decreased the production of TNF-α and increased interleukin-10 in the BALF. These results firstly indicate that LF may protect against LPS-induced ALI in mice.

[Slide platelet aggregation test used as a monitor for patient treated with anti-pletelet drugs].

The aim was to verify the effectiveness of slide platelet aggregation test (SPAT) to monitor the inhibition effect of anti-platelet drugs. A group of eight healthy volunteers was examined for SPAT value and T(50) (time necessary for reaching 50% of total aggregation) induced by ADP, arachidonic acid (AA) and cationic propyl gallate (c-PG) respectively before and after administration of ASA in dose of 100 mg/day for 3 days. The group of 41 inpatients at the Department of Cardiovascular Disease treated with anti-platelet drugs and the group of 327 healthy blood donors were also examined for SPAT. The SPAT value of healthy volunteer samples stored at room temperature were measured hourly for four hours. The results showed that: (1) no significant difference was detected between the T(50) before and after ASA administration in health volunteer group when ADP was used as inducer, but a significant difference was detected in this group when AA or c-PG was used as inducer. There was significant linear correlation between SPAT value and T(50) induced by c-PG in health volunteer group before and after administration of ASA (r = 0.998, P = 0.000); (2) there was no significant difference between the SPAT value of health volunteer group before administration of ASA and the SPAT value of health blood donors group (P = 0.853), but there was a significant difference between the SPAT values before and after administration of ASA in health volunteer group (P = 0.000). There was significant difference when the SPAT value of the inpatients treated with anti-platelet drugs was compared with that of healthy blood donor group and with that of health volunteer group before and after administration of ASA (P = 0.000). The cut-off value of SPAT in health blood donor group was 44.6 +/- 11.7 seconds, reference value was from 21.1 seconds to 68.0 seconds; (3) there was no significant difference between SPAT values when platelets samples stored at room temperature for 1, 2, 3, 4 hours (P = 0.815). In conclusion, SPAT can rapidly monitor the inhibition effect of anti-platelet drugs and SPAT may have the similar clinic value with T(50) induced by c-PG.