Ubiquitin reduces pulmonary cell adhension molecules and TNF-α level in ALI of mouse
何振扬1 邢娟1
Department of Crtical Care Medicine of HaiNan Provincial Hospital
【Abstact】Objective To access effects of ubiquitin on pulmonary intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and tumor necrosis factors-α (TNF-α) in acute lung injury of mouse induced by cecal ligation and perforation (CLP). Methods Sixty mice were devided randomly into five groups with twelve mice in each group, ie. CLP group, SHAM group, UB1 group (10mg/kg), UB2 group (5mg/kg) and UB3 group(1mg/kg). Mice of SHAM group underwent sham operation, and other four groups underwent CLP. Six hours after surgery, mice of three UB groups received ubiquitin by caudal vein injection while CLP and SHAM group received vehicle. Seven hours after surgery, blood and lungs of all mice were collected. ICAM-1, VCAM-1 and TNF-α level of 9% lung homogenate and serum TNF-α level were measured by ELISA. Results Pulmonary ICAM-1, VCAM-1 and TNF-α level of three UB groups were lower than CLP and SHAM group, and there were several comparisons with a statistically significant difference. Serum TNF-α level of three UB groups were slightly lower than CLP group, but far higher than SHAM group. Pulmonary ICAM-1 level, VCAM-1 level and serum TNF-α level of UB3 group were lower than UB1 and UB2 group, and there was a significant difference in VCAM-1 between UB3 and UB1 group. Pulmonary TNF-α level of UB3 group was slightly higher than UB1 and UB2 group. Conclusion Exogenous ubiquitin not only significantly inhibits the increases of pulmonary ICAM-1, VCAM-1 and TNF-α level in acute lung injury of mice induced by CLP, but also lowers the increases elicited by operation and stress. But ubiquitin doesn’t effect serum TNF-α obviously. With a decline in doses, ubiquitin’s inhibition of pulmonary ICAM-1 and VCAM-1level gradually increases while inhibition of pulmonary TNF-α level decreases.
