We previously reported that
beta-SQAG9 liposome, a
sulfonoglycolipid extracted from sea urchin intestines, had a protective effect against hepatic
ischemia reperfusion (I/R) injury. In this study, we made a detailed investigation of this protective effect and its mechanism. Rats were pretreated either with
beta-SQAG9 liposome (treated group) or with
phosphate-buffered
saline solution (control group). Thereafter, they were subjected to partial hepatic I/R. The serum levels of
aspartate aminotransferase,
alanine aminotransferase, and
lactate dehydrogenase were measured, and histological damage was evaluated with
hematoxylin and
eosin staining. To investigate the protective mechanism of
beta-SQAG9 liposome on I/R injury, the serum levels and the tissue
messenger RNA levels of
TNF-alpha and IL-1beta were measured, and polymorphonuclear neutrophil (PMN) infiltration was histologically evaluated by immunohistochemistry. Moreover, to investigate an interaction between
beta-SQAG9 liposome and
L-selectin on PMNs, flow cytometric analysis and immunofluorescence were performed.
beta-SQAG9 liposome reduced the hepatic I/R injury. The pretreatment with
beta-SQAG9 liposome reduced the PMN infiltration into the liver parenchyma. On the other hand, there was no apparent difference in the serum levels and the tissue
messenger RNA levels of the proinflammatory
cytokines between the two groups. Thus,
beta-SQAG9 liposome might reduce the hepatic I/R injury by inhibition of the PMN infiltration into the liver parenchyma, which was independent of the regulation of
cytokine production. Moreover, we demonstrated that
beta-SQAG9 liposome specifically bound to
L-selectin on PMN cell surface, which mediated the PMN infiltration.
beta-SQAG9 liposome might competitively antagonize
L-selectin on PMNs and suppress the subsequent PMN infiltration, resulting in the reduction in I/R injury.