BACKGROUND: Ischemia-reperfusion (I/R) injury occurs in various situations, including transplantation, trauma, and shock. We previously reported that the synthetic beta-SQDG (18:0), which was derived from sulfoquinovosyl diacylglycerol of the sea urchin, possessed immunosuppressive effects, such as inhibition of T-cell responses in human allogenic human mixed lymphocyte reactions (MLR) and skin allograft survival in rats. beta-SQAG9 was synthesized from beta-SQDG (18:0) to improve structural stability in aqueous solution with the same biological activities to bind to CD62L (L-selectin) and CD62P (P-selectin) in vitro. We hypothesized that beta-SQAG9 might attenuate leukocyte rolling on the endothelium and neutrophil infiltration in which L-selectin and P-selectin are key molecules. We investigated the protective effect of beta-SQAG9 against hepatic I/R injury. METHODS: Male Lewis rats were divided into 6 groups: sham, control, and treatment. Rats in the control, and the treatment groups were subjected to hepatic ischemia for 30 minutes. They were injected with PBS or beta-SQAG9 at doses of 5, 10, 25, and 50 mg/kg into the penile vein immediately before reperfusion. To assess the damage to the hepatic parenchyma, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were measured and histological evaluation was performed at 6 hours after reperfusion. RESULTS: In the group treated with beta-SQAG9 at a dose of 10 mg/kg, AST, ALT, and LDH were significantly reduced, and the amount of neutrophil infiltration also was significantly reduced. CONCLUSIONS: Our data suggest that SQAG-9 (10 mg/kg) reduces the warm hepatic I/R injury.

Animals↗

PubMedDate not supplied

Immunohistochemical localization of glycosaminoglycans with the use of monoclonal antibodies in salivary pleomorphic adenomas.

Immunohistochemical identification of glycosaminoglycans (GG) in salivary pleomorphic adenomas (63 cases) was made to evaluate chondrogenesis in modified myoepithelial cell regions. Monoclonal antibodies (MoAbs) to GGs were used in conjunction with specific enzyme digestion, and chondroitin 4S proteoglycan (C4SPG), chondroitin 6S PG(C6SPG), dermatan sulfate PG(DSPG), heparan sulfate PG(HSPG) and keratan sulfate PG(KSPC) were identified. Modified myoepithelial cells showing fibrillar and plasmatoid shapes contained KSPG (68%), DSPG (32%) and CSPG(C6SPG:22%, C4SPG:33%). Foci of chondroidally changed cells stained intensely for KSPG (53%), and less so for CSPG(C6SPG:22%, C4SPG:33%), and DSPG (19%). Perinuclear matrix in chondroidal tissue reacted most strongly. Almost all types of modified myoepithelial cells, or outer layer tumor cells of tubulo-ductal structures, produced or synthesized CSPG, DSPG, and HSPG. Certain cells located in hyalinous and myxomatous tissues may undergo chondroidal metaplasia, and clusters of such cells may produce GGs and PGs in the perinuclear zone similar to those GGs in matrix synthesized in chondroidal tissue. GG-synthesizing cells might continuously produce KSPG until the cartilage matrix is completed.

Adenoma↗