Ohnuma S
Department of Orthopedic Surgery, Akita University School of Medicine, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1994 Nov;68(11):953-60.
Calcium pyrophosphate dihydrate (CPPD) crystal-induced inflammation subsides spontaneously, and there have been few reports on its mechanism. It has recently been proposed that lipoproteins in the inflammatory synovial fluid played a role in the recovery from crystal-induced arthritis. This study investigated the inhibitory effect of lipoprotein on the inflammation-inducing activity of CPPD crystals in vitro and in vivo. Lipoproteins (very low density lipoprotein--VLDL, and low density lipoprotein-LDL) were isolated from human serum (in vitro) and rat serum (in vivo) by the sequential ultracentrifugal technique. In the in vitro studies, saline with lipoproteins was mixed with CPPD crystals, and co-incubated with isolated polymorphonuclear leukocytes (PMN). The production of superoxide anion (O-(2)) was measured as an index of inflammatory activity. In the in vivo studies, suspensions of CPPD crystals and rat lipoprotein solutions, were injected into the rat air pouch. The total number of white blood cells (WBC), crystal-containing WBCs, and concentrations of beta-glucronidase and prostaglandin (PG) E2, were measured. In the in vitro studies, O-(2) production by PMNs was more significantly suppressed after treating the CPPD crystals with VLDL or LDL than when the crystals were not treated with VLDL or LDL. In the in vivo studies, treatment of the CPPD crystals with lipoproteins significantly decreased the number of WBC and crystal-containing WBC, as well as the concentration of beta-glucronidase, and tended to depress the concentration of PGE2. These findings suggested that lipoproteins, especially LDL in inflammatory synovial fluid played an important role in the recovery from CPPD crystal-induced arthritis.
二水焦磷酸钙(CPPD)晶体诱导的炎症可自发消退,关于其机制的报道较少。最近有人提出,炎性滑液中的脂蛋白在晶体诱导的关节炎恢复过程中发挥了作用。本研究调查了脂蛋白在体外和体内对CPPD晶体炎症诱导活性的抑制作用。通过连续超速离心技术从人血清(体外)和大鼠血清(体内)中分离脂蛋白(极低密度脂蛋白-VLDL和低密度脂蛋白-LDL)。在体外研究中,将含有脂蛋白的盐水与CPPD晶体混合,并与分离的多形核白细胞(PMN)共同孵育。测量超氧阴离子(O-(2))的产生作为炎症活性指标。在体内研究中,将CPPD晶体悬浮液和大鼠脂蛋白溶液注入大鼠气袋。测量白细胞(WBC)总数、含晶体的WBC数量以及β-葡萄糖醛酸酶和前列腺素(PG)E2的浓度。在体外研究中,与未用VLDL或LDL处理的晶体相比,用VLDL或LDL处理CPPD晶体后,PMN产生的O-(2)受到更显著的抑制。在体内研究中,用脂蛋白处理CPPD晶体可显著减少WBC和含晶体的WBC数量,以及β-葡萄糖醛酸酶的浓度,并倾向于降低PGE2的浓度。这些发现表明,脂蛋白,尤其是炎性滑液中的LDL,在CPPD晶体诱导的关节炎恢复中起重要作用。