Hidaka T, Inokuchi T, Nakamura Y, Kotegawa M, Sugiyama M, Ogura R
Department of Medical Biochemistry, Kurume University School of Medicine, Japan.
Exp Mol Pathol. 1991 Oct;55(2):135-42. doi: 10.1016/0014-4800(91)90048-3.
16,16-Dimethyl PGE2 (dmPGE2) is known to protect against cellular damage in various tissues. Histological and biochemical approaches were used to examine the effect of this prostaglandin on hepatocellular damage in an experimental Reye's syndrome model produced in rats by 4-pentenoic acid. Chronic intraperitoneal administration of 4-pentenoic acid induced an accumulation of fatty droplets throughout the hepatic lobules along with mitochondrial abnormalities including swelling, disappearance of christae, and heterogeneity of matrix. These abnormalities were more intense in the marginal zone and successively decreased nearer to the central vein. Such hepatic abnormalities were markedly reduced by the combined administration of dmPGE2 with 4-pentenoic acid. Biochemical examination confirmed that dmPGE2 was able to inhibit the accumulation of hepatic triglyceride seen after the treatment with 4-pentenoic acid alone. These results indicated that dmPGE2 can prevent characteristic hepatocellular damage in this experimental Reye's syndrome model, suggesting that the involvement of prostaglandins should be taken into account in discussing the etiology and management of this syndrome.
已知16,16-二甲基前列腺素E2（dmPGE2）可保护多种组织免受细胞损伤。采用组织学和生化方法，在4-戊烯酸诱导的大鼠实验性瑞氏综合征模型中，研究了这种前列腺素对肝细胞损伤的影响。慢性腹腔注射4-戊烯酸会导致整个肝小叶出现脂肪滴积聚，同时伴有线粒体异常，包括肿胀、嵴消失和基质异质性。这些异常在边缘区更为明显，并在靠近中央静脉处逐渐减轻。dmPGE2与4-戊烯酸联合给药可显著减轻此类肝脏异常。生化检查证实，dmPGE2能够抑制单独使用4-戊烯酸治疗后出现的肝脏甘油三酯积聚。这些结果表明，dmPGE2可预防该实验性瑞氏综合征模型中的特征性肝细胞损伤，提示在讨论该综合征的病因和治疗时应考虑前列腺素的参与。
