Stachura J, Tarnawski A, Ivey K J, Mach T, Bogdal J, Szczudrawa J, klimczyk B
Gastroenterology. 1981 Aug;81(2):211-7.
We studied whether 16,16--dimethyl prostaglandin E2 (dmPGE2) may prevent acute liver damage induced by carbon tetrachloride (CCl4) in the rat. One hundred thirty male rats were divided into the following groups: (1) controls, (2) rats given CCl4 6670 mg/kg body wt subcutaneously, (3) rats pretreated with 5 micrograms/kg dmPGE2 given subcutaneously 30 min before, and 8 and 24 h after CCl4 administration, and (4) animals given dmPGE2 only as in group 3. Liver damage was assessed by biochemical studies (SGPT, serum alkaline phosphatase, and bilirubin) and by histology. In rats receiving CCl4 alone, SGPT activities were significantly elevated to 1024 +/- 82 U/L, 1270 +/- 120 U/L, 386 +/- 48 U/L and 208 +/- 20 U/L at 24, 48, 96, and 120 h after CCl4 respectively. In animals pretreated with dmPGE2 before CCl4, SGPT activities were 201 +/- 24 U/L, 55 +/- 4.6 U/L, 28 +/- 4 U/L, and 24 +/- 4 U/L at 24, 48, 96, and 120 h after CCl4, respectively (p less than 0.01, versus animals receiving CCl4 only). Histologically, livers of rats treated with CCl4 alone showed severe centrilobular necrosis at 24 and 48 h. Livers of animals pretreated with dmPGE2 before CCl4 did not show necrosis. It is concluded that dmPGE2 protects the liver against cell necrosis induced by CCl4 in the rat.
我们研究了16,16-二甲基前列腺素E2（dmPGE2）是否可以预防大鼠四氯化碳（CCl4）诱导的急性肝损伤。130只雄性大鼠被分为以下几组：（1）对照组；（2）皮下注射6670mg/kg体重CCl4的大鼠；（3）在CCl4给药前30分钟、给药后8小时和24小时皮下注射5μg/kg dmPGE2预处理的大鼠；（4）仅按第3组方式给予dmPGE2的动物。通过生化研究（谷丙转氨酶、血清碱性磷酸酶和胆红素）和组织学评估肝损伤。单独接受CCl4的大鼠，在CCl4给药后24、48、96和120小时，谷丙转氨酶活性分别显著升高至1024±82U/L、1270±120U/L、386±48U/L和208±20U/L。在CCl4给药前用dmPGE2预处理的动物，在CCl4给药后24、48、96和120小时，谷丙转氨酶活性分别为201±24U/L、55±4.6U/L、28±4U/L和24±4U/L（与仅接受CCl4的动物相比，p<0.01）。组织学上，单独接受CCl4处理的大鼠肝脏在24和48小时显示严重的小叶中心坏死。在CCl4给药前用dmPGE2预处理的动物肝脏未显示坏死。结论是，dmPGE2可保护大鼠肝脏免受CCl4诱导的细胞坏死。
