Prostaglandin protection of carbon tetrachloride-induced liver cell necrosis in the rat.
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.
D015064:16,16-Dimethylprostaglandin E2 / Q000494:pharmacology*; D000410:Alanine Transaminase / Q000097:blood; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001663:Bilirubin / Q000097:blood; D002251:Carbon Tetrachloride; D008099:Liver / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D009336:Necrosis / Q000139:chemically induced / Q000517:prevention & control*; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology*; D051381:Rats
D011459:Prostaglandins E, Synthetic; D002251:Carbon Tetrachloride; D000410:Alanine Transaminase; D000469:Alkaline Phosphatase; D015064:16,16-Dimethylprostaglandin E2; D001663:Bilirubin