Journal of Nippon Medical School: Vol.68 No.2 page.154

Home > List of Issue > Table of Contents > Abstract

Journal of Nippon Medical School

Select Language
in Japanese < > in English

Full Text of this Article

in Japanese PDF (1.2M)

ArticleTitle The Protective Effect of Hepatocyte Growth-Promoting Factor (pHGF) Against Carbon Tetrachloride-Induced Acute Liver Injury in Rats -II. Protective Effects on Cell Membrane Injury-

AuthorList Wei Dai¹, Shigeru Sato² and Goro Asano¹

Affiliation ¹Department of Pathology and ²Central Institute for Electron Microscopic Researches, Nippon Medical School

Language JA

Volume 68

Issue 2

Year 2001

Page 154-164

Received July 11, 2000

Accepted October 11, 2000

Keywords acute liver injury, carbon tetrachloride, ultrastructure, pHGF, liver function

Abstract To examine the protective effects of hepatocyte growth-promoting factor (pHGF) against carbon tetrachloride (CCl₄) -induced acute liver injury in rats, the pathological changes were observed by light and electron microcopy, and the serum GOT and GPT levels were measured. Acute liver injury was produced by the injection of CCl₄(2ml/kg BW) in two groups of animals, of which one received pHGF (300μg/kg BW) via the tail vein after 4 hrs. In the group treated with CCl₄ alone, serum GOT and GPT were significantly elevated (1280±228 and 187±73 IU/l, respectively) 6 hrs after injection, indicating the induction of liver injury by CCl₄. They reached a peak (3836±654 and 1022±230 IU/l, respectively) at 48 hrs and declined thereafter, but did not completely recover after 72 hrs. PAS-negative cells were observed around the central veins after 6 hrs and most of the hepatocytes were PAS-negative at 12 hrs. PAS-positive cells began to appear and increased in number after 24 hrs. There were scarcely any PAS-negative cells remaining in the lobules after 72 hrs. In the group treated with CCl₄ followed by pHGF, serum GOT and GPT levels were significantly lower than in the CCl₄-treated group, and abundant PAS-positive hepatocytes were observed. Also, all hepatocytes were PAS-positive (as in normal liver) after 72 hrs. Administration of pHGF resulted in a decrease in the ultrastructural changes in rats with CCl₄-induced liver injury such as vacuolation, cisternae formation and dilatation of the rough endoplasmic reticulum. These results suggest that pHGF acts to stabilize cell membranes, thereby providing protection against CCl₄-induced hepatic injury.

Correspondence to Wei Dai, Department of Pathology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan

ArticleTitle	The Protective Effect of Hepatocyte Growth-Promoting Factor (pHGF) Against Carbon Tetrachloride-Induced Acute Liver Injury in Rats -II. Protective Effects on Cell Membrane Injury-
AuthorList	Wei Dai¹, Shigeru Sato² and Goro Asano¹
Affiliation	¹Department of Pathology and ²Central Institute for Electron Microscopic Researches, Nippon Medical School
Language	JA
Volume	68
Issue	2
Year	2001
Page	154-164
Received	July 11, 2000
Accepted	October 11, 2000
Keywords	acute liver injury, carbon tetrachloride, ultrastructure, pHGF, liver function
Abstract	To examine the protective effects of hepatocyte growth-promoting factor (pHGF) against carbon tetrachloride (CCl₄) -induced acute liver injury in rats, the pathological changes were observed by light and electron microcopy, and the serum GOT and GPT levels were measured. Acute liver injury was produced by the injection of CCl₄(2ml/kg BW) in two groups of animals, of which one received pHGF (300μg/kg BW) via the tail vein after 4 hrs. In the group treated with CCl₄ alone, serum GOT and GPT were significantly elevated (1280±228 and 187±73 IU/l, respectively) 6 hrs after injection, indicating the induction of liver injury by CCl₄. They reached a peak (3836±654 and 1022±230 IU/l, respectively) at 48 hrs and declined thereafter, but did not completely recover after 72 hrs. PAS-negative cells were observed around the central veins after 6 hrs and most of the hepatocytes were PAS-negative at 12 hrs. PAS-positive cells began to appear and increased in number after 24 hrs. There were scarcely any PAS-negative cells remaining in the lobules after 72 hrs. In the group treated with CCl₄ followed by pHGF, serum GOT and GPT levels were significantly lower than in the CCl₄-treated group, and abundant PAS-positive hepatocytes were observed. Also, all hepatocytes were PAS-positive (as in normal liver) after 72 hrs. Administration of pHGF resulted in a decrease in the ultrastructural changes in rats with CCl₄-induced liver injury such as vacuolation, cisternae formation and dilatation of the rough endoplasmic reticulum. These results suggest that pHGF acts to stabilize cell membranes, thereby providing protection against CCl₄-induced hepatic injury.
Correspondence to	Wei Dai, Department of Pathology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan