Although hepatic ischemia-reperfusion (IR) injury is partially mediated by tumor necrosis factor-alpha (TNF), we recently found that low-dose TNF before IR is hepatoprotective. We examined the seemingly conflicting roles of TNF in mediating liver injury in a partial hepatic IR model using TNF gene k
Involvement of tumor necrosis factor-α in development of hepatic injury in galactosamine-sensitized mice
✍ Scribed by Ieharu Hishinuma; Jun-Ichi Nagakawa; Kazuo Hirota; Kaname Miyamoto; Kazuo Tsukidate; Takashi Yamanaka; Kou-Ichi Katayama; Isao Yamatsu
- Book ID
- 102849769
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 549 KB
- Volume
- 12
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
Intravenous injection of lipopolysaccharide and Dg a l a c t d e , at doses of 0.2 pg/kg and 800 mg/kg, respectively, elicited massive hepatic necrosis within 24 hr in C3HMeN mice. The plasma L-alanine aminotransferase (ALT, E.C. 2.6.1.2) or L-aspartate aminotransferase (AST, E.C. 2.6.1.1) activities at this point reached more than 2,000 IUL. However, overt hepatic injury as evaluated by the plasma aminotransferase activities did not develop in mice in which only lipoplysaccharide or only D-galactosamine was injected.
No tumor necrosis factolclike activities could be detected in the plasma of galactosarmn * e-and lipopolysaccharide-iqjected mice as determined by the assay of cytotoxicity to highly tumor necrosis factor-sensitive L-P3 cells through the experimental period of 24 hr.
📜 SIMILAR VOLUMES
Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Activation of nuclear factor kappa B (NF-kappa B) and expression of apoptotic Bcl-2 family members w