TY - JOUR
T1 - Effects of minocycline on Fas-mediated fulminant hepatitis in mice
AU - Chu, Heng-Cheng
AU - Lin, Yi-Ling
AU - Sytwu, Huey-Kang
AU - Lin, Shin-Hua
AU - Liao, Ching-Len
AU - Chao, You-Chen
N1 - 被引用次數：18
Export Date: 22 March 2016
CODEN: BJPCB
通訊地址: Liao, C.-L.161, Sec. 6, Min-Chuan E Road, Neihu, Taipei 114, Taiwan; 電子郵件： [email protected]
化學物質/CAS: caspase 3, 169592-56-7; caspase 9, 180189-96-2; cytochrome c, 9007-43-6, 9064-84-0; liver extract, 72980-85-9; minocycline, 10118-90-8, 11006-27-2, 13614-98-7; protein Bid, 260235-79-8; Antibodies, Monoclonal; Antigens, CD95; Fas protein, mouse; Minocycline, 10118-90-8; Receptors, Tumor Necrosis Factor; anti-Fas monoclonal antibody
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PY - 2005
Y1 - 2005
N2 - Minocycline has anti-inflammatory and antiapoptotic effects on cartilage, neurons and periodontal tissues, and both properties are central to the pharmaceutical treatment of liver diseases. We investigated the effects of minocycline on fulminant hepatitis in C57BL/6J mice induced by lethal challenge of the activating anti-Fas antibody, Jo2. Intraperitoneal injection of Jo2 (0.6 μg g -1) to mice resulted in fulminant hepatitis, as evidenced by increase of serum alanine/aspartate transaminase activities and histopathological alterations in liver sections, as well as animal death. Nevertheless, mice pretreated with three doses of minocycline (5 mg kg -1) resisted this lethal effect significantly. Minocycline treatment improved the survival kinetics, although to a lesser extent, when mice were challenged simultaneously with Jo2 or even treated 30 min after the lethal challenge. Jo2-induced activation of caspase-3 or -9 in liver tissues was inhibited by minocycline pretreatment, and yet the direct addition of minocycline to liver extracts from Jo2-challenged mice failed to block caspase activation in vitro. Moreover, minocycline efficiently suppressed the release of cytochrome c from mitochondria of the liver tissues from Jo2-challenged mice. In contrast, caspase-8 activation and Bid truncation triggered by Jo2 were not diminished by minocycline pretreatment in mouse livers. Our results suggest that easing of Fas-triggered fulminant hepatitis by minocycline may involve a mitochondrial apoptotic pathway, probably through preventing cytochrome c release and thereby blocking downstream caspase activation.
AB - Minocycline has anti-inflammatory and antiapoptotic effects on cartilage, neurons and periodontal tissues, and both properties are central to the pharmaceutical treatment of liver diseases. We investigated the effects of minocycline on fulminant hepatitis in C57BL/6J mice induced by lethal challenge of the activating anti-Fas antibody, Jo2. Intraperitoneal injection of Jo2 (0.6 μg g -1) to mice resulted in fulminant hepatitis, as evidenced by increase of serum alanine/aspartate transaminase activities and histopathological alterations in liver sections, as well as animal death. Nevertheless, mice pretreated with three doses of minocycline (5 mg kg -1) resisted this lethal effect significantly. Minocycline treatment improved the survival kinetics, although to a lesser extent, when mice were challenged simultaneously with Jo2 or even treated 30 min after the lethal challenge. Jo2-induced activation of caspase-3 or -9 in liver tissues was inhibited by minocycline pretreatment, and yet the direct addition of minocycline to liver extracts from Jo2-challenged mice failed to block caspase activation in vitro. Moreover, minocycline efficiently suppressed the release of cytochrome c from mitochondria of the liver tissues from Jo2-challenged mice. In contrast, caspase-8 activation and Bid truncation triggered by Jo2 were not diminished by minocycline pretreatment in mouse livers. Our results suggest that easing of Fas-triggered fulminant hepatitis by minocycline may involve a mitochondrial apoptotic pathway, probably through preventing cytochrome c release and thereby blocking downstream caspase activation.
KW - Caspase
KW - Cytochrome c
KW - Fas
KW - Fulminant hepatitis
KW - Minocycline
KW - Mitochondria
KW - caspase 3
KW - caspase 9
KW - cytochrome c
KW - Fas antibody
KW - Fas antigen
KW - jo2 antibody
KW - liver extract
KW - minocycline
KW - protein Bid
KW - unclassified drug
KW - alanine aminotransferase blood level
KW - animal experiment
KW - animal model
KW - animal tissue
KW - antiinflammatory activity
KW - apoptosis
KW - article
KW - aspartate aminotransferase blood level
KW - controlled study
KW - disease model
KW - drug effect
KW - enzyme activation
KW - enzyme release
KW - hepatitis
KW - histopathology
KW - kinetics
KW - liver mitochondrion
KW - male
KW - mouse
KW - mouse strain
KW - nonhuman
KW - priority journal
KW - survival
KW - Animals
KW - Antibodies, Monoclonal
KW - Antigens, CD95
KW - Dose-Response Relationship, Drug
KW - Liver
KW - Liver Failure, Acute
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Receptors, Tumor Necrosis Factor
U2 - 10.1038/sj.bjp.0706079
DO - 10.1038/sj.bjp.0706079
M3 - Article
SN - 0007-1188
VL - 144
SP - 275
EP - 282
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
IS - 2
ER -
