dc.contributor.author |
Demirel, Ulvi |
|
dc.contributor.author |
Harputoğlu, Muhsin Murat Muhip |
|
dc.contributor.author |
Seçkin, Yüksel |
|
dc.contributor.author |
Çıralık, Harun |
|
dc.contributor.author |
Temel, İsmail |
|
dc.contributor.author |
Özyalın, Fatma |
|
dc.contributor.author |
Otlu, Barış |
|
dc.contributor.author |
Yılmaz, Bilgiç |
|
dc.contributor.author |
Dinçtürk, Mehmet Sarp |
|
dc.contributor.author |
Aladağ, Hülya |
|
dc.date.accessioned |
2017-07-15T07:23:43Z |
|
dc.date.available |
2017-07-15T07:23:43Z |
|
dc.date.issued |
2011 |
|
dc.identifier.citation |
Demirel, U. Harputoğlu, M. M. M. Seçkin, Y. Çıralık, H. Temel, İ. Özyalın, F. Otlu, B. Yılmaz, B. Dinçtürk, M. S. Aladağ, H. (2011). An antibody of TNF alpha did not prevent thioacetamide induced hepatotoxicity in rats. Human & experimental toxicology. 30(7) 560–566. |
tr_TR |
dc.identifier.issn |
0960-3271 |
|
dc.identifier.uri |
http://hdl.handle.net/11616/7382 |
|
dc.description.abstract |
Tumor necrosis factor (TNF)-a antibodies have been shown to reduce liver damage in different models. We
investigated the effects of infliximab (a TNF-a antibody) on liver damage in thioacetamide (TAA)-induced hepatotoxicity
in rats. Group 1 (n ¼ 8) was the control group. In group 2 (n ¼ 8), the TAA group, the rats received
300 mg/kg intraperitoneal (ip) TAA daily for 2 days. In group 3 (n ¼ 8), the TAA þ Infliximab (INF) group,
infliximab (5 mg/kg ip daily) was administered 48 hours before the first dose of TAA daily for 2 days and
was maintained for 4 consecutive days. In group 4 (n ¼ 8), the INF group, the rats received only ip infliximab
(5 mg/kg) daily. Livers were excised for histopathological and biochemical tests (thiobarbituric-acid-reactive
substances [TBARS], and myeloperoxidase [MPO]). Serum ammonia, aspartate transaminase (AST), alanine
transaminase (ALT), TNF-a, liver TBARS and MPO levels, and liver necrosis and inflammation scores in the
TAA group were significantly higher than in the control and INF groups (all p < 0.01). All parameters except
AST were not significantly different between TAA and TAA þ INF. In conclusion, our results suggest that oxidative
stress plays an important role in TAA-induced hepatotoxicity, and infliximab does not improve oxidative
liver damage. |
tr_TR |
dc.language.iso |
eng |
tr_TR |
dc.publisher |
Human&experimental toxicology |
tr_TR |
dc.rights |
info:eu-repo/semantics/openAccess |
tr_TR |
dc.subject |
Infliximab |
tr_TR |
dc.subject |
Tumor necrosis factor-a |
tr_TR |
dc.subject |
Thioacetamide |
tr_TR |
dc.subject |
Oxidative stress |
tr_TR |
dc.subject |
Liver |
tr_TR |
dc.title |
An antibody of TNF alpha did not prevent thioacetamide induced hepatotoxicity in rats |
tr_TR |
dc.type |
article |
tr_TR |
dc.relation.journal |
Human&experimental toxicology |
tr_TR |
dc.contributor.department |
İnönü Üniversitesi |
tr_TR |
dc.contributor.authorID |
101949 |
tr_TR |
dc.identifier.volume |
30 |
tr_TR |
dc.identifier.issue |
7 |
tr_TR |
dc.identifier.startpage |
560 |
tr_TR |
dc.identifier.endpage |
566 |
tr_TR |