The effects of montelukast against amikacin-induced acute renal damage.
OBJECTIVE
The therapeutic and protective effects of montelukast against amikacin-induced acute renal damage were investigated.


METHODS
35 Wistar albino female rats were divided into 5 groups as follows: Group I: Control; Group II: Control+montelukast; Group III: Amikacin; Group IV: Amikacin+montelukast; Group V: Montelukast+amikacin. At the end of the experiment, the kidney tissues and the blood of rats were collected. Malondialdehyde (MDA), myeloperoxidase (MPO), and reduced glutathione (GSH) levels were determined from kidney tissues. Blood urea nitrogen (BUN), creatinine (Cr), TNF-alpha, and IL-1beta levels were assessed in the serum. In addition the kidney tissues were examined histologically.


CONCLUSIONS
The MDA, MPO, BUN, and Cr levels of group III significantly increased when compared to groups I and II. These parameters of group IV decreased when compared to group III. In addition, GSH levels significantly increased when compared to the first three groups. MDA, BUN and Cr levels of group V did not reach significant level in comparison with the control group. The most significant histological damage was observed in the group III followed by the groups IV and V. Immunohistochemically, group III showed a significantly increased apoptotic staining. In group IV, it was observed that montelukast treatment reduced the expression of apoptotic cells.


CONCLUSIONS
Montelukast treatment after amikacin injection could reduce the amikacin-induced kidney damage.
Department of Anatomy, School of Medicine, Inonu University, Malatya, Turkey. evren.kose@inonu.edu.tr
E
E
Kose
A
A
Beytur
Z
Z
Dogan
Z
Z
Ekincioglu
N
N
Vardi
K
K
Cinar
Y
Y
Turkoz
H
H
Soysal
N
N
Ekinci
D000085:Acetates / Q000494:pharmacology*; D000208:Acute Disease; D000583:Amikacin; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D003521:Cyclopropanes; D019610:Cytoprotection; D004195:Disease Models, Animal; D005260:Female; D005978:Glutathione / Q000378:metabolism; D007150:Immunohistochemistry; D053583:Interleukin-1beta / Q000097:blood; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D011804:Quinolines / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D000085:Acetates; D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D003521:Cyclopropanes; D053583:Interleukin-1beta; D011804:Quinolines; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D000583:Amikacin; D003404:Creatinine; D009195:Peroxidase; D005978:Glutathione; C093875:montelukast