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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Ren+Fail
2018 ; 40
(1
): 423-434
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N-acetylcysteine suppresses colistimethate sodium-induced nephrotoxicity via
activation of SOD2, eNOS, and MMP3 protein expressions
#MMPMID30035652
Ceylan B
; Ozansoy M
; K?l?ç Ü
; Yozgat Y
; Ercan Ç
; Y?ld?z P
; Aslan T
Ren Fail
2018[Nov]; 40
(1
): 423-434
PMID30035652
show ga
OBJECTIVE: To investigate the molecular mechanisms of colistimethate
sodium-induced nephrotoxicity and the protective effect of N-acetylcysteine (NAC)
against nephrotoxicity. METHODS: Twenty-eight Wistar rats were divided into four
groups comprised of control, colistin, NAC, and colistin-NAC co-treatment,
respectively. Serum creatinine and urine N-acetyl-?-d-glucosaminidase (NAG)
levels were measured at different time intervals. Histological changes,
apoptosis, total oxidant and antioxidant status, and the expression levels of
endothelial nitric oxide synthase (eNOS), superoxide dismutase 2 (SOD2), and
matrix metalloproteinase 3 (MMP3) were evaluated in renal tissue. RESULTS: In the
colistin group, post-treatment creatinine levels were higher than pretreatment
levels (p?=?.001). There was a significant increase in urine NAG level following
colistin treatment on day 10, compared to the baseline value and the first day of
treatment (p?=?.001 and .0001, respectively). Urine NAG levels were higher in the
colistin group on the 10th day of treatment than in the other groups (p?.01).
Colistin treatment increased the apoptosis index and renal histological damage
score (RHDS) significantly and these changes were reversed in NAC co-treatment
(RHSD and apoptosis index were 45 and 0 for sterile saline group, 29 and 2 for
NAC group, 122 and 7 for colistin group, and 66 and 2 for colistin?+?NAC group).
We observed no difference between groups regarding total antioxidant and total
oxidant status in the kidneys. The expression levels of eNOS, SOD2, and MMP3
decreased significantly in the kidneys of colistin-treated rats; these changes
were reversed in the kidneys of NAC co-treated rats. CONCLUSIONS:
N-acetylcysteine prevented colistin-induced nephrotoxicity through activation of
expression levels of SOD2, eNOS, and MMP3.
|Acetylcysteine/*pharmacology/therapeutic use
[MESH]