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The CHOP knockout and wild type mice with or without UUO were used.
2
UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment.
3
Increased renal iron content was observed in UUO mice, which was reduced by DFO treatment.
4
The expression of IRAK-M increased within 2 d after UUO in obstructed compared with unobstructed kidneys.
5
This analytical approach was applied on mice with unilateral ureteral obstruction (UUO) inducing chronic kidney disease.
6
Additionally, increased autophagy and tubular cell damage were more severe in UUO-treated GSTA4 KO mice than in WT mice.
7
C57Bl6 mice were submitted to left UUO and killed after 7 and 14 days.
8
To confirm these results, we applied this technique to a rat UUO therapeutic model with the anti-fibrotic reagent Fasudil.
9
Transient tubular cell proliferation seemed unable to counteract the apoptosis since tubular atrophy was apparently present by day 11 of UUO.
10
In the UUO group, the level of BUN and Scr, and the level of apoptosis and oxidative stress were all increased.
11
Methods: Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days.
12
CHOP deficiency could also ameliorate lipid peroxidation and endogenous antioxidant enzymes depletion, tubular apoptosis, and inflammatory cells infiltration in the UUO kidneys.
13
Conclusion: These findings suggest an important role for apoptosis and its regulatory proteins in the processes of tubular atrophy and fibrogenesis following UUO.
14
After UUO there was no significant change of tubular interstitial damage and interstitial fibrosis in neither of these mice compared to wildtype counterparts.
15
Our data demonstrate that HMGB1 is an essential contributor in facilitating M1 polarization at the early stage of UUO.
16
The expression of Bax protein was inhibited on day 3 when compared with that of the SO group, but increased with time following UUO.