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Tempol Protects Against Acute Renal Injury by Regulating PI3K/Akt/mTOR and GSK3?
Signaling Cascades and Afferent Arteriolar Activity
#MMPMID29870982
Zhang G
; Wang Q
; Wang W
; Yu M
; Zhang S
; Xu N
; Zhou S
; Cao X
; Fu X
; Ma Z
; Liu R
; Mao J
; Lai EY
Kidney Blood Press Res
2018[]; 43
(3
): 904-913
PMID29870982
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BACKGROUND/AIMS: Free radical scavenger tempol is a protective antioxidant
against ischemic injury. Tubular epithelial apoptosis is one of the main changes
in the renal ischemia/reperfusion (I/R) injury. Meanwhile some proteins related
with apoptosis and inflammation are also involved in renal I/R injury. We tested
the hypothesis that tempol protects against renal I/R injury by activating
protein kinase B/mammalian target of rapamycin (PKB, Akt/mTOR) and glycogen
synthase kinase 3? (GSK3?) pathways as well as the coordinating apoptosis and
inflammation related proteins. METHODS: The right renal pedicle of C57Bl/6 mouse
was clamped for 30 minutes and the left kidney was removed in the study. The
renal injury was assessed with serum parameters by an automatic chemistry
analyzer. Renal expressions of Akt/mTOR and GSK3? pathways were measured by
western blot in I/R mice treated with saline or tempol (50mg/kg) and compared
with sham-operated mice. RESULTS: The levels of blood urea nitrogen (BUN),
creatinine and superoxide anion (O2.-) increased, and superoxide dismutase (SOD)
and catalase (CAT) decreased significantly after renal I/R injury. However,
tempol treatment prevented the changes. Besides, I/R injury reduced renal
expression of p-Akt, p-GSK3?, p-mTOR, Bcl2 and increased NF-?B, p-JNK and p53 in
kidney, tempol significantly normalized these changes. In addition, renal I/R
injury reduced the response of afferent arteriole to Angiotensin II (Ang II),
while tempol treatment improved the activity of afferent arteriole. CONCLUSION:
Tempol attenuates renal I/R injury. The protective mechanisms seem to relate with
activation of PI3K/Akt/mTOR and GSK3? pathways, inhibition of cellular damage
markers and inflammation factors, as well as improvement of afferent arteriolar
activity.
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