NQDI 1, An Inhibitor of ASK1 Attenuates Acute Ischemic Renal Injury by Modulating Oxidative Stress and Cell Death

ISSN: 1875-6182 (Online)
ISSN: 1871-5257 (Print)

Volume 15, 3 Issues, 2017

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Cardiovascular & Hematological Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Cardiovascular & Hematological Agents

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Debabrata Mukherjee
Department of Internal Medicine Texas Tech University
El Paso, TX

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NQDI 1, An Inhibitor of ASK1 Attenuates Acute Ischemic Renal Injury by Modulating Oxidative Stress and Cell Death

Cardiovascular & Hematological Agents in Medicinal Chemistry, 11(3): 179-186.

Author(s): Eman El Eter.

Affiliation: Physiology Department, Medical College & King Khalid University Hospital, King Saud University, P.O.BOX 2925(29), Riyadh 11461, Saudi Arabia.


Apoptosis signal-regulating kinase 1 (ASK1) is among the signaling events that lead to postischemic cell death. Inhibition of ASK1 pathway protected hearts from ischemic damage. The present study evaluated the renal protective effects of NQDI 1, an inhibitor of ASK1, in an animal model of acute ischemic renal failure. Male Wistar rats were subjected to right nephrectomy and clamping of left renal pedicle for 45 min, or sham operation. The administration of NQDI 1 attenuated renal dysfunction and histological changes characteristic for renal ischemia/reperfusion injury (IRI). Apoptosis of renal tissues, as detected by TUNEL staining, was also reduced together with p53 protein expression, and renal levels of MDA and SOD with NQDI 1 administration and BCL2 was up regulated. In conclusion, inhibition of ASK1 is of therapeutic potential against acute ischemic renal injury. Its protective effects are mediated via inhibition of apoptosis and oxidative stress.


Acute kidney disease, apoptosis, ASK1, Bcl-2, oxidative stress, p53, renal ischemia reperfusion injury.

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Article Details

Volume: 11
Issue Number: 3
First Page: 179
Last Page: 186
Page Count: 8
DOI: 10.2174/18715257113119990085
Price: $58

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