Reduction of amphotericin B-induced renal tubular apoptosis by N-acetylcysteine.

REDUCTION OF AMPHOTERICIN B INDUCED RENAL TUBULAR APOPTOSIS BY N-ACETYLCYSTEINE Running Title: N-acetylcystein and amphotericin B nephrotoxicity

Effect of ground black seeds (Nigella sativa L.) on renal tubular cell apoptosis induced by ischemia/reperfusion injury in the rats

Objective(s): The aim of this study was to evaluate the effects of ground black seeds on renal tubular cell apoptosis following ischemia/reperfusion (I/R) injury in rats. Materials and Methods: Forty male Wistar rats were randomly allocated into 5 equal groups including Sham, I/R model and three I/R+ black seeds (5, 10 and 20%)-treated groups. I/R groups’ kidneys were subjected to 60 min of isc...

Effects of Pretreatment with Pentoxyfilline and N-acetylcysteine on Renal Injury Following Induction of Liver Ischemia-Reperfusion

Background & Aims: Liver ischemia-reperfusion (IR) is one of the common consequences of liver surgery, especially during liver transplantation which results in organ dysfunction. Acute hepatic injury causes systematic inflammatory responses which may finally lead to functional disturbances in remote organs such as heart, lungs and kidneys. In this study, the effects of a potent inhibitor of inf...

Nephroprotective Effects of N-Acetylcysteine Amide against Contrast-Induced Nephropathy through Upregulating Thioredoxin-1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats

Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury (AKI) due to apoptosis induced in renal tubular cells. Our previous study demonstrated the novel N-acetylcysteine amide (NACA); the amide form of N-acetyl cysteine (NAC) prevented renal tubular cells from contrast-induced apoptosis through inhibiting p38 MAPK pathway in vitro. In the present study, we...

Apoptosis contributes to amphotericin B-induced nephrotoxicity.

The aim of this study was to investigate whether apoptosis contributes to nephrotoxicity caused by amphotericin B (AmB). By detecting apoptosis-specific DNA fragmentation, it is demonstrated that proximal tubular cells (LLC-PK(1)) and medullary interstitial cells (RMIC) respond with programmed cell death when treated with therapeutic doses of AmB. Concomitant application of AmB and recombinant ...