الفهرس 
Possible modulatory effect of certain drug in acute kidney injury induced by ischemia/reperfusion in rats
AbstractOnly 14 pages are availabe for public view
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Abstract
Despite the documented renoprotective effect of pentoxifylline (PTX), a non-selective phosphodiesterase-4 inhibitor, the studies appraised only its anti-inflammatory/-oxidant/-apoptotic capacities without assessment of the possible involved trajectories. Here, we evaluated the potential role of galectin-3 and the ASK-1/NF-кp65 signaling pathway with its upstream/downstream signals in an attempt to unveil part of the cascades involved in the PTX renotherapeutic effect using a renal bilateral ischemia/ reperfusion (I/R) model. Rats were randomized into sham-operated, renal I/R (45 min/72h) and PTX (100 mg/kg; p.o) treated groups.Post-treatment with PTX for 3 days improved renal function and abated serum levels of cystatin C, creatinine, BUN and renal KIM-1 content, effects that were reflected on an improvement of the I/R-induced renal histological changes. On the molecular level, PTX reduced renal contents of galectin-3, ASK-1 with its two downstream molecules ERK1/2 and JNK, as well as NF-{u049B}B p65 and HMGB1.This inhibitory effect extended also to suppress neutrophil infiltration, evidenced by diminishing ICAM-1 and MPO, as well as inflammatory cytokines (TNF-Ü /IL-18), oxidative stress (MDA/TAC), and caspase-3. Evidently, the PTX novel renotherapeutic effect involved in part the inhibition of galectin-3 and ASK-1/ERK1/2 & JNK/NF-{u049B}B/HMGB-1 trajectories to mitigate renal I/R injury and to provide basis for its anti-inflammatory, anti-oxidant, and anti-apoptotic impacts