Background
Acetaminophen also name paracetamol is apopular antipyretic and analgesic drug, in alarge doses produces a cute kidney injury either in human and animals. The
Conclusions
We provided a novel treatment against acetaminophen induced-nephrotoxicity with targeting renal oxidative stress, inflammation, apoptosis with elevation of Aquaporin 1 (AQP1) level.
Methods
Rats were divided into four groups: control, celastrol-treated, acetaminophen-exposed, and a group receiving both acetaminophen and celastrol. After 24 hours, blood samples were taken and kidney tissues were harvested for histological and molecular analyses. The findings shed light on the protective effects of celastrol against acetaminophen-induced nephrotoxicity, offering insights into its therapeutic potential.
Results
paracetamol oral intake altered renal histology with significantly P< 0.05 increased serum creatinine, blood urea nitrogen (BUN), and homogenate malonaldhyde (MDA), and immunoexpression of tumor necrosis- alpha (TNF-α), interleukin-6 (IL-6), caspase-3, Bcl-2-associated X- protein (Bax). Furthermore, it decreases homogenate level of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and gene expression of nuclear factor erythroid 2-related factor 2 (Nrf2), and haem oxygenase-1 (HO-1). Meanwhile, intraperitoneal injection of celastrol with acetaminophen reaffirms the previous results. Conclusions: We provided a novel treatment against acetaminophen induced-nephrotoxicity with targeting renal oxidative stress, inflammation, apoptosis with elevation of Aquaporin 1 (AQP1) level.