Impact of date palm pollen (Phoenix dactylifera) treatment on paracetamol-induced hepatorenal toxicity in rats

Abstract

Abstract Background Consumption of plant-derived nutraceuticals and crude drugs in Arab traditional medicine is widely believed to confer beneficial effects in liver and kidney diseases. Fruits from the date palm Phoenix dactylifera L. are a rich source of nutrients and bioactive phytochemicals which possess a myriad of pharmacological effects. Herein, we examined the impact of Date Palm Pollen (DPP) aqueous suspension treatment on paracetamol (APAP) [Acetaminophen (APAP)] triggered hepatorenal damage in rats and further explored the underlying putative mechanism. Methods Thirty Wistar rats were assigned to five groups (n = 6/group). Group I was control group; animals in group II were administered APAP 1000 mg/kg body weight (b.w.) intraperitonealy (i.p.); Group III and IV administered APAP plus date palm pollen with doses of 50, 100 mg/kg b.w and group V were administered APAP plus Silymarin (SIL) 10 mg/kg b.w. (i.p) respectively. Various biochemical parameters and histological assessment were evaluated in serum and tissue homogenate. Results Pretreatment with DPP aqueous suspensions (50 and 100 mg/kg b.w.) significantly (p < 0.05) thwarted APAP triggered alterations in serum biomarkers of liver damage [aspartate transaminase (AST), alanine aminotransferase (ALT), γ-glutamyl transferase (GGT) and alkaline phosphatase (ALP)], serum albumin as well as bilirubin. DPP treatment further mitigated APAP triggered dyslipidemia associated with hepatic damage by influencing APAP elicited changes in serum levels of cholesterol, triglycerides, HDL, LDL and VLDL. DPP treatment significantly (p < 0.05) ameliorated extrahepatic manifestations of APAP toxicity by influencing alterations in parameters of renal function (creatinine, urea and uric acid) as well serum electrolytes (Sodium, Potassium and Calcium). DPP treatment further influenced APAP-induced histological lesions by curtailing necrosis and inflammatory changes in the hepatic and renal architecture, respectively. Furthermore, DPP treatment modulated APAP-induced redox imbalance in the hepatic and renal tissue by blunting the increase of malondialdehyde (MDA) as well as decrease of nonprotein sulfhydryls (NP-SH) significantly (p < 0.05) when compared with control. The protective effect of DPP was further confirmed histologically. Conclusions The present observations point to an hepatorenal protective effects of acute DPP treatment in APAP-intoxicated rats which is underpinned by its robust antioxidant properties.