Background: The use of natural products is an essential way to new pharmaceutical leads for the discovery and development of new drugs to treat diseases. Propolis (Pro) is a natural resinous product produced by honey bees. It has a strong cytoprotective effect against various exogenous toxic agents. The current study was designed to evaluate the possible protective effect of propolis against the toxicity of aluminum chloride (AlCl 3) on hepatorenal structure and function in male white albino rats. Methods: Thirty mature males of albino rat, Rattus rattus, weighing about 80-90g were divided into five groups contained 6 rats each. The first group acts as a control (received only saline solution); the second group (Al) had given orally 40 mg/kg b.w. of AlC1 3 , the third group (Pro) had administrated orally 150 mg/kg b.w. of propolis and the fourth group (Al+Pro) had given 40 mg/kg b.w. of AlCl 3 in the morning and 150 mg/kg b.w. of propolis in the evening. These four groups had given the treatments for two months. The fifth group (Al-Pro) had given 40 mg/kg b.w. of AlC1 3 chloride for one month then had given 40 mg/kg b.w. of AlCl 3 combined with 150 mg/kg b.w. of propolis for another month. Results: The AlCl 3-treated group showed a significant increase in the activities of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), acid phosphatase (AP), and lactate dehydrogenase (LDH) in the plasma. Also, glucose, total protein, albumin, creatinine, uric acid, urea, cholesterol, and triglycerides in the plasma were significantly increased. The histological examination for the liver and kidney sections revealed marked histopathological alternations. The treatment with propolis combined with AlCl 3 improved the previous mentioned biochemical and histological alterations induced by AlCl3. Conclusion: It can be concluded that the combination of propolis with AlCl 3 alleviated the toxic effects of AlCl 3. The propolis has protective influences on the hepatorenal structure and function and could be able to resist AlCl 3 intoxication.

Background: Acrylamide has been reported to induce hepato-and nephrotoxicity. The present investigation aims to alleviate the dangerous effects at the histopathological and physiological levels of acrylamide by bee venom and its extracted bradykinin-potentiating factor (BPF). Seventy-five adult male mice were divided into 15 groups: a control (G1) 15 animals for 30 (G1.1), 45 (G 1.2), and 60 (G 1.3) days of experimental periods; acrylamide-administered G2.1, G2. 2, and G2.3 received acrylamide orally (10 mg/kg b.w) daily for 30, 45, and 60 days. Chips-administered G3.1, G3.2, and G3.3 were fed one third of its daily diet by chips for 30, 45, and 60 days. Bee venom-and BPF-treated G4.1 and G4.2 were i.p. injected with bee venom (1.319 mg/kg b.w.) and BPF (2.314 mg/kg b.w.), respectively, day after the other day for 60 days. G5.1 and G5.2 received acrylamide orally (10 mg/kg b.w) combined either with i.p. by bee venom (1.319 mg/kg b.w.) or BPF (2.314 mg/kg b.w.) respectively day after the other day for 60 days. G6.1 and G6.2 were fed one third of its daily diet by chips for 60 days combined either with i.p. by bee venom (1.319 mg/kg b.w.) or with BPF (2.314 mg/kg b.w.), respectively, day after the other day for 60 days. Results: The results showed that acrylamide administration and chips feeding groups suffer from alteration and histopathological changes in liver and kidney tissues that were accompanied with the increase in liver and kidney physiological biomarker (ALT, AST, urea, creatinine, uric acid) and the decrease in the albumin levels. Acrylamide or chips combined with either bee venom or BPF showed improvement in the level of physiological and histopathological studies. Conclusion:The study concluded the protective role of bee venom and its extracted BPF against acrylamide-and chips-induced hepato-and nephrotoxicity.

Background: Acrylamide is reported for its toxicity on the central and the peripheral nervous system and causes paralysis. Bee venom (BV) and bradykinin-potentiating factor (BPF) have been documented for their potential therapeutic effects as anti-neuroinflammation. The study aimed to ameliorate the neurotoxic effects of acrylamide or chips by using BV or its extracted BPF. Mice were divided into 15 subgroups: control (G1.1, G1.2, G1.3) at 30, 45, and 60 days, respectively; acrylamide-(10 mg/kg b.w.; orally daily) administered subgroup for 30 days (G2.1), 45 days (G2.2), and 60 days (G2.3); chips feeding group (1/3 of daily diet) for 30 days (G3.1), 45 days (G3.2), and 60 days (G3.3); bee venom-treated group for 60 days (1.319 mg/kg b.w.) (G4.1); BPF-treated group for 60 days (2.314 mg/kg b.w.) (G4.2), day after the other day; and acrylamide-or chips-administered groups combined either with BV (G5.1, G6.1) or BPF treatment (G5.2, G6.2) for 60 days. Results: The results indicated that the approximate LD50 for BV and BPF equal to 13.19 mg/kg and 23.14 mg/kg, respectively, and the extracted BPF contains 15 amino acids. Also, the results showed abnormal gait in mice of acrylamide-administered groups which was accompanied by histopathological changes in the hippocampus, cerebellum, and cerebral cortex. A marked gradual increase of alpha-synuclein expression was noted at the studied region in the acrylamide-and chips-treated groups at 60 days of treatment as compared to control. Both BV-and BPF-treated groups either separately or in co-administration with acrylamide or with chips did not show any histopathological changes in the studied regions with downregulated expression of alpha-synuclein. Conclusion: The study concluded the neuroprotective effect of BV and its extracted BPF against neurotoxicity induced by acrylamide or chips administration.