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Bee pollen has been used as an apitherapy agent for several centuries to treat burns, wounds, gastrointestinal disorders, and various other diseases. The aim of our study was to investigate the hepatoprotective effects of chestnut bee pollen against carbon tetrachloride (CCI4)-induced liver damage. Total phenolic content, flavonoid, ferric reducing/antioxidant power, and DPPH radical activity measurements were used as antioxidant capacity determinants of the pollen. The study was conducted in rats as seven groups. Two different concentrations of chestnut bee pollens (200 and 400 mg/kg/day) were given orally and one group was administered with silibinin (50 mg/kg/day, i.p.) for seven days to the rats following the CCI4 treatment. The protective effect of the bee pollen was monitored by aspartate transaminase (AST) and alanine transaminase (AST) activities, histopathological imaging, and antioxidant parameters from the blood and liver samples of the rats. The results were compared with the silibinin-treated and untreated groups. We detected that CCI4 treatment induced liver damage and both the bee pollen and silibinin-treated groups reversed the damage; however, silibinin caused significant weight loss and mortality due, severe diarrhea in the rats. The chestnut pollen had showed 28.87 mg GAE/g DW of total phenolic substance, 8.07 mg QUE/g DW of total flavonoid, 92.71 mg Cyn-3-glu/kg DW of total anthocyanins, and 9 mg β-carotene/100 g DW of total carotenoid and substantial amount of antioxidant power according to FRAP and DPPH activity. The results demonstrated that the chestnut bee pollen protects the hepatocytes from the oxidative stress and promotes the healing of the liver damage induced by CCI4 toxicity. Our findings suggest that chestnut bee pollen can be used as a safe alternative to the silibinin in the treatment of liver injuries.

Melatonin, the main secretory product of the pineal gland, has been shown to be potentially effective in prevention of numerous types of neurodegenerative disorders in which free radical processes are involved. Homocysteine (Hcy), an independent risk factor for atherosclerosis, undergoes auto-oxidation and generates reactive oxygen species. The purpose of this study was to test whether intracerebroventricular (ICV) injection of Hcy leads to neural lipid peroxidation and also to investigate the protective effects of melatonin on the brain tissue from oxidative stress of Hcy. Adult male Wistar rats under anaesthesia were injected ICV with Hcy at a dose of 143 microg/kg. Melatonin was administered intraperitoneally to a group of rats for three consecutive days before Hcy injection. The rats were decapitated and brain tissues were removed and hippocampus, cortex and cerebellum were dissected. There was a significant development of oxidative stress as indicated by an increase in malondialdehyde in hippocampus, cortex and cerebellum of rats injected with Hcy, whereas melatonin prevented the elevation of lipid peroxidation. Furthermore, melatonin significantly increased glutathione levels and glutathione peroxidase activity in all brain regions. The present study demonstrates that Hcy, in high levels, may be a causal factor in generation of free radicals in the brain and it may be one of the mechanisms which cause neurodegeneration in elderly people. It also shows that melatonin could potentially be beneficial in prevention of neurodegeneration caused by hyperhomocysteinemia.

Our results suggest that honey, propolis, pollen, and royal jelly significantly enhanced the healing of CCl4-induced liver damage, partially due to their antioxidant properties and bioavailability.

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