The protective effects of intrahippocampal application of green tea leaf extract on aluminium-induced brain toxicity

Abstract

Diets have attracted great interest on the account of growing evidence of their beneficial effects on human health. Green tea has been used for a very long time as a folk remedy for a wide array of diseases. The well-known green tea beverage is made from a plant Camellia sinensis. The healthy properties of green tea are linked closely to its content of phenolic compounds, particularly to the (-)-epigallocatechin-3-gallate. It has been proposed that green tea may have a beneficial impact on a number of brain functions, as well as on neurodegenerative disorder prevention in humans and in various animal models, including Alzheimer's disease (AD). A large number of scientific studies have supported some of these assumptions. In the case of AD, aluminium may have an important role in the disease aetiology/pathogenesis/precipitation. However, aluminium has biological effects in the green tea plant, where it is a cofactor for polyphenol biosynthesis. Consequently, leaves of green tea accumulate and store large quantities of this element during the plant growth. Thus, it was intriguing whether the unilateral intrahippocampal application of green tea leaf extract (GTLE) and aluminium chloride would have any interaction, measured by the biochemical parameters in six brain structures: the forebrain cortex, striatum, basal forebrain, hippocampus, brain stem and cerebellum, of the adult male Wistar rats. It was found that GTLE given alone demonstrated biochemical effects not only in the ipsilateral hippocampus, but also spread into the five other examined structures at the same side, as well as into the identical brain structures on the contralateral hemisphere. In fact, there were no differences in the activity of superoxide dismutase, cytochrome c oxidase (COX) and acetylcholinesterase (AChE) between the right and the corresponding left brain structures. Moreover, the activity of COX and AChE were significantly higher when compared to the control group. Out of the three observed parameters, the content of reduced glutathione (GSH), superoxide anion and nitrites, aluminium itself demonstrated the strongest effects towards GSH, which was significantly reduced in all structures, compared to the control group. The changes were identical in the ipsi- and contralateral corresponding structures. Howewer, the application of GTLE just before aluminium prevented the reduction of GSH induced by aluminium, and significantly increased its content compared to the control group. Also, the content of superoxide anion was significantly reduced in most structures compared to the control, and to the aluminium-treated group as well. The obtained results of GTE in the aluminium-induced neurotoxicity are in accordance with the antioxidant effects of GTLE. Also, it is clear that GTE administered alone did not demonstrate neurotoxic effects as did the solution of aluminium chloride, but, on the contrary, showed the opposite, neuroprotective effects. To sum up, GTLE has proved to manifest strong antioxidant effects in the brain of healthy rats, and in the cases of neurotoxicity induced by aluminum, as well.