Aging is the process of progressive accumulation of changes over time, which is additionally connected with increasing susceptibility to some diseases and ultimately leads to death. Aging is associated mainly with loss of permanent cells, e.g. in heart, skeletal muscle and brain. During aging neurons die mainly in the apoptotic way. Apoptosis can be divided into three phases: initiation, execution and degradation. During the execution phase activation of specific enzymes, caspases, is observed. These enzymes are responsible for initiation of the death machinery. Caspase-9 is connected with the internal pathway of apoptosis, which begins at the mitochondrium in response to apoptotic stimulants, such as free radicals, UV radiation or chemotherapeutics. Before the executive phase starts, cytochrome c leaks from the mitochondrium to the cytoplasm, where it joins to the protein Apaf-1 and procaspase-9 and forms a complex called the apoptosome. Then procaspase-9 is converted by autolysis to caspase-9, which subsequently activates procaspase-3 to the active form which ultimately leads to apoptosis. Immunohistochemical analysis demonstrated a small decrease in caspase-9 and caspase-3 activation during normal aging and an increase in this process after application of stress factors. Also increased apoptosis in the cerebrum after administration of a drug for Alzheimer disease, memantine, to aging rats was observed. Taken together, the results obtained in this study seem to confirm the neuroprotective effect of memantine on increasing levels of cells with active caspase-3 and active caspase-9. It probably improves caspase-dependent apoptosis in the aging brain.
Green tea contains many polyphenolic constitutes, which might prevent non-alcoholic fatty liver disease (NAFLD). We aimed to investigate whether green tea extract (GTE) given at doses reflecting habitual consumption of green tea beverages prevents development of NAFLD in rats fed a high-fat diet (HFD). Twenty-four male Wistar rats were randomly divided into four equal groups (two study and two control groups). The study groups received a HFD (approximately 50% energy from fat), enriched with 1.1% and 2.0% GTE, respectively, for a total of 56 days. The control groups were fed a HFD alone and normal standardised diet (low-fat diet), respectively, for the same period of time. The percentage of hepatocytes affected by steatosis in the HFD group (median [1 st-3 rd quartile]: 25% [12-34%]) was higher (p < 0.033 and p < 0.050, respectively) than in the HFD-2.0%GTE group (9% [3-18%]) and normal diet group (10% [5-18%]). No significant differences were observed for the group consuming HFD-1.1%GTE, in which intermediate results were observed (15% [4-30%]). This finding points towards the hepatoprotective potential of GTE in preventing dietary-induced liver steatosis. In view of the increasing incidence of overweight and obesity a simple and cheap dietary modification, such as GTE supplementation, could prove to be useful clinically.
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