Ameliorative effect of Centella asiatica on memory dysfunction in D-galactose–induced senescence mice

Abstract

Aging is a biological process, characterized by the gradual loss of physiological functions by unknown mechanism. Accumulating evidence suggests that mitochondrial dysfunction and oxidative stress play major roles in aging. D-galactose induced neurotoxicity is well known animal model for studying of aging and related oxidative damage and memory impairment. Centella asiatica, Indian pennywort has been documented in the treatment of various neurological disorders including aging. Therefore, present study has been conducted in order to explore the possible role of Centella asiatica against D-galactose induced cognitive impairment, oxidative and mitochondrial dysfunction in mice. D-galactose (100 mg/kg) was administered subcutaneously in male Swiss albino mice. Animals were treated with Centella asiatica (150 and 300 mg/kg, p.o. daily for a period of six weeks. On the 20th, 21st & 42nd day after D-galactose administration, Morris water maze and elevated plus maze were performed for assessment of memory. Cytoplasmic and nuclear fractions of whole brain were prepared for the quantification of oxidative stress parameters (lipid peroxidation, nitrite concentration, superoxide dismutase, catalase and non-protein thiols), mitochondrial enzymes activity and acetylcholinestrease level. Chronic administration of D-galactose or six weeks significantly impaired behavioral (Morris water maze, elevated plus maze and locomotor activity), oxidative defense and impaired mitochondrial enzymes complex (I, II and III) activities as compared to sham group. Six weeks Centella asiatica treatment significantly improved behavioral alterations, oxidative damage and mitochondrial enzyme complex activities as compared to control (D-galactose). Centella asiatica also attenuated enhanced acetylcholine esterase enzyme level in D-galactose senescence mice. In conclusion, results of this study illustrate that Centella asiatica ameliorates memory dysfunction and biochemical, mitochondrial dysfunction in D-galactose induced senescence mice.