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Centella asiatica Attenuates D-Galactose-Induced Cognitive Impairment, Oxidative and Mitochondrial Dysfunction in Mice

By Anil Kumar, Atish Prakash and Samrita Dogra


D-galactose induced neurotoxicity is well known model for studying aging and related oxidative damage and memory impairment. Aging is a biological process, characterized by the gradual loss of physiological functions by unknown mechanism. 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. Chronic administration of D-galactose (100 mg/kg s.c.) for a period of six weeks significantly impaired cognitive task (both in both Morris water maze and elevated plus maze) and oxidative defense (Increased lipid peroxidation, nitrite concentration and decreased activity of superoxide dismutase, catalase and non-protein thiols) and impaired mitochondrial complex (I, II and III) enzymes activities as compared to sham group. Six weeks Centella asiatica (150 and 300 mg/kg, p.o) treatment significantly improved behavioral alterations, oxidative damage and mitochondrial enzyme complex activities as compared to contro l (D-galactose). Centella asiatica also attenuated enhanced acetylcholine esterase enzyme level in D-galactose senescence mice. Present study highlights the protective effect of Centella asiatica against D-galactose induced behavioral, biochemical and mitochondrial dysfunction in mice

Topics: Research Article
Publisher: SAGE-Hindawi Access to Research
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Provided by: PubMed Central

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  1. (1990). 2,3,23-trihydroxy-urs-12-ene and its derivatives, processes for their preparation and their use,”
  2. (2009). A .K u m a r ,S .D o g r a ,a n dA .P r a k a s h ,“ E ffect of carvedilol on behavioral, mitochondrial dysfunction, and oxidative damage against d-galactose induced senescence in mice,”
  3. (2002). A .N a v a r r o
  4. (1956). Aging: a theory based on free radical and radiation chemistry,”
  5. Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids,”
  6. (2003). Antioxidative activity and total polyphenolic compounds of leaf, root and petiole of four accessions of Centella asiatica (L.) urban,”
  7. (1981). Assays for differentiation of glutathione
  8. C r i v e l l o ,I .H .R o s e n b e r g ,G .E .D a l l a l ,D .B i e l i n s k i ,a n d
  9. (1971). Catalase,” in
  10. (2006). Centella asiatica (L.) leaf extract treatment during the growth spurt period enhances hippocampal CA3 neuronal dendritic arborization
  11. (2005). Centella asiatica treatment during postnatal period enhances learning and memory
  12. (2006). Chronic systemic Dgalactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: protective effects of R-α-lipoic acid,”
  13. (1996). Clinical Chemistry,M o s b y ,S t .
  14. (1949). Determination of serum proteins by means of Biuret reaction,” The J o u r n a lo fB i o l o g i c a lC h e m i s t r y ,
  15. (1997). Dopamine oxidation alters mitochondrialrespirationandinducespermeabilitytransition in brain mitochondria: implications for Parkinson’s disease,”
  16. (2005). e i ,L .L i ,Q .S o n g ,H .A i ,J .C h u ,a n dW .L i ,“ B e h a v i o u r a l study of the D-galactose induced aging model in C57BL/6J mice,”Behavioural Brain Research,vol.157,no.2,pp.245–251,
  17. (1961). E l l m a n ,K .D .C o u r t n e y ,V .A n d r e s ,a n dR .M . Featherstone, “A new and rapid colorimetric determinationof acetylcholinesterase activity,” Biochemical Pharmacology,v o l .
  18. (2009). Enhancement of amygdaloid neuronal dendritic arborization by fresh leaf juice of Centella asiatica (Linn) during growth spurt period
  19. (1992). Evaluation of learning and memory mechanisms employing elevated plus-maze in rats and mice,”
  20. (1996). Evidence that specific mtDNA point mutations may not accumulate in skeletal muscle during normal human aging,”
  21. (1978). Generation of superoxide radical during autoxidation ofhydroxylamine andanassayforsuperoxide dismutase,”
  22. (1997). Genetic and functional changes in mitochondria associatedwithaging,”Physiological Reviews,v ol.77,no .2,p p .
  23. (2009). H s i e h ,W .M .W u ,a n dM .L .H u ,“ S o yi s o fl a v o n e s attenuate oxidative stress and improve parameters related to aging and Alzheimer’s disease in C57BL/6J mice treated with d-galactose,” Food and Chemical Toxicology,v o l .4 7 ,n o .3 ,p p .
  24. (2002). ie ta l . ,“ M e l a t o n i nr e d u c e s memory changes and neural oxidative damage in mice treated withD-galactose,”Journal ofPineal Research,v ol.32,no .3,p p .
  25. (2001). Improving effects of SSF on memory deficits and pathological changes of neural and immunological systems in senescent mice,”
  26. (2007). J.Long,X.Wang,H.Gaoetal.,“D-Galactosetoxicityinmiceis associated with mitochondrial dysfunction: protecting effects of mitochondrial nutrient R-alpha-lipoic acid,”
  27. (2003). L i u ,a n dR .Y .W u ,“ E s t a b l i s h m e n to f the mimetic aging effect in mice caused by
  28. (2002). M.H.V.KumarandY.K.Gupta,“Effect ofdifferent extracts of Centella asiatica on cognition and markers of oxidative stress in rats,”
  29. (1997). Mechanism of cellular 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) reduction,”
  30. (1966). Mechanisms of lipid peroxide formation in animal tissues,”
  31. (1989). Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases,”
  32. (1995). Modelling the effects of agerelatedmtDNAmutationaccumulation;Complex Ideficiency, superoxide and cell death,”
  33. (2010). Naringin alleviates cognitive impairment, mitochondrial dysfunction and oxidative stress induced by d-galactose
  34. (2009). Neuroprotective effects of Centella asiatica against intracerebroventricular colchicine—induced cognitive impairment and oxidative stress,”
  35. (1999). P.V.Sharma,DravyagunaVignana,ChaukhambaPublications Vishwa Bharati Academy,
  36. (2009). Paeonol attenuates neurotoxicity and ameliorates cognitive impairment induced by d-galactose in ICR mice,”
  37. (2008). Possible involvement of advanced glycation end-products (AGEs) in the pathogenesis of Alzheimer’s disease,”
  38. (1967). Preparation of succinate dehydrogenase and reconstitution of succinate oxidase,”
  39. (1967). Preparations and properties of soluble
  40. (2007). Protective effect of Centella asiatica extract and powder on oxidative stress
  41. (1999). Protective effects ofasiaticosidederivatives againstbeta-amyloid neurotoxicity,”
  42. (1999). S o n g ,M .B a o ,D .L i ,a n dY .M .L i ,“ A d v a n c e dg l y c a t i o n
  43. (2003). T r o e n ,“ T h eb i o l o g yo fa g i n g ,
  44. (2001). The role of AGEs in aging: causation or correlation,”
  45. (1959). Tissue sulfhydryl groups,”
  46. (1997). Turrens, “Superoxide production by the mitochondrial respiratory chain,”