Effect of Centella asiatica leaf powder on oxidative markers in brain regions of prepubertal mice in vivo and its in vitro efficacy to ameliorate 3-NPA-induced oxidative stress in mitochondria

• Published in: Phytomedicine (Stuttgart) 2008-11, Vol.15 (11), p.971-984
• Main Authors: Shinomol, George K., Muralidhara
• Format: Article
• Language: English
• Subjects: 3-NPA; Animals; Antioxidants - metabolism; Biomarkers - metabolism; Brain - drug effects; Brain - metabolism; Brain regions; Centella; Centella asiatica; Enzymes - metabolism; Glutathione - metabolism; Hydrogen Peroxide - metabolism; In vitro; Male; Malondialdehyde - metabolism; Mice; Mitochondria - drug effects; Mitochondria - metabolism; Nitro Compounds - adverse effects; Oxidative markers; Oxidative Stress - drug effects; Plant Leaves; Plants, Medicinal; Prepubertal mice mitochondria; Propionates - adverse effects; Protein Carbonylation - drug effects; Puberty; Reactive Oxygen Species - metabolism; Triterpenes - pharmacology
• ISSN: 0944-7113; 1618-095X
• DOI: 10.1016/j.phymed.2008.04.010

Centella asiatica (CA) is a common medicinal plant used in the ayurvedic system of medicine to treat various ailments and as a memory enhancer. Despite its extensive usage in children, data on its ability to modulate neuronal oxidative stress in prepubertal rodents are limited. Hence in the present study we have addressed primarily two questions (i) whether dietary intake of CA leaf powder possess the propensity to modulate endogenous oxidative markers in mouse brain regions and (ii) the efficacy of CA aqueous extract to abrogate 3-nitropropionic acid (3-NPA)-induced oxidative stress in brain mitochondria in vitro. Prepubertal male mice were fed CA-incorporated diet (0.5 and 1%) for 4 weeks, and biochemical markers of oxidative stress in brain regions were determined. Mice fed CA showed significant diminution in the levels of malondialdehyde (30–50%), reactive oxygen species (32–42%) and hydroperoxide levels (30–35%), which was accompanied by enhanced activities of antioxidant enzymes in all brain regions. While the levels of reduced glutathione and total thiols were elevated, the protein carbonyl content was decreased in brain among CA-fed mice. Interestingly, the oxidative markers among brain mitochondria of CA-fed mice were also significantly diminished (malondialdehyde, 25%; ROS, 30%; hydroperoxides, 35% and protein carbonyls, 28%). Further, the aqueous extract of CA showed significant free radical scavenging activity determined in established chemical test systems (viz., DPPH, superoxide and hydroxyl radical scavenging activity). Furthermore, the aqueous extract of CA markedly ameliorated the 3-NPA induced oxidative stress response in brain mitochondria under in vitro exposure,. Taken together, these data suggest that CA has the propensity to modulate both endogenous and neurotoxicant induced oxidative impairments in the brain and may be effectively employed as a neuroprotective adjuvant to abrogate oxidative stress in vivo.