Centella asiatica or known as ‘pegaga’ in Malaysia, is a popular medicinal herb, which is being used as main ingredient or incorporated into various herbal products. Apart from efficacy, the chemical profile and potential toxic effect of the plant are two important aspects of concern towards ensuring product satisfaction and safety of consumers. This paper reports the qualitative and quantitative chemical analysis of the leaf ethanolic extract of C. asiatica using LCMS/MS. The acute toxiciy effect of the extract and selected marker chemical constituents were further analysed using a zebrafish model. Twenty constituents, were identified and the main chemical marker constituents of the plant viz asiaticoside, asiatic acid, and madecassic acid were further quantified. Asiaticoside was found to be present in higher concentration than the other marker constituents. Meanwhile in the acute toxicity test, the LD50 of the extract on the zebrafish model was determined to be 1250 mg/L while 100% mortality was observed at the highest test concentration of 2500 mg/L. However, acute toxicity evaluation on four marker triterpenoids of the herb, i.e asiatic acid, madecassic acid, asiaticoside and madecassoside, indicated them to be quite safe on the zebrafish model, with no mortality shown for test concentrations between 10 to 500 mg/kg BW.
Dietary deficiency of ω3 fatty acid during development leads to impaired cognitive function. However, the effects of multiple generations of ω3 fatty-acid deficiency on cognitive impairment remain unclear. In addition, we sought to test the hypothesis that the cognitive impairments of ω3 fatty-acid-deficient mice are mediated through the arachidonic acid-cyclooxygenase (COX) pathway. To address these issues, C57BL/6J mice were bred for 3 generations and fed diets either deficient (DEF) or sufficient (SUF) in ω3 fatty acids. At postnatal day 21, the F3 offspring remained on the dam's diet or were switched to the opposite diet, creating 4 groups. In addition, 2 groups that remained on the dam's diet were treated with a COX inhibitor. At 19 wk of age, spatial-recognition memory was tested on a Y-maze. Results showed that 16 wk of SUF diet reversed the cognitive impairment of F3 DEF mice. However, 16 wk of ω3 fatty-acid-deficient diet impaired the cognitive performance of the F3 SUF mice, which did not differ from that of the F3 DEF mice. These findings suggest that the cognitive deficits after multigenerational maintenance on ω3 fatty-acid-deficient diet are not any greater than are those after deficiency during a single generation. In addition, treatment with a COX inhibitor prevented spatial-recognition deficits in F3 DEF mice. Therefore, cognitive impairment due to dietary ω3 fatty-acid deficiency appears to be mediated by the arachidonic acid-COX pathway and can be prevented by 16 wk of dietary repletion with ω3 fatty acids or COX inhibition.