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Amla (Emblica officinalis Gaertn.) prevents dyslipidaemia and oxidative stress in the ageing process

Takako Yokozawaa1 c1, Hyun Young Kima1, Hyun Ju Kima1, Tsutomu Okuboa2, Djoing-Chi Chua2 and Lekh Raj Junejaa2

a1 Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan

a2 Bio-nutrition Division, Taiyo Kagaku Co. Ltd, 1–3 Takaramachi, Yokkaichi 510-0844, Japan


Amla (Emblica officinalis Gaertn.) is widely used in Indian medicine for the treatment of various diseases. We have investigated the effects of amla on the lipid metabolism and protein expression involved in oxidative stress during the ageing process. SunAmla or ethyl acetate extract of amla, a polyphenol-rich fraction, was administered at a dose of 40 or 10 mg/kg body weight per d for 100 d to young rats aged 2 months and aged rats aged 10 months. The lipid levels, such as cholesterol and TAG, in serum and liver were markedly elevated in aged control rats, while they were significantly decreased by the administration of amla. The PPARα is known to regulate the transcription of genes involved in lipid and cholesterol metabolism. The PPARα protein level in liver was reduced in aged control rats. However, the oral administration of amla significantly increased the hepatic PPARα protein level. In addition, oral administration of amla significantly inhibited the serum and hepatic mitochondrial thiobarbituric acid-reactive substance levels in aged rats. Moreover, the elevated expression level of bax was significantly decreased after the oral administration of amla, while the level of bcl-2 led to a significant increase. Furthermore, the expressions of hepatic NF-κB, inducible NO synthase (iNOS), and cyclo-oxygenase-2 (COX-2) protein levels were also increased with ageing. However, amla extract reduced the iNOS and COX-2 expression levels by inhibiting NF-κB activation in aged rats. These results indicate that amla may prevent age-related hyperlipidaemia through attenuating oxidative stress in the ageing process.

(Received October 07 2006)

(Revised December 06 2006)

(Accepted December 19 2006)


c1 *Corresponding author: Dr Takako Yokozawa, fax +81 76 434 5068, email yokozawa@inm.u-toyama.ac.jp


Abbreviations: COX-2, cyclo-oxygenase-2; EtOAc, ethyl acetate; IκB-α, inhibitor binding protein κB-α; iNOS, inducible NO synthase; PMSF, phenylmethyl sulfonyl fluoride; TBA, 2-thiobarbituric acid