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WHO monographs on selected medicinal plants - travolekar.ru

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<str<strong>on</strong>g>WHO</str<strong>on</strong>g> <str<strong>on</strong>g>m<strong>on</strong>ographs</str<strong>on</strong>g> <strong>on</strong> <strong>selected</strong> <strong>medicinal</strong> <strong>plants</strong><br />

the liver was also increased in animals treated with the rhizome extract.<br />

Intragastric administrati<strong>on</strong> of a methanol extract of the c<strong>ru</strong>de d<strong>ru</strong>g to mice,<br />

at a dose of 670.0 mg/kg bw, suppressed carb<strong>on</strong> tetrachloride-induced<br />

hepatotoxicity (26).<br />

Inducti<strong>on</strong> of liver injury in 16 mice by injecti<strong>on</strong> of carb<strong>on</strong> tetrachloride<br />

(CCl 4<br />

) for 9 weeks was reduced by the rhizome. Eight animals were<br />

fed the c<strong>ru</strong>de d<strong>ru</strong>g extract (12.0 mg/kg bw) daily, for 10 days before CCl 4<br />

injecti<strong>on</strong>. C<strong>on</strong>trol mice (n = 6) were injected with olive oil for the same<br />

period. Se<strong>ru</strong>m markers of liver injury and histology of liver tissues were<br />

studied. Hepatic glutathi<strong>on</strong>e, total thiol, glucose-6-phosphate dehydrogenase,<br />

catalase, lipid peroxidati<strong>on</strong> and plasma membrane-bound Na + /K +<br />

ATPase were also assessed. Feeding the c<strong>ru</strong>de d<strong>ru</strong>g extract to CCl 4<br />

-treated<br />

mice reduced se<strong>ru</strong>m alanine aminotransferase, aspartate aminotransferase,<br />

liver glutathi<strong>on</strong>e, catalase and membrane-bound Na + /K + ATPase.<br />

Histological lesi<strong>on</strong>s of liver and lipid peroxidati<strong>on</strong> were also significantly<br />

fewer in these animals (27).<br />

Intragastric administrati<strong>on</strong> of a dried 75% methanol extract of the<br />

powdered rhizomes, at a dose of 150.0 mg/kg bw inhibited the inducti<strong>on</strong><br />

of N-nitrosodiethylamine-induced hepatocarcinogenesis and prevented<br />

lipid peroxide formati<strong>on</strong> as well as reducing the levels of aniline hydrase<br />

and -glutamyl transpeptidase (28). Intragastric administrati<strong>on</strong> of a 95%<br />

ethanol extract of the c<strong>ru</strong>de d<strong>ru</strong>g at a dose of 12.0–25.0 mg/kg bw for<br />

7 days reduced galactosamine and m<strong>on</strong>ocrotaline-induced hepatotoxicity<br />

(29, 30). The effect of an iridoid glycoside c<strong>on</strong>taining an extract of the rhizome<br />

<strong>on</strong> the carcinogenic resp<strong>on</strong>se and <strong>on</strong> hepatic and renal antioxidant<br />

enzymes of rats treated with 1,2-dimethylhydrazine hydrochloride was<br />

investigated (15). 1,2-dimethylhydrazine hydrochloride-induced hepatic<br />

carcinogenic resp<strong>on</strong>se and necrosis were inhibited by oral administrati<strong>on</strong><br />

of the extract at doses of 40.0 and 200.0 mg/kg bw. Liver -glutamyl transpeptidase<br />

was reduced to 0.22 ± 0.04 and 0.18 ± 0.03 nmol/mg protein,<br />

respectively, by the treatment. Depleti<strong>on</strong> of hepatic and renal antioxidant<br />

enzymes such as catalase and superoxide dismutase levels induced by 1,2-<br />

dimethylhydrazine hydrochloride was reversed by the treatment, and elevated<br />

lipid peroxidati<strong>on</strong> in liver, kidney and se<strong>ru</strong>m was reduced. Renal<br />

glutathi<strong>on</strong>e S-transferase and hepatic glutathi<strong>on</strong>e levels which had been<br />

depleted by 1,2-dimethylhydrazine hydrochloride were also increased.<br />

Oral administrati<strong>on</strong> of a standardized iridoid glycoside fracti<strong>on</strong> of the<br />

c<strong>ru</strong>de d<strong>ru</strong>g (25.0 mg/kg bw daily for 15 days), significantly reduced the<br />

increases in the activities of tau-glutamyl transpeptidase, 5´-nucleotidase,<br />

acid phosphatase and acid rib<strong>on</strong>uclease, and decreased the activities of succinate<br />

dehydrogenase and glucose-6-phosphatase in liver, and the level of<br />

264

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