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Pharmaceutical Biology 2010-Dec

Antitumor activity of Sansevieria roxburghiana rhizome against Ehrlich ascites carcinoma in mice.

Vain rekisteröityneet käyttäjät voivat kääntää artikkeleita
Kirjaudu sisään Rekisteröidy
Linkki tallennetaan leikepöydälle
Pallab Kanti Haldar
Biswakanth Kar
Asis Bala
Sanjib Bhattacharya
Upal Kanti Mazumder

Avainsanat

Abstrakti

BACKGROUND

Sansevieria roxburghiana Schult. & Schult. f. (Agavaceae) is a herbaceous perennial plant traditionally used for coughs, rheumatism; as an expectorant, febrifuge, purgative, and tonic.

OBJECTIVE

To evaluate the hydroalcoholic extract of S. roxburghiana rhizome (HASR) for antitumor activity against Ehrlich ascites carcinoma (EAC) in Swiss albino mice.

METHODS

Twenty-Four hours after intraperitoneal inoculation of tumor (EAC) cells in mice, HASR was administered at 50 and 100 mg/kg body weight for nine consecutive days. On day 10 half of the mice were sacrificed and rest were kept alive for assessment of increase in life-span. The antitumor effect of HASR was assessed by evaluating tumor volume, packed cell count, viable and non-viable tumor cell count, median survival time and increase in life-span of EAC bearing hosts. Hematological profiles and serum biochemical parameters were estimated. Further, antioxidant properties were assessed by estimating lipid peroxidation, reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT).

CONCLUSIONS

HASR showed a significant (p < 0.001) decrease in tumor volume, packed cell volume and viable cell count and increased the life span of EAC bearing mice. Hematological and serum biochemical profiles were restored to normal levels in HASR treated mice as compared to EAC control. HASR treatment significantly (p <0.001) decreased lipid peroxidation and recovered GSH, SOD and CAT towards normal as compared to EAC control.

CONCLUSIONS

The present study demonstrates that S. roxburghiana rhizome exhibited remarkable antitumor activity in Swiss mice that is plausibly attributable to its augmenting endogenous antioxidant mechanisms.

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