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Protective Activities of Cistanoside A on CCl4 Induced Hepatotoxicity in Mice

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407 ISSN 0326-2383

KEY WORDS: Cistanoside A, CCl4, Free radical, Hepatoprotection, Respiratory chain.

* Author to whom correspondence should be addressed. E-mail:louria@126.com

Latin American Journal of Pharmacy

(formerly

Acta Farmacéutica Bonaerense)

Lat. Am. J. Pharm.

31

(3): 407-13 (2012)

Regular Article Received: April 15, 2011 Revised version: June 3, 2011 Accepted: June 5, 2011

Protective Activities of

Cistanoside

A

on CCl

4

Induced Hepatotoxicity in Mice

Huiying LUO

1,2

*, Juan LI

3

, Lijuan WANG

1,2

& Lijuan ZHU

1,2

1

Department of Pharmacology, Gansu College of Traditional Chinese Medicine.

Av. Dingxi, 30, Lanzhou, 730000, P.R.China

2

Key Laboratory of Pharmacology and Toxicology for Traditional Chinese Medicine of Gansu Province.

Av. Dingxi, 30, Lanzhou, 730000, P.R.China

3

Centre for Molecular Biology, the first hospital of Lanzhou University,

Av. Donggang 90, Lanzhou, 730000, P.R.China

SUMMARY. To evaluate the protective efficacy of Cistanoside A (C.A), a phenylethanol glycoside isolated from Cistanche deserticola, on CCl4induced hepatotoxicity in mice, 50 animals were divided into five

dif-ferent protocols, and hepatic functional index were detected by diagnostic kits. Histological changes were compared by H&E stain. Activities of mitochondrial antioxidant enzymes (GST, SOD, and CAT) and res-piratory marker enzymes (MDH, SDH, NADH dehydrogenase, and cytochrome c oxidases) were mea-sured. To confirm the effect of C.A on free radical, tests on the free radical scavenging activities were also carried out in vitro. We found treatment with C.A (10, 20 mg/kg o.p. for 7 days) could significantly amelio-rated the levels of hepatic function indices (AST, ALT, ALP and LDH) (P < 0.05). The biochemical results were also confirmed by histopathological examination. C.A treatment decreased the ballooning degenera-tion, moderated the hepatocytes apoptosis, and alleviated centrilobular and bridging necrosis which were observed in the CCl4 control group. Following experiments revealed that C.A could increase the activities of mitochondrial antioxidant enzymes (GST, SOD, and CAT) and respiratory marker enzymes (MDH, SDH, NADH dehydrogenase, and cytochrome c oxidases) (P < 0.05). In vitro, C.A exhibited strong scav-enging activities for DPPH radical and superoxide anion radical. Our results revealed that C.A possess protective activities on CCl4induced hepatotoxicity in mice, which was involved with increasing free

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