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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2011.1
- 수록면
- 47 - 56 (10page)
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Objectives : This study investigated whether the water extract of Spatholobi Caulis (SCE) has the ability to protect hepatocyte against oxidative stress induced by tert-butylhydroperoxide (tBHP) in vitro and $CCl_4$ in vivo. Methods : In vitro, HepG2 cells pre-treated with Spatholobi Caulis water extract (1, 3, 10, $30{\mu}g$/ml) for 12h and further incubated with tBHP ($100{\mu}M$) for the next 12h. Cell viability was assessed by MTT assay. In vivo, rats were orally administrated with the aqueous extract of Spatholobi Caulis (SCE; 50, 100 mg/kg) for 4 days and then, injected with $CCl_4$ 1 mg/kg body weight to induce acute liver damage. Results : Treatment with SCE inhibited cell death induced by tBHP, as evidenced by alterations in the levels of the proteins associated with apoptosis:SCE prevented a decrease in $Bcl_2$, and cleavage of poly(ADP-ribose)polymerase and pro-caspase-3. Moreover, SCE inhibited the ability of tBHP to generate $H_2O_2$ production, thereby restoring GSH content. Moreover, SCE treatments in rats effectively decreased liver injuries induced by a single dose of $CCl_4$, as evidenced by decreases in hepatic degeneration and inflammation as well as plasma alanine aminotransferase and lactate dehydrogenase activities. Consistently, treatments of SCE also protected liver in rats stimulated by $CCl_4$, as indicated by restoration GSH and prevention of MDA in the liver. Conclusions : SCE has the ability 1) to protect hepatocyte against oxidative stress induced by tBHP and 2) to prevent $CCl_4$-inducible acute liver toxicity. Present findings may be informative not only in elucidating the pharmacological mechanism of Spatholobi Caulis, but in determining its potential application for oxidative cellular damage in the liver.
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참고문헌 (39)
참고문헌 신청
Korean Central Association of Cancer Registries of Ministry of Health and Welfare / 2006 and 2007 cancer rates
Ramadori G / 2008 / Physiology and pathophysiology of liver inflammation, damage and repair / J Physiol Pharmacol 59(Suppl 1):107~117
Effendi K / 2010 / Molecular pathology in early hepatocarcinogenesis / Oncology 78(2):157~160
Papa S / 2009 / Mechanisms of liver disease： cross-talk between the NF-kappaB and JNK pathways / Biol Chem 390(10):965~976
Liu J / 2009 / Role of oxidative stress in cadmium toxicity and carcinogenesis / Toxicol Appl Pharmacol 238(3):209~214
Ramadori G / 2008 / Physiology and pathophysiology of liver inflammation, damage and repair / J Physiol Pharmacol 59(Suppl 1):107~117
Effendi K / 2010 / Molecular pathology in early hepatocarcinogenesis / Oncology 78(2):157~160
Papa S / 2009 / Mechanisms of liver disease： cross-talk between the NF-kappaB and JNK pathways / Biol Chem 390(10):965~976
Liu J / 2009 / Role of oxidative stress in cadmium toxicity and carcinogenesis / Toxicol Appl Pharmacol 238(3):209~214
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