Effect of Cassia fistula Linn. leaf extract on diethylnitrosamine induced hepatic injury in rats

Pradeep, Kannampalli; Chandrasekaran, Victor Raj Mohan; Gobianand, Kuppannan; Karthikeyan, S.

doi:10.1016/j.cbi.2006.12.011

Cited by 79 publications

(54 citation statements)

References 34 publications

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“…The higher serum aminotransferase activities could be the result of leakage from damaged liver cell membranes after doxorubicin treatment. 18) In our study, pretreatment of berberine provided dramatic suppress from damage of mice and ameliorated liver function by lowering serum ALT and AST levels. The protective effect of berberine against doxorubicin was also evaluated in the livers from a histopathologic point of view.…”

Section: Discussionsupporting

confidence: 51%

Protective Effects of Berberine on Doxorubicin-Induced Hepatotoxicity in Mice

Zhao

Zhang

Tong

et al. 2012

Biological & Pharmaceutical Bulletin

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Doxorubicin, a very potent and often used anti-cancer drug, is largely limited due to the dose-related toxic effects. The present study investigated whether berberine, a natural product alkaloid, can reduce the liver injury induced by doxorubicin. Mice of either gender were randomly divided into four groups: the control group, doxorubicin group, berberine group, and berberine doxorubicin group. In the tests, body weight, general condition and mortality of the mice were observed, and serum alanine aminotransferase and aspartate transaminase levels were determined to evaluate liver function. Furthermore, the liver was excised for determination of the weight changes, as well as histopathological analysis in the tissues. Mortality rate and significant decline in body weight, and increased plasma alanine aminotransferase and aspartate transaminase activities were observed in doxorubicin-treated mice. These changes were significantly prevented by pretreatment with berberine. Histopathological studies showed that doxorubicin caused structural injuries, such as vascular congestion, inflammatory cell infiltration, hepatocellular degeneration and necrosis, fibrosis in the liver. These histopathological changes were largely attenuated by berberine pretreatment. These findings indicate that berberine has the hepatoprotective effect on doxorubicin-induced liver injury in mice.

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Section: Discussionsupporting

confidence: 51%

Protective Effects of Berberine on Doxorubicin-Induced Hepatotoxicity in Mice

Zhao

Zhang

Tong

et al. 2012

Biological & Pharmaceutical Bulletin

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“…The hepatoprotective property of the hexane leaf extract of this plant against carbon tetrachloride-and paracetamol-induced hepatotoxicity was demonstrated in rats (Bhakta et al, 1999(Bhakta et al, , 2001. Studies conducted in this laboratory have shown the protective properties of the ethanol leaf extract of Cassia fistula in post-treatment of carbon tetrachloride-induced liver damage in rats (Pradeep et al, 2005).…”

Section: Introductionmentioning

confidence: 92%

Antiulcer activity of ethanol leaf extract ofCassia fistula

Karthikeyan

Gobianand

2010

Pharmaceutical Biology

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“…Furthermore, Kiruthiga et al [57], showed, that administration of silymarin enhanced the activities of antioxidant enzymes, SOD, CAT, glutathione peroxidase (GPx), GR and glutathione-S-transferase (GST), together with a decrease in the levels of MDA, a marker for lipid peroxidation, in erythrocytes exposed to H 2 O 2 . Also, silymarin exhibited an excellent hepatoprotective and antioxidant properties by restoring the hepatic marker enzyme activities and reversing the oxidant-antioxidant imbalance during diethylnitrosamine-induced oxidative stress in rats [58].…”

Section: Discussionmentioning

confidence: 98%

“…Repeated exposure to lower doses of DMN as small as 10 and 20 mg/kg causes sub-acute and chronic liver injury with varying degrees of necrosis, fibrosis, and nodular regeneration [11,12]. Metabolism of DMN produces formaldehyde and methanol, coupled with hydrogen peroxide (H 2 O 2 ), superoxide anion (O 2 -), hydroxyl radicals (OH Á ), and reacting with nucleic acids and proteins to form methylated macromolecules, resulting in oxidative stress causing liver damage [13]. Conventional or synthetic drugs used in the treatment of liver fibrosis are sometimes inadequate and can have serious adverse effects [14].…”

Section: Introductionmentioning

confidence: 99%