Hepatocellular toxicity of kava leaf and root extracts

Lüde, Saskia; Török, Michael; Dieterle, S.; Jäggi, René; Büter, Karin Berger; Krähenbühl, Stephan

doi:10.1016/j.phymed.2007.11.003

Cited by 30 publications

(24 citation statements)

References 39 publications

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“…These findings suggest that depletion of glutathione is not the primary mechanism by which kavalactones induce hepatic injury. This is further supported by another study which found no significant increase in the ratio of oxidised to reduced glutathione (GSSG/GSH) in HepG2 cells treated with methanolic or acetonic extracts of kava root (Lude et al, 2008). However, a statistically significant increase in this ratio was found in cells treated with a methanolic leaf extract, suggesting that other kava constituents such as pipermethystine (which is present mainly in kava leaves) may deplete available glutathione.…”

Section: Discussionsupporting

confidence: 52%

Macrophage depletion ameliorates kavalactone damage in the isolated perfused rat liver

et al. 2012

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-Liver toxicity is a side effect observed with some herbal treatments, including Piper methysticum. The possible mechanisms responsible include inflammation subsequent to activation of liver macrophages and oxidative damage. Hepatotoxicity of the pharmacologically active component of Piper methysticum (kavalactones) was tested in isolated, perfused livers from rats which were pretreated with the macrophage intoxicant gadolinium chloride. Perfusions without kavalactones in gadolinium chloride pretreated and untreated livers were included as negative controls. Serial liver lobe biopsies were collected to measure temporal changes in available (reduced) hepatic glutathione. There were no statistically significant changes in reduced glutathione over the course of perfusion in any experimental group. Liver damage was observed using electron microscopy. Hepatic sinusoids displayed extensive damage to the endothelium in kavalactone-perfused, rat livers. This damage was significantly reduced by pre-treatment with gadolinium chloride. Hence liver macrophages may be a factor in liver injury induced by Piper methysticum. Characterisation and modulation of the liver macrophage response may enable the development of strategies to avoid these hepatic side effects.

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Section: Discussionsupporting

confidence: 52%

Macrophage depletion ameliorates kavalactone damage in the isolated perfused rat liver

et al. 2012

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“…In chronic inflammation or cirrhosis the stellate cells play an important role in hepatic fibrogenesis by the deposition of type I and III collagen within the sinusoidal space [33]. Meanwhile, other studies failed to show potential liver morphological changes [34,35]. This might be due to the lower dosage used in these studies.…”

Section: Histological Resultsmentioning

confidence: 92%

Kava extract drug

El-Kholy¹,

El-Salam

2011

The Egyptian Journal of Histology

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“…Many studies have reported that natural plants and/or their naturally occurring compounds, acacetin ( (Hsu et al, 2007), Piper methysticum Forster (Lude et al, 2008), Physalis angulata and Physalis peruviana (Wu et al, 2004), traditional herbal medicines; are potential inhibitors of tumor cell proliferation and apoptotic inducers in hepatoma cells. In fact, many plant derivatives have been used as anticancer agents in clinical patients (Katz, 2001).…”

Section: Discussionmentioning

confidence: 99%

Anti-invasion and apoptosis induction of chlorella (Chlorella sorokiniana) in Hep G2 human hepatocellular carcinoma cells

Chung¹,

Peng

Chu

et al. 2012

Journal of Functional Foods

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Apoptosis Invasion Human hepatocellular carcinoma cells Hep G2 cells A B S T R A C T The effects of 80% ethanolic extract derived from commercial granule chlorella (GPE) on cell viability, invasion capacity and apoptosis in human hepatoma cell line (Hep G2 cells) were investigated. The results demonstrated that GPE decreased cell viability, induced apoptosis and showed invasion inhibitory effects in the Hep G2 cells. GPE-triggered apoptosis was confirmed by 4 0 -6-diamidino-2-phenyindole (DAPI) staining and comet assay. GPE promoted an increase of reactive oxygen species (ROS) and Ca 2+ , and loss of mitochondrial membrane potential (DWm) accompanied by cytochrome c release that was due to the decrease of Bcl-2 in the Hep G2 cells. GPE also induced the protein levels of apoptosisinducing factor (AIF), increased the levels of caspase-3, -8 and -9, and stimulated the levels of fatty acid synthase (Fas) and Fas ligand (FasL) in the Hep G2 cells. Additionally GPE inhibited invasion of Hep G2 cells by down-regulation of the expression of matrix metalloproteinase (MMP)-2 and -9. Furthermore, cellular glutathione content and superoxide dismutases (SOD) activities were significantly reduced and thiobarbituric acid-reactive substances (TBARS) levels were significantly increased after GPE treatment. These results suggest that GPE can induce cytotoxicity on Hep G2 cells and inhibit the invasive capacity of malignant cells.

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Hepatocellular toxicity of kava leaf and root extracts

Cited by 30 publications

References 39 publications

Macrophage depletion ameliorates kavalactone damage in the isolated perfused rat liver

Macrophage depletion ameliorates kavalactone damage in the isolated perfused rat liver

Kava extract drug

Anti-invasion and apoptosis induction of chlorella (Chlorella sorokiniana) in Hep G2 human hepatocellular carcinoma cells

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