Enhanced induction of mitochondrial damage and apoptosis in human leukemia HL-60 cells by the Ganoderma lucidum and Duchesnea chrysantha extracts

Kim, Kug Chan; Kim, Jin Sik; Son, Jung Kyu; Kim, In Gyu

doi:10.1016/j.canlet.2006.02.014

Cited by 64 publications

(47 citation statements)

References 16 publications

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“…In addition to western therapies for cancer prevention, there are also studies on anti-tumor effects of herbal medicines such as D. bulbifera, Tripterygium wilfordii, and Andrographis paniculata (Shamon et al, 1997;Gao et al, 2002;Kumar et al, 2004). Compatibility is a main principle of Chinese medicinal herbs, and some reports have demonstrated that compatibility may lead to eliminating toxicity or reinforcing bioactivities (Kim et al, 2007;Gao et al, 2009). Ferulic acid is the main bioactive component of A. sinensis root, and our results from ALT/AST assays and histological observations are the first to demonstrate that ferulic acid prevents diosbulbin B-induced liver injury.…”

Section: Discussionmentioning

confidence: 99%

Ferulic acid prevents liver injury and increases the anti-tumor effect of diosbulbin B in vivo

Wang

Sheng

et al. 2014

J. Zhejiang Univ. Sci. B

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Abstract:The present study is designed to investigate the protection by ferulic acid against the hepatotoxicity induced by diosbulbin B and its possible mechanism, and further observe whether ferulic acid augments diosbulbin Binduced anti-tumor activity. The results show that ferulic acid decreases diosbulbin B-increased serum alanine transaminase/aspartate transaminase (ALT/AST) levels. Ferulic acid also decreases lipid peroxide (LPO) levels which are elevated in diosbulbin B-treated mice. Histological evaluation of the liver demonstrates hydropic degeneration in diosbulbin B-treated mice, while ferulic acid reverses this injury. Moreover, the activities of copper-and zinc-containing superoxide dismutase (CuZn-SOD) and catalase (CAT) are decreased in the livers of diosbulbin B-treated mice, while ferulic acid reverses these decreases. Further results demonstrate that the mRNA expressions of CuZn-SOD and CAT in diosbulbin B-treated mouse liver are significantly decreased, while ferulic acid prevents this decrease. In addition, ferulic acid also augments diosbulbin B-induced tumor growth inhibition compared with diosbulbin B alone. Taken together, the present study shows that ferulic acid prevents diosbulbin B-induced liver injury via ameliorating diosbulbin B-induced liver oxidative stress injury and augments diosbulbin B-induced anti-tumor activity.

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Section: Discussionmentioning

confidence: 99%

Ferulic acid prevents liver injury and increases the anti-tumor effect of diosbulbin B in vivo

Wang

Sheng

et al. 2014

J. Zhejiang Univ. Sci. B

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“…2B). Treating cells with GDE alone resulted in about 30% of the cells undergoing apoptosis after 48 h of treatment (14). Combining GDE with 2 Gy of γ-radiation increased the Figure 1.…”

Section: Combined Treatment With Gde and Radiation Enhances Apoptosismentioning

confidence: 94%

“…A previous study in this laboratory demonstrated that combined treatment with extracts of the medicinal mushroom Ganoderma lucidum and the herb Duchesnea chrysantha (GDE) causes an enhanced induction of mitochondrial damage and apoptosis as well as growth inhibition in human leukemia HL-60 cells (14). Moreover, the combination of these extracts was selectively toxic to the leukemic cells, whereas no cytotoxic effect was observed in the normal human peripheral blood mononuclear cells, raising the possibility that this strategy has the potential for therapeutic selectivity.…”

Section: Introductionmentioning

confidence: 99%

Enhancement of radiation response with combined Ganoderma lucidum and Duchesnea chrysantha extracts in human leukemia HL-60 cells

Kim

Jun²,

Kim³

et al. 2008

Int J Mol Med

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Abstract. We previously demonstrated that combined treatment with extracts of the medicinal mushroom Ganoderma lucidum and the herb Duchesnea chrysantha (GDE) significantly suppresses cell growth and selectively induces apoptosis in human leukemia HL-60 cells, but not in normal cells. GDE's mechanism of action and its activity against HL-60 cells suggest that it could be suitable for the combined-modality treatment of hematological malignancies. In the present study, we examined whether treatment with a combination of GDE and ionizing radiation enhances the therapeutic effect. We demonstrated that, when used in combination with radiation at a clinically relevant dose of 2 Gy, GDE further suppressed cell proliferation and induced apoptosis as well as micronuclei formation in HL-60 cells, leading to increased cell death. Furthermore, GDE pretreatment not only reduced radiation-induced G 2 /M-phase arrest, but also induced G 1 -phase arrest. These events are associated with the inhibition of cyclin-dependent kinase 1 (CDK1) phosphorylation and the dephosphorylation of retinoblastoma protein (pRB). Collectively, these data show that combined treatment with GDE and radiation enhances radiation-induced apoptosis and overall cell death. These findings may be clinically relevant and suggest a novel therapeutic strategy for increasing the efficacy of radiotherapy.

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“…Many agents can induce, directly or indirectly, apoptosis by insult to the mitochondria [34,35] . Apoptosis could cause loss of Δψm and release of cytochrome C into cytosol, and induce caspase-9-dependent activation of caspase-3 [13] .…”

Section: Discussionmentioning

confidence: 99%

Scutellaria barbate extract induces apoptosis of hepatoma H22 cells via the mitochondrial pathway involving caspase-3

Dai¹,

Wang²,

Li³

et al. 2008

WJG

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of cell cycle, the percentage of cells in S phase was significantly decreased, while the percentage of cells in G 1 phase was increased. Flow cytometry assay also showed that ESB had a positive effect on apoptosis. Typical apoptotic morphologies such as condensation and fragmentation of nuclei and blebbing membrane of apoptotic cells could be observed under transmission electron microscope and fluorescence microscope. To further investige the molecular mechanism behind ESB-induced apoptosis, ESB-treated cells rapidly lost their mitochondrial transmembrane potential, released mitochondrial cytochrome C into cytosol, and induced caspase-3 activity in a dose-dependent manner. CONCLUSION: ESB can effectively inhibit the proliferation and induce apoptosis of H22 cells involving loss of mitochondrial transmembrane potential, release of cytochrome C, and activation of caspase-3. INTRODUCTIONScutellaria barbata D.Don (S. barbata) is a perennial herb, also known as Ban-Zhi-Lian (barbat sskullcap) in traditional Chinese medicine. It is mainly distributed in southern China and has been used as an antitumor agent for lung cancer, digestive system cancer, hepatoma, breast cancer, and chorioepithelioma as well as an anti-inflammatory agent and a diuretic in China and Korea [1][2][3][4][5][6][7][8][9] . Extracts from S. barbata (ESB) have in vitro growth inhibitory effects on a number of human cancers including leukemia, colon cancer, hepatoma and skin cancer [4][5][6][7][8][9][10] . However, its antitumor mechanism still remains unclear.It was reported that many Chinese herbs have anticancer properties and induce apoptosis [11] . Three apoptotic pathways have been addressed, including the mitochondrial pathway [12,13] , death receptor pathway [14] , and endoplasmic reticulum stress-mediated apoptosis pathway [15] . The mitochondrial pathway initiates apoptosis in most physiological and pathological situations. Permeabilization outside mitochondrial membrane plays the most important role in mitochondrial apoptosis. In the mitochondria-initiated pathway, mitochondria undergoing permeability transition release apoptogenic proteins such as cytochrome C or apoptosis-inducing factor from the mitochondrial intermembrane space into the cytosol [16] . Released cytochrome C can activate caspase-9, and activated caspase-9 in turn cleaves and activates executioner caspase-3. After caspase-3 activation, some specific substrates for caspase-3 such as poly (ADP-ribose) and polymerase (PARP) are cleaved, and eventually lead to apoptosis [17] . In this study, S. barbata extract showed anti-tumor activity in vitro and could inhibit the growth of mouse H22 hepatoma cells by inhibiting cell apoptosis and cytotoxic effects, demonstrating that the extract from S. barbata can strongly inhibit cell proliferation and induce apoptosis of H22 cells through the mitochondrial dysfunction pathway. MATERIALS AND METHODSReagents and animals N e w b ov i n e s e r u m ( G i b c o, U S A ) , R P M I -1 6 4 0 medium(Gibco, USA), propidium iodide (PI) (Sigma, ...

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Enhanced induction of mitochondrial damage and apoptosis in human leukemia HL-60 cells by the Ganoderma lucidum and Duchesnea chrysantha extracts

Cited by 64 publications

References 16 publications

Ferulic acid prevents liver injury and increases the anti-tumor effect of diosbulbin B in vivo

Ferulic acid prevents liver injury and increases the anti-tumor effect of diosbulbin B in vivo

Enhancement of radiation response with combined Ganoderma lucidum and Duchesnea chrysantha extracts in human leukemia HL-60 cells

Scutellaria barbate extract induces apoptosis of hepatoma H22 cells via the mitochondrial pathway involving caspase-3

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