Enhancement of Arsenic Trioxide (As<sub>2</sub>O<sub>3</sub>)- Mediated Apoptosis Using Berberine in Human Neuroblastoma SH-SY5Y Cells

Kim, Dae Won; Ahan, Song Ho; Kim, Tae Young

doi:10.3340/jkns.2007.42.5.392

Cited by 35 publications

(23 citation statements)

References 27 publications

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“…Furthermore, berberine was found to maintain the cytotoxic effects of rapamycin on the HCC cells with a lower concentration of rapamycin, suggesting that berberine may minimize rapamycin-induced immunosuppression by allowing a lower dose of rapamycin to be used. Similar synergistic anticancer results have been reported in SH-SY5Y human neuroblastoma cells, where a low dose combination of berberine and As 2 O 3 , an anticancer agent that induces various side effects at high concentrations, was found to markedly decrease cell viability compared with treatment with a low dose of berberine or As 2 O 3 alone (17). Berberine is a small molecule, which is easily isolated from a large number of traditional medicinal plants and has strong anticancer properties without significant side effects (9,10).…”

Section: Discussionsupporting

confidence: 77%

Berberine sensitizes rapamycin-mediated human hepatoma cell death in vitro

Guo

Yan

Gao

et al. 2014

Molecular Medicine Reports

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Rapamycin is clinically used as an immunosuppressant. Increasing evidence suggests that rapamycin has an important inhibitory role in the development and progression of different types of cancer and that it is a promising candidate for cancer chemotherapy. Berberine is an isoquinoline alkaloid isolated from medicinal plant species, which has been used in traditional Chinese medicine with no significant side effects. Recent research has demonstrated that berberine has anticancer activity against various types of cancer, mediated through the suppression of mammalian target of rapamycin (mTOR). The present study aimed to investigate the in vitro synergistic anticancer effect of combined treatment of rapamycin at various concentrations (0, 10, 50, 100 and 200 nM) and berberine (62.5 µM) in SMMC7721 and HepG2 hepatocellular carcinoma (HCC) cell lines, and the potential underlying molecular mechanism. The combined use of rapamycin and berberine was found to have a synergistic cytotoxic effect, with berberine observed to maintain the cyotoxic effect of rapamycin on HCC cells at a lower rapamycin concentration. Moreover, the cells treated with the combination of the two agents exhibited significantly decreased protein levels of phosphorylated (p)‑p70S6 kinase 1 (Thr389), the downstream effector of mTOR, compared with the cells treated with rapamycin or berberine alone. Furthermore, overexpression of cluster of differentiation (CD) 147, a transmembrance glycoprotein associated with the anticancer effects of berberine, was found to upregulate p‑mTOR expression and inhibit cell death in SMMC7721 cells co‑treated with rapamycin and berberine. In conclusion, the findings of the present study suggest that the combined use of rapamycin and berberine may improve HCC therapy through synergistically inhibiting the mTOR signaling pathway, which is at least in part, mediated through CD147.

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Section: Discussionsupporting

confidence: 77%

Berberine sensitizes rapamycin-mediated human hepatoma cell death in vitro

Guo

Yan

Gao

et al. 2014

Molecular Medicine Reports

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“…On the other hand, Ber was found to affect the production of ROS (21). Therefore, we further observed the effects of Ber and/or yohimbine on cardiac TBARS content and SOD activity in mice.…”

Section: Ber and Yohimbine Prevent Lps-provoked Myocardial Dysfunctiomentioning

confidence: 69%

Pretreatment with Berberine and Yohimbine Protects Against LPS-Induced Myocardial Dysfunction Via Inhibition of Cardiac I-κBα Phosphorylation and Apoptosis in Mice

Wang¹,

Li²,

Wang³

et al. 2011

Shock

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Myocardial dysfunction is a common complication in sepsis and significantly contributes to the mortality of patients with septic shock. Our previous study demonstrated that pretreatment with berberine (Ber) protected against the lethality induced by LPS, which was enhanced by yohimbine, an [alpha]2-adrenergic receptor antagonist, and Ber combined with yohimbine also improved survival in mice subjected to cecal ligation and puncture. However, no studies have examined whether Ber and yohimbine reduce LPS-induced myocardial dysfunction. Here, we report that pretreatment with Ber, Ber combined with yohimbine, or yohimbine significantly reduced LPS-induced cardiac dysfunction in mice. LPS-provoked cardiac apoptosis, I-[kappa]B[alpha] phosphorylation, IL-1[beta], TNF-[alpha], and NO production were attenuated by pretreatment with Ber and/or yohimbine, whereas cardiac Toll-like receptor 4 mRNA expression, malondialdehyde content, and superoxide dismutase activity were not affected. These data demonstrate for the first time that pretreatment with Ber and/or yohimbine prevents LPS-induced myocardial dysfunction in mice through inhibiting myocardial apoptosis, cardiac I-[kappa]B[alpha] phosphorylation, and TNF-[alpha], IL-1[beta], and NO production, suggesting that activation of [alpha]2-adrenergic receptor in vivo may be responsible at least in part for LPS-induced cardiac dysfunction, and Ber in combination with yohimbine may be a potential agent for preventing cardiac dysfunction during sepsis.

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“…Combination of radiation with 5 and 10 µM berberine significantly increases the radio‐sensitivity of A549 cells, in which both autophagy and cell‐cycle G2/M arrest occur [Peng et al, 2008]. Combined treatment with As 2 O 3 and berberine also has an anti‐cancer effect in human neuroblastoma SH‐SY5Y cells that function through a mitochondria/caspase‐3 dependent‐signaling pathway [Kim et al, 2007]. Here, we have shown that berberine induces apoptotic and autophagic cell death in HCC cells, but further investigation is required to fully characterize the concomitant mediators and determinant switches of cell death induced by berberine alone or in combination with other therapies in cancer cell models and animal models.…”

Section: Discussionmentioning

confidence: 99%

Berberine induces autophagic cell death and mitochondrial apoptosis in liver cancer cells: The cellular mechanism

Wang

Feng

Zhu

et al. 2010

J of Cellular Biochemistry

262

170

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Extensive studies have revealed that berberine, a small molecule derived from Coptidis rhizoma (Huanglian in Chinese) and many other plants, has strong anti-tumor properties. To better understand berberine-induced cell death and its underlying mechanisms in cancer, we examined autophagy and apoptosis in the human hepatic carcinoma cell lines HepG2 and MHCC97-L. The results of this study indicate that berberine can induce both autophagy and apoptosis in hepatocellular carcinoma cells. Berberine-induced cell death in human hepatic carcinoma cells was diminished in the presence of the cell death inhibitor 3-methyladenine, or following interference with the essential autophagy gene Atg5. Mechanistic studies showed that berberine may activate mitochondrial apoptosis in HepG2 and MHCC97-L cells by increasing Bax expression, the formation of permeable transition pores, cytochrome C release to cytosol, and subsequent activation of the caspases 3 and 9 execution pathway. Berberine may also induce autophagic cell death in HepG2 and MHCC97-L cells through activation of Beclin-1 and inhibition of the mTOR-signaling pathway by suppressing the activity of Akt and up-regulating P38 MAPK signaling. This is the first study to describe the role of Beclin-1 activation and mTOR inhibition in berberine-induced autophagic cell death. These results further demonstrate the potential of berberine as a therapeutic agent in the emerging list of cancer therapies with novel mechanisms.

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Enhancement of Arsenic Trioxide (As₂O₃)- Mediated Apoptosis Using Berberine in Human Neuroblastoma SH-SY5Y Cells

Cited by 35 publications

References 27 publications

Berberine sensitizes rapamycin-mediated human hepatoma cell death in vitro

Berberine sensitizes rapamycin-mediated human hepatoma cell death in vitro

Pretreatment with Berberine and Yohimbine Protects Against LPS-Induced Myocardial Dysfunction Via Inhibition of Cardiac I-κBα Phosphorylation and Apoptosis in Mice

Berberine induces autophagic cell death and mitochondrial apoptosis in liver cancer cells: The cellular mechanism

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Enhancement of Arsenic Trioxide (As2O3)- Mediated Apoptosis Using Berberine in Human Neuroblastoma SH-SY5Y Cells

Cited by 35 publications

References 27 publications

Berberine sensitizes rapamycin-mediated human hepatoma cell death in vitro

Berberine sensitizes rapamycin-mediated human hepatoma cell death in vitro

Pretreatment with Berberine and Yohimbine Protects Against LPS-Induced Myocardial Dysfunction Via Inhibition of Cardiac I-κBα Phosphorylation and Apoptosis in Mice

Berberine induces autophagic cell death and mitochondrial apoptosis in liver cancer cells: The cellular mechanism

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Enhancement of Arsenic Trioxide (As₂O₃)- Mediated Apoptosis Using Berberine in Human Neuroblastoma SH-SY5Y Cells