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Last Updated: 2 months ago

Possible Interaction: Emodin and Gemcitabine

supplement:

Emodin

Research Papers that Mention the Interaction

Emodin and gemcitabine combination treatments resulted in decreased cell proliferation and increased apoptosis in Bxpc-3/Gem cells.
International journal of oncology  •  2013  |  View Paper
Interestingly, emodin increases the sensitivity of pancreatic cancers to other chemotherapeutic agents such as gemcitabine.
Immunopharmacology and immunotoxicology  •  2013  |  View Paper
Emodin enhanced the SW1990/Gem cell sensitivity to gemcitabine in a time-dependent manner.
Emodin monotherapy or combination with gemcitabine both decreased the gene and protein expression levels of MDR-1 (P-gp), NF-κB and Bcl-2 and inhibited the function of P-gp, but increased the expression levels of Bax, cytochrome-C (cytosol), caspase-9 and -3, and promoted cell apoptosis.
Emodin promoted cell apoptosis of the gemcitabine-resistant cell line SW1990/Gem in a dose-dependent manner.
This demonstrated that emodin had a reversing effect on the gemcitabine-resistant cell line SW1990/Gem, possibly via decreasing the function of P-gp and activating the mitochondrial apoptosis pathway in vitro.
International journal of oncology  •  2012  |  View Paper
Emodin potentiated the antitumor effects of gemcitabine in pancreatic cancer, which was related to the down-regulation of NF-κB.
Furthermore, emodin combined with gemcitabine induced a higher percentage of growth inhibition and apoptosis in both pancreatic cancer cell lines compared to gemcitabine alone.
Molecular medicine reports  •  2011  |  View Paper
CONCLUSION Emodin could potentiate the inhibition of pancreatic cancer growth induced by gemcitabine both in vitro and in vivo, which might be achieved by up-regulating the expression of Bax and down-regulating the expression of Bcl-2.
CONCLUSION Emodin could potentiate the inhibition of pancreatic cancer growth induced by gemcitabine both in vitro and in vivo, which might be achieved by up-regulating the expression of Bax and down-regulating the expression of Bcl-2.
Emodin combined with gemcitabine could significantly inhibit the growth of pancreatic xenograft tumors, increase the positive expression of Bax in tumor tissues, obviously decrease the positive expressions of Ki-67 and Bcl-2 (P < 0.05).
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine  •  2012  |  View Paper
…,emodin … gemcitabine on pancreatic caner cells in vitro and in vivo by inhibiting the activity of NF-κB. Here, for the first time, we demonstrated that … VEGF, MMP-2, MMP-9, and eNOS), and reduced eNOS phosphorylation, as evidenced by both immunohistochemistry and western blot analysis of implanted tumors.
…,emodin … gemcitabine on pancreatic caner cells in vitro and in vivo by inhibiting the activity of NF-κB. Here, for the first time, we demonstrated that … VEGF, MMP-2, MMP-9, and eNOS), and reduced eNOS phosphorylation, as evidenced by both immunohistochemistry and western blot analysis of implanted tumors.
PloS one  •  2012  |  View Paper
Our research demonstrated that the combination of emodin and gemcitabine resulted in significantly reduced tumor volumes compared to gemcitabine or emodin treatment alone.
International journal of oncology  •  2012  |  View Paper
In addition to in vitro results, emodin in combination with gemcitabine is much more effective as an antitumor agent compared to either agent alone in the orthotopic tumor model.
The results show that pretreatment of cells with emodin followed by gemcitabine induced a higher percentage of growth inhibition and apoptosis of pancreatic cancer cells than that of gemcitabine alone.
Yao xue xue bao = Acta pharmaceutica Sinica  •  2011  |  View Paper
Collectively, emodin enhanced the activity of gemcitabine in tumor growth suppression via inhibition of Akt and NF-κB activation, thus promoting the mitochondrial-dependent apoptotic pathway.
Emodin is an active component of Chinese medicinal herbs and can inhibit the activation of Akt and NF-κB. In this study, we investigated whether emodin could enhance the anticancer effect of gemcitabine on pancreatic cancer in vivo.
International journal of oncology  •  2011  |  View Paper
Gemcitabine upregulated the expression of XIAP and NF-κB, while emodin or emodin plus gemcitabine downregulated them compared to the control group in vitro.
Ki-67 prolif-eration index and TUNEL assay results also showed that emodin enhanced tumor apoptosis induced by gemcitabine in vivo.
The combination of emodin and gemcitabine showed more significant reduction in the T/NT ratio, SUV and tumor weight compared to monotherapy.
This study suggests that emodin enhances the antitumor effect of gemcitabine in SW1990 pancreatic cancer in vitro and in vivo, which may be via the downregulation of NF-κB expression, thus inhibiting the expression of XIAP.
International journal of oncology  •  2011  |  View Paper
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