Herbal medicines as adjuvants for cancer therapeutics - PubMed (original) (raw)

Herbal medicines as adjuvants for cancer therapeutics

Chong-Zhi Wang et al. Am J Chin Med. 2012.

Abstract

In the United States, many patients, including cancer patients, concurrently take prescription drugs and herbal supplements. Co-administration of prescription medicines and herbal supplements may have negative outcomes via pharmacodynamic and pharmacokinetic herb-drug interactions. However, multiple constituents in botanicals may also yield beneficial pharmacological activities. Botanicals could possess effective anticancer compounds that may be used as adjuvants to existing chemotherapy to improve efficacy and/or reduce drug-induced toxicity. Herbal medicines, such as ginseng, potentiated the effects of chemotherapeutic agents via synergistic activities, supported by cell cycle evaluations, apoptotic observations, and computer-based docking analysis. Since botanicals are nearly always administrated orally, the role of intestinal microbiota in metabolizing ginseng constituents is presented. Controlled clinical studies are warranted to verify the clinical utility of the botanicals in cancer chemoprevention.

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Figures

Figure 1

Figure 1

Chemical structures of representative ginsenosides characterized from American ginseng. Two major groups of ginsenosides are listed. PPD: protopanaxadiol; PPT: protopanaxatriol; G: ginsenoside; Q: quinquenoside; F: floralquinquenoside. Adapted from (Qi et al., 2011a).

Figure 2

Figure 2

Synergistic antiproliferative effects of ginseng extract and 5-FU in human HCT-116 colorectal cancer cells. Cell growth decreased significantly with the combined treatment of ginseng extract (0.2 and 0.3 mg/mL) and 5-FU (10, 50 and 100 μM) than with 5-FU alone. Ctrl: control; GE: ginseng extract. *, P < 0.01 vs. corresponding groups of 5-FU only. Adapted from (Fishbein et al., 2009).

Figure 3

Figure 3

Panaxadiol enhances antiproliferative effects of irinotecan in HCT-116 cells. The combination of panaxadiol and irinotecan significantly enhanced antiproliferative effects in the cells. PD: panaxadiol; IRN: irinotecan. *, P < 0.05; **, P < 0.01, vs. corresponding groups of IRN only. Adapted from (Du et al., 2012).

Figure 4

Figure 4

Effects of irinotecan and panaxadiol on cell cycle in HCT-116 cells. (A) Representative histograms of cell cycle distribution. (B) Percentage of each cell cycle phase with various treatments or with control. PD: panaxadiol; IRN: irinotecan. Adapted from (Du et al., 2012).

Figure 5

Figure 5

Effects of irinotecan and panaxadiol on HCT-116 cell apoptosis and expression of caspases 3 and 9. (A) Representative scatter plots of PI (y-axis) vs. annexin V (x-axis). (B) Irinotecan and/or panaxadiol on expression of caspases 3 and 9. Cells were treated with irinotecan 10 μM and/or panaxadiol 10 μM. Ctrl: control; PD: panaxadiol; IRN: irinotecan. *P < 0.05 vs. corresponding control groups. Adapted from (Du et al., 2012).

Figure 6

Figure 6

Metabolic pathways of ginsenoside Rb1. “ → ” denotes major pathways; “ formula image ” denotes additional pathways. [P]: metabolites detected in plasma; [U]: metabolites in urine; [F]: metabolites in feces; [B]: metabolites in bile. ig: metabolites after oral administration; iv: metabolites after intravenous injection. Compound K (C–K) is a pharmacologically active ginsenoside metabolite. Adapted from (Qi et al., 2011b).

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