Horse Chestnut

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Summary of Research and Conclusions

Although horse chestnut has not generally been considered an anticancer agent, one in-vitro study found that horse chestnut saponins are cytotoxic to cancer cells.78 In this book, we include horse chestnut not as a cyto-toxic compound but as one that can protect the vascula-ture and reduce edema. Through these actions, it should be able to inhibit angiogenesis, metastasis, and invasion. Even though anticancer studies on animals and humans have not yet been done, it seems likely that horse chestnut has a role in cancer treatment.

Discussion

Horse chestnut (Aesculus hippocastanum) is used in Western herbal medicine to treat diseases of the venous system. In Germany, preparations of horse chestnut are approved to treat diseases such as thrombophlebitis, varicose veins, and many types of edema. Aesculus extracts are the second most prescribed herbal monoprepa-ration in Germany, with annual retail sales of $103 million (U.S. dollars).79 In Chinese herbal medicine, the seed of a related plant, A. chinensis, is used to treat malnutrition and other digestive difficulties at a dose of 3 to 9 grams in decoction. Japanese herbal medicine prescribes the seed of A. turbinata, another related plant, to treat digestive difficulties and promote absorption.80

Horse chestnut extract is effective against many forms of edema, including brain edema (see Tables 8.1 and F.1). For example, oral administration of 50 to 200 mg/kg in rats and 100 to 200 mg/kg in mice inhibited chemically induced increases in vascular permeability.81 The human equivalents are about 810 milligrams to 3.2 grams. In a recent meta-analysis of placebo-controlled human trials, horse chestnut extract was superior to placebo in alleviating signs and symptoms of chronic ve nous insufficiency.82 The primary active compound in horse chestnut extract is the saponin escin, although other compounds such as flavonoids and the coumarin derivative esculin may add to its effects. The common dose of escin itself is 100 to 150 milligrams per day. For example, an oral dose of 100 milligrams per day decreased leg edema in humans.83 In animal experiments, escin was 600 times more potent than the flavon-oid rutin in reducing edema.84

Escin is actually a group of related complex saponins. These saponins contain additional acids and a greater number of sugar molecules than other saponins or gly-cosides we discuss. The yield of escin from dried horse chestnut seeds is roughly 1.9 to 3.8 percent.85,86 Commercial standardized horse chestnut extracts usually contain 16 to 21 percent escin.87

The potential anticancer actions of escin are listed in Table 21.7. At least one in-vitro study reported that escin directly inhibited cancer cell proliferation. In that study, the IC50 for Ehrlich ascites cells was about 10 mM; normal cells were affected only at much higher concentrations.78 Although escin is known to cause direct cytotoxicity, the actions in the table are those that may inhibit cancer by indirect, noncytotoxic means. Such actions will likely be the most prominent in vivo.

Estimated Therapeutic and LOAEL Doses of Escin

Because of the poor pharmacokinetic characteristics of escin, cytotoxic concentrations can probably not be achieved in the plasma. Indeed, based on pharmacoki-netic and in-vitro data, the cytotoxic dose appears to be about 100 grams, which is 1,000-fold higher than the dose commonly prescribed in noncancerous conditions. Therefore, escin is best used for its potential to inhibit

TABLE 21.8 ESTIMATED THERAPEUTIC AND LOAEL DOSES

FOR ESCIN*

DESCRIPTION

DOSE (mg/day)

Required dose as scaled from animal anti-edema studies

150 to 600

Required dose as determined from human antiinflammatory or anti-edema studies

100 to 150

Required cytotoxic dose as determined from pharmacokinetic calculations

100 grams

Commonly prescribed human dose in noncancerous conditions

100 to 150

Estimated LOAEL dose

150

Tentative dose recommendation for further research

150

See Appendix J for details.

TABLE 21.9 ESTIMATED THERAPEUTIC AND LOAEL DOSES

FOR RUSCOGENINS

DESCRIPTION

DOSE (mg/day)

Required cytotoxic dose as determined from pharmacokinetic calculations

1,500*

Commonly prescribed human dose in noncancerous conditions

100

Estimated LOAEL dose

130

Tentative dose recommendation for further research

100 to 130

See Appendix J for details. ^ Based on an average clearance value obtained from other simple triterpenoids and saponins.

cancer progression by indirect means. The commonly prescribed escin dose in noncancerous conditions is 100 to 150 milligrams per day. This dose might be sufficient to cause anticancer effects through indirect actions, if horse chestnut is used with other anticancer compounds. Although the LOAEL dose is uncertain, adverse effects may occur at doses significantly above 150 milligrams (see Appendix J).

Dose estimates for escin are summarized in Table 21.8. The tentative dose recommendation of 150 milligrams is based on the upper range of the commonly prescribed dose.

Butcher's Broom

Summary of Research and Conclusions

Like horse chestnut, butcher's broom has not generally been thought of as an anticancer agent. However, at least one in-vitro study suggested that saponins from butcher's broom are cytotoxic to cancer cells.88 Here we are interested in its ability to protect the vasculature and reduce edema, and thus its potential to inhibit an-giogenesis, metastasis, and invasion. As with horse chestnut, the efficacy of butcher's broom in cancer treatment remains to be proven in animals or humans.

Discussion

Butcher's broom (Ruscus aculea-tus) is an evergreen bush native to the Mediterranean region. It has been used extensively in herbal medicine to treat varicose veins, hemorrhoids, and edema, although it has not received as much research in this area as horse chestnut. The active ingredients include a group of saponins known as ruscogenins, which have vasoconstrictive and anti-inflammatory effects in vivo (see Tables 8.1 and F.1).

The potential anticancer actions of butcher's broom are the same as those for horse chestnut (see Table 21.7). In addition, cytotoxic effects are possible. Some ruscogenins inhibited proliferation of human leukemia cells in vitro, with an IC50 of about 4 mM.88

Estimated Therapeutic and LOAEL Doses of Butcher's Broom

As stated, butcher's broom is regarded here as an indirect-acting, rather than a cytotoxic compound. Nonetheless, there is a possibility ruscogenins could induce direct cytotoxic effects, with the benefits of synergism. Using a target in-vivo concentration of 15 pM, the required ruscogenin dose needed to cause cytotoxic effects would be about 1.5 grams per day. This dose is greater than the approximate 100-milligram dose commonly prescribed in noncancerous conditions. It is also above the estimated LOAEL dose of 130 milligrams (see Appendix J). Accordingly, at least a 12-fold increase in potency due to synergism would be required to produce direct inhibitory effects. Although this size of increase is theoretically possible, the 1.5-gram target dose is based on very limited pharmacokinetic and in-vitro data. Therefore, while direct effects may be possible in syner-gistic combinations, it is best at this stage to think of ruscogenins as indirect-acting compounds.

TABLE 21.10 POTENTIAL ANTICANCER ACTIONS OF GINSENG

ACTIVITY

KNOWN EFFECTS

Chapters 9 and 10: Invasion and Metastasis

Inhibit cell migration

x

Inhibit platelet aggregation

x

Chapters 11 and 12: Immune System

Stimulate the immune system

x

Dose estimates for ruscogenins are summarized in Table 21.9. The tentative dose recommendation is listed as 100 to 130 milligrams, where the lower value is equal to the commonly prescribed dose and the higher is the estimated LOAEL dose.

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