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Characterization of bioactive ginsen...

Popovich, David Glen.

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Characterization of bioactive ginsenosides extracted from native and processed North American ginseng plant components.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Characterization of bioactive ginsenosides extracted from native and processed North American ginseng plant components./
Author:	Popovich, David Glen.
Description:	163 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-08, Section: B, page: 3790.
Contained By:	Dissertation Abstracts International65-08B.
Subject:	Agriculture, Food Science and Technology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NQ93166
ISBN:	0612931668

Characterization of bioactive ginsenosides extracted from native and processed North American ginseng plant components.
Popovich, David Glen.

Characterization of bioactive ginsenosides extracted from native and processed North American ginseng plant components. - 163 p.

Source: Dissertation Abstracts International, Volume: 65-08, Section: B, page: 3790.

Thesis (Ph.D.)--The University of British Columbia (Canada), 2004.

Ginseng root is one of the oldest and most utilized traditional herbal ingredients. Ginseng has been used to treat many diverse ailments. Compounds in ginseng known as ginsenosides, which are also known as steroidal saponins, are generally thought to be the most bioactive component. However, ginseng contains up to 30 different ginsenosides and the type and proportion of ginsenosides depends on the source of ginseng and portion of the plant material used. The overall objective was to identify, evaluate and recover sources of bioactive ginsenosides. In this thesis, the main ginsenosides that showed a propensity to inhibit cultured cancer cell viability were identified and a LC50 (concentration to inhibit 50% cell viability) was determined in three distinct cell lines. Generally, ginsenoside aglycones 20(S)-protopanaxadiol (PD) and 20(S)-protopanaxadiol (PT) and ginsenoside Rh2 were identified to have affected cell viability in all three cell lines. Specifically, the LC50 values for PD (13 mug/mL), ginsenoside Rh2 (15 mug/mL), PT (19 mug/mL) and ginsenoside Rh1 (210 mug/mL) were established in cultured leukemia cells (THP-1). In intestinal 407 cells (Int-407), a non malignant embryonic intestinal cell line established via HeLa cell contamination, the LC50 values were determined for PD (23 mug/mL), PT (26 mug/mL) and ginsenoside Rh2 (53 mug/mL). In comparison, LC50 for PD and PT were 24 mug/mL and Rh2 was 55 mug/mL in cultured Caco-2 cells, an adenocarcinoma intestinal cell line. Generally, cell cycle analysis showed that these specific ginsenosides which inhibited cell viability also resulted in a build up of sub-G1 cells, a characteristic of apoptosis. Furthermore, treatments that showed the greatest increase (P ≤ 0.05) in sub-G1 cells also had the largest (P ≤ 0.05) release of lactate dehydrogenase (LDH), a useful bio-marker for membrane integrity. It was concluded that specific structure-function relationships exist for bioactive ginsenosides. The sources of rare bioactive ginsenosides, such as Rh2 have only been attributed to Asian red ginseng root. However, ginsenoside Rh2 was found in this study in North American ginseng leaf, an underutilized resource, as a product of applying thermal energy during extraction procedure. Furthermore, Rh2 formation was shown to be a function of heating time and a breakdown product of more abundant ginsenosides (e.g. Rb1 and Rd). Specific mechanistic studies with PD, PT, Rh2 and an enriched Rh2 North American ginseng leaf extract in THP-1 and Caco-2 cells showed that both ginsenoside concentration and exposure time were factors causing cytotoxicity. Generally, test ginsenosides increased both the buildup of apoptotic and necrotic cells while having a varying effect on Caspase-3 activity. In conclusion, the findings of this thesis indicate that variable bioactive response of ginsenosides may be explained on the basis of hydrophobic/hydrophilic balance of the compounds. Moreover, the bioactivity observed was more associated with non-specific changes in cell membrane function than specific trigger mechanism of programmed cell death.

ISBN: 0612931668Subjects--Topical Terms:

1017813
Agriculture, Food Science and Technology.

Characterization of bioactive ginsenosides extracted from native and processed North American ginseng plant components.
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520 $a Ginseng root is one of the oldest and most utilized traditional herbal ingredients. Ginseng has been used to treat many diverse ailments. Compounds in ginseng known as ginsenosides, which are also known as steroidal saponins, are generally thought to be the most bioactive component. However, ginseng contains up to 30 different ginsenosides and the type and proportion of ginsenosides depends on the source of ginseng and portion of the plant material used. The overall objective was to identify, evaluate and recover sources of bioactive ginsenosides. In this thesis, the main ginsenosides that showed a propensity to inhibit cultured cancer cell viability were identified and a LC50 (concentration to inhibit 50% cell viability) was determined in three distinct cell lines. Generally, ginsenoside aglycones 20(S)-protopanaxadiol (PD) and 20(S)-protopanaxadiol (PT) and ginsenoside Rh2 were identified to have affected cell viability in all three cell lines. Specifically, the LC50 values for PD (13 mug/mL), ginsenoside Rh2 (15 mug/mL), PT (19 mug/mL) and ginsenoside Rh1 (210 mug/mL) were established in cultured leukemia cells (THP-1). In intestinal 407 cells (Int-407), a non malignant embryonic intestinal cell line established via HeLa cell contamination, the LC50 values were determined for PD (23 mug/mL), PT (26 mug/mL) and ginsenoside Rh2 (53 mug/mL). In comparison, LC50 for PD and PT were 24 mug/mL and Rh2 was 55 mug/mL in cultured Caco-2 cells, an adenocarcinoma intestinal cell line. Generally, cell cycle analysis showed that these specific ginsenosides which inhibited cell viability also resulted in a build up of sub-G1 cells, a characteristic of apoptosis. Furthermore, treatments that showed the greatest increase (P ≤ 0.05) in sub-G1 cells also had the largest (P ≤ 0.05) release of lactate dehydrogenase (LDH), a useful bio-marker for membrane integrity. It was concluded that specific structure-function relationships exist for bioactive ginsenosides. The sources of rare bioactive ginsenosides, such as Rh2 have only been attributed to Asian red ginseng root. However, ginsenoside Rh2 was found in this study in North American ginseng leaf, an underutilized resource, as a product of applying thermal energy during extraction procedure. Furthermore, Rh2 formation was shown to be a function of heating time and a breakdown product of more abundant ginsenosides (e.g. Rb1 and Rd). Specific mechanistic studies with PD, PT, Rh2 and an enriched Rh2 North American ginseng leaf extract in THP-1 and Caco-2 cells showed that both ginsenoside concentration and exposure time were factors causing cytotoxicity. Generally, test ginsenosides increased both the buildup of apoptotic and necrotic cells while having a varying effect on Caspase-3 activity. In conclusion, the findings of this thesis indicate that variable bioactive response of ginsenosides may be explained on the basis of hydrophobic/hydrophilic balance of the compounds. Moreover, the bioactivity observed was more associated with non-specific changes in cell membrane function than specific trigger mechanism of programmed cell death.
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