Egb761, a ginkgo biloba extract, is effective against atherosclerosis in vitro, and in a rat model of type 2 diabetes

Soo Lim, Ji Won Yoon, Seon Mee Kang, Sung Hee Choi, Bong Jun Cho, Min Kim, Ho Seon Park, Hyun Ju Cho, Hayley Shin, Young Bum Kim, Hyo Soo Kim, Hak Chul Jang, Kyong Soo Park

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Background: EGb761, a standardized Ginkgo biloba extract, has antioxidant and antiplatelet aggregation and thus might protect against atherosclerosis. However, molecular and functional properties of EGb761 and its major subcomponents have not been well characterized. We investigated the effect of EGb761 and its major subcomponents (bilobalide, kaemferol, and quercetin) on preventing atherosclerosis in vitro, and in a rat model of type 2 diabetes. Methods and Results: EGb761 (100 and 200 mg/kg) or normal saline (control) were administered to Otsuka Long-Evans Tokushima Fatty rats, an obese insulin-resistant rat model, for 6 weeks (from 3 weeks before to 3 weeks after carotid artery injury). Immunohistochemical staining was performed to investigate cell proliferation and apoptosis in the injured arteries. Cell migration, caspase-3 activity and DNA fragmentation, monocyte adhesion, and ICAM-1/VCAM-1 levels were explored in vitro. Treatment with EGb761 dose-dependently reduced intima-media ratio, proliferation of vascular smooth muscle cells (VSMCs) and induced greater apoptosis than the controls. Proliferation and migration of VSMCs in vitro were also decreased by the treatment of EGb761. Glucose homeostasis and circulating adiponectin levels were improved, and plasma hsCRP concentrations were decreased in the treatment groups. Caspase-3 activity and DNA fragmentation increased while monocyte adhesion and ICAM-1/VCAM-1 levels decreased significantly. Among subcomponents of EGb761, kaemferol and quercetin reduced VSMC migration and increased caspase activity. Conclusions: EGb761 has a protective role in the development of atherosclerosis and is a potential therapeutic agent for preventing atherosclerosis.

Original languageEnglish
Article numbere20301
JournalPLoS ONE
Volume6
Issue number6
DOIs
StatePublished - 8 Jun 2011

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Ginkgo biloba
Medical problems
atherosclerosis
noninsulin-dependent diabetes mellitus
Type 2 Diabetes Mellitus
Rats
Atherosclerosis
animal models
blood vessels
smooth muscle
myocytes
DNA fragmentation
extracts
caspase-3
cell movement
monocytes
quercetin
adhesion
apoptosis
Vascular Smooth Muscle

Cite this

@article{8708b0aa6594424e95ac469eb30b75f6,
title = "Egb761, a ginkgo biloba extract, is effective against atherosclerosis in vitro, and in a rat model of type 2 diabetes",
abstract = "Background: EGb761, a standardized Ginkgo biloba extract, has antioxidant and antiplatelet aggregation and thus might protect against atherosclerosis. However, molecular and functional properties of EGb761 and its major subcomponents have not been well characterized. We investigated the effect of EGb761 and its major subcomponents (bilobalide, kaemferol, and quercetin) on preventing atherosclerosis in vitro, and in a rat model of type 2 diabetes. Methods and Results: EGb761 (100 and 200 mg/kg) or normal saline (control) were administered to Otsuka Long-Evans Tokushima Fatty rats, an obese insulin-resistant rat model, for 6 weeks (from 3 weeks before to 3 weeks after carotid artery injury). Immunohistochemical staining was performed to investigate cell proliferation and apoptosis in the injured arteries. Cell migration, caspase-3 activity and DNA fragmentation, monocyte adhesion, and ICAM-1/VCAM-1 levels were explored in vitro. Treatment with EGb761 dose-dependently reduced intima-media ratio, proliferation of vascular smooth muscle cells (VSMCs) and induced greater apoptosis than the controls. Proliferation and migration of VSMCs in vitro were also decreased by the treatment of EGb761. Glucose homeostasis and circulating adiponectin levels were improved, and plasma hsCRP concentrations were decreased in the treatment groups. Caspase-3 activity and DNA fragmentation increased while monocyte adhesion and ICAM-1/VCAM-1 levels decreased significantly. Among subcomponents of EGb761, kaemferol and quercetin reduced VSMC migration and increased caspase activity. Conclusions: EGb761 has a protective role in the development of atherosclerosis and is a potential therapeutic agent for preventing atherosclerosis.",
author = "Soo Lim and Yoon, {Ji Won} and Kang, {Seon Mee} and Choi, {Sung Hee} and Cho, {Bong Jun} and Min Kim and Park, {Ho Seon} and Cho, {Hyun Ju} and Hayley Shin and Kim, {Young Bum} and Kim, {Hyo Soo} and Jang, {Hak Chul} and Park, {Kyong Soo}",
year = "2011",
month = "6",
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language = "English",
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Egb761, a ginkgo biloba extract, is effective against atherosclerosis in vitro, and in a rat model of type 2 diabetes. / Lim, Soo; Yoon, Ji Won; Kang, Seon Mee; Choi, Sung Hee; Cho, Bong Jun; Kim, Min; Park, Ho Seon; Cho, Hyun Ju; Shin, Hayley; Kim, Young Bum; Kim, Hyo Soo; Jang, Hak Chul; Park, Kyong Soo.

In: PLoS ONE, Vol. 6, No. 6, e20301, 08.06.2011.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Egb761, a ginkgo biloba extract, is effective against atherosclerosis in vitro, and in a rat model of type 2 diabetes

AU - Lim, Soo

AU - Yoon, Ji Won

AU - Kang, Seon Mee

AU - Choi, Sung Hee

AU - Cho, Bong Jun

AU - Kim, Min

AU - Park, Ho Seon

AU - Cho, Hyun Ju

AU - Shin, Hayley

AU - Kim, Young Bum

AU - Kim, Hyo Soo

AU - Jang, Hak Chul

AU - Park, Kyong Soo

PY - 2011/6/8

Y1 - 2011/6/8

N2 - Background: EGb761, a standardized Ginkgo biloba extract, has antioxidant and antiplatelet aggregation and thus might protect against atherosclerosis. However, molecular and functional properties of EGb761 and its major subcomponents have not been well characterized. We investigated the effect of EGb761 and its major subcomponents (bilobalide, kaemferol, and quercetin) on preventing atherosclerosis in vitro, and in a rat model of type 2 diabetes. Methods and Results: EGb761 (100 and 200 mg/kg) or normal saline (control) were administered to Otsuka Long-Evans Tokushima Fatty rats, an obese insulin-resistant rat model, for 6 weeks (from 3 weeks before to 3 weeks after carotid artery injury). Immunohistochemical staining was performed to investigate cell proliferation and apoptosis in the injured arteries. Cell migration, caspase-3 activity and DNA fragmentation, monocyte adhesion, and ICAM-1/VCAM-1 levels were explored in vitro. Treatment with EGb761 dose-dependently reduced intima-media ratio, proliferation of vascular smooth muscle cells (VSMCs) and induced greater apoptosis than the controls. Proliferation and migration of VSMCs in vitro were also decreased by the treatment of EGb761. Glucose homeostasis and circulating adiponectin levels were improved, and plasma hsCRP concentrations were decreased in the treatment groups. Caspase-3 activity and DNA fragmentation increased while monocyte adhesion and ICAM-1/VCAM-1 levels decreased significantly. Among subcomponents of EGb761, kaemferol and quercetin reduced VSMC migration and increased caspase activity. Conclusions: EGb761 has a protective role in the development of atherosclerosis and is a potential therapeutic agent for preventing atherosclerosis.

AB - Background: EGb761, a standardized Ginkgo biloba extract, has antioxidant and antiplatelet aggregation and thus might protect against atherosclerosis. However, molecular and functional properties of EGb761 and its major subcomponents have not been well characterized. We investigated the effect of EGb761 and its major subcomponents (bilobalide, kaemferol, and quercetin) on preventing atherosclerosis in vitro, and in a rat model of type 2 diabetes. Methods and Results: EGb761 (100 and 200 mg/kg) or normal saline (control) were administered to Otsuka Long-Evans Tokushima Fatty rats, an obese insulin-resistant rat model, for 6 weeks (from 3 weeks before to 3 weeks after carotid artery injury). Immunohistochemical staining was performed to investigate cell proliferation and apoptosis in the injured arteries. Cell migration, caspase-3 activity and DNA fragmentation, monocyte adhesion, and ICAM-1/VCAM-1 levels were explored in vitro. Treatment with EGb761 dose-dependently reduced intima-media ratio, proliferation of vascular smooth muscle cells (VSMCs) and induced greater apoptosis than the controls. Proliferation and migration of VSMCs in vitro were also decreased by the treatment of EGb761. Glucose homeostasis and circulating adiponectin levels were improved, and plasma hsCRP concentrations were decreased in the treatment groups. Caspase-3 activity and DNA fragmentation increased while monocyte adhesion and ICAM-1/VCAM-1 levels decreased significantly. Among subcomponents of EGb761, kaemferol and quercetin reduced VSMC migration and increased caspase activity. Conclusions: EGb761 has a protective role in the development of atherosclerosis and is a potential therapeutic agent for preventing atherosclerosis.

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