Preventive Effects of Ginseng Against Atherosclerosis

Atherosclerosis Clinical Trial

— PEGASUS  

Official title:

Preventive Effects of Ginseng Against Atherosclerosis and Subsequent Ischemic Stroke: A Randomized Controlled Trial

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT02796664
• Other study ID #: KGC2016-26
• Status: Completed
• Phase: N/A
• Start date: June 23, 2016
• Est. completion date: July 4, 2018

Study information

• Verified date: August 2021
• Source: Asan Medical Center
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

This study is a 12-month, double-blind, randomized, placebo-controlled trial. The purpose of this study is to determine whether ginseng is effective in the prevention of atherosclerosis and subsequent ischemic stroke. High-risk patients with severe atherosclerosis in the major intracranial arteries and extracranial carotid artery were enrolled.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 58
• Est. completion date: July 4, 2018
• Est. primary completion date: July 4, 2018
• Accepts healthy volunteers: No
• Gender: All
• Age group: 20 Years to 80 Years

Eligibility

"Inclusion Criteria"

Patients were included if they

1. were aged 20 to 80 years;

2. had occlusion or severe stenosis (= 70%) of extracranial carotid artery and major intracranial arteries (intracranial carotid artery, middle cerebral artery, anterior cerebral artery, intracranial vertebral, basilar, or posterior cerebral artery) as documented by cerebral catheter angiography;

3. had any risk factor for stroke, such as hypertension, diabetes mellitus, hypercholesterolemia, smoking, alcohol drinking, or previous stroke history;

4. had no adverse reactions to administration of ginseng; and

5. agreed to participate in the trial.

"Exclusion Criteria"

Patients were excluded if they

1. did not agree to participate in the trial;

2. had any genetic cerebrovascular diseases;

3. had adverse reactions to contrast medium;

4. were pregnant or planning to be pregnant;

5. had a history of cardioembolic stroke;

6. had an emboligenic cardiac disease such as atrial fibrillation, valve disease, congestive heart failure, or recent myocardial infarction;

7. had a risk of stroke of other determined etiology according to the TOAST classification;

8. had undergone any neurointervention procedure or surgery, such as intra-arterial thrombolysis, angioplasty procedures, carotid endarterectomy, or bypass surgery;

9. had chronic kidney disease (GFR < 30 ml/min); or

10. had severe hepatic dysfunction.

Related Conditions & MeSH terms

• Atherosclerosis
• Ischemic Stroke
• Stroke

Intervention

Dietary Supplement:
• Ginseng
Korean Red Ginseng extract tablet (0.5 grams/tablet, 2 tablets twice a day) daily for 12 months.
• Placebo
Placebo (0.5 grams/tablet, 2 tablets twice a day) daily for 12 months.

Locations

Country	Name	City	State
Korea, Republic of	Asan Medical Center	Seoul

Sponsors (2)

Lead Sponsor	Collaborator
Dae Chul Suh	Korea Ginseng Corporation

Country where clinical trial is conducted

Korea, Republic of, 

References & Publications (10)

Aleshin S, Strokin M, Sergeeva M, Reiser G. Peroxisome proliferator-activated receptor (PPAR)ß/d, a possible nexus of PPARa- and PPAR?-dependent molecular pathways in neurodegenerative diseases: Review and novel hypotheses. Neurochem Int. 2013 Oct;63(4):322-30. doi: 10.1016/j.neuint.2013.06.012. Epub 2013 Jun 25. Review. — View Citation

Bao C, Wang Y, Min H, Zhang M, Du X, Han R, Liu X. Combination of ginsenoside Rg1 and bone marrow mesenchymal stem cell transplantation in the treatment of cerebral ischemia reperfusion injury in rats. Cell Physiol Biochem. 2015;37(3):901-10. doi: 10.1159/000430217. Epub 2015 Sep 18. — View Citation

Chen LM, Zhou XM, Cao YL, Hu WX. Neuroprotection of ginsenoside Re in cerebral ischemia-reperfusion injury in rats. J Asian Nat Prod Res. 2008 May-Jun;10(5-6):439-45. doi: 10.1080/10286020801892292. — View Citation

He B, Chen P, Yang J, Yun Y, Zhang X, Yang R, Shen Z. Neuroprotective effect of 20(R)-ginsenoside Rg(3) against transient focal cerebral ischemia in rats. Neurosci Lett. 2012 Sep 27;526(2):106-11. doi: 10.1016/j.neulet.2012.08.022. Epub 2012 Aug 19. — View Citation

Hong KS. Blood Pressure Management for Stroke Prevention and in Acute Stroke. J Stroke. 2017 May;19(2):152-165. doi: 10.5853/jos.2017.00164. Epub 2017 May 31. Review. — View Citation

Kernan WN, Viscoli CM, Furie KL, Young LH, Inzucchi SE, Gorman M, Guarino PD, Lovejoy AM, Peduzzi PN, Conwit R, Brass LM, Schwartz GG, Adams HP Jr, Berger L, Carolei A, Clark W, Coull B, Ford GA, Kleindorfer D, O'Leary JR, Parsons MW, Ringleb P, Sen S, Spence JD, Tanne D, Wang D, Winder TR; IRIS Trial Investigators. Pioglitazone after Ischemic Stroke or Transient Ischemic Attack. N Engl J Med. 2016 Apr 7;374(14):1321-31. doi: 10.1056/NEJMoa1506930. Epub 2016 Feb 17. — View Citation

Liu XY, Zhou XY, Hou JC, Zhu H, Wang Z, Liu JX, Zheng YQ. Ginsenoside Rd promotes neurogenesis in rat brain after transient focal cerebral ischemia via activation of PI3K/Akt pathway. Acta Pharmacol Sin. 2015 Apr;36(4):421-8. doi: 10.1038/aps.2014.156. Epub 2015 Mar 16. — View Citation

Yang Y, Li X, Zhang L, Liu L, Jing G, Cai H. Ginsenoside Rg1 suppressed inflammation and neuron apoptosis by activating PPAR?/HO-1 in hippocampus in rat model of cerebral ischemia-reperfusion injury. Int J Clin Exp Pathol. 2015 Mar 1;8(3):2484-94. eCollection 2015. — View Citation

Zheng M, Xin Y, Li Y, Xu F, Xi X, Guo H, Cui X, Cao H, Zhang X, Han C. Ginsenosides: A Potential Neuroprotective Agent. Biomed Res Int. 2018 May 8;2018:8174345. doi: 10.1155/2018/8174345. eCollection 2018. Review. — View Citation

Zhou Y, Li HQ, Lu L, Fu DL, Liu AJ, Li JH, Zheng GQ. Ginsenoside Rg1 provides neuroprotection against blood brain barrier disruption and neurological injury in a rat model of cerebral ischemia/reperfusion through downregulation of aquaporin 4 expression. Phytomedicine. 2014 Jun 15;21(7):998-1003. doi: 10.1016/j.phymed.2013.12.005. Epub 2014 Jan 22. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Other	Drug Compliance	We calculated average drug compliance based on the number of remained drugs at each follow-up.	At twelve months after randomization.
Primary	The Composite of Cerebral Ischemic Stroke and Transient Ischemic Attack	The 1-year composite of cerebral ischemic stroke and transient ischemic attack downstream to an atherosclerotic lesion	Twelve months after randomization.
Primary	Modified Rankin Scale	Presence of other cerebro-cardiovascular morbidity or mortality assessed by aggravation of patient status (modified Rankin Scale). The modified Rankin Scale is ranging from 0 to 5. The higher scale indicates the worse outcome.	Twelve months after randomization.
Secondary	The Changes in Volumetric Blood Flow (ml/Sec) in Intracranial Vessels.	The changes in volumetric blood flow (ml/sec) in intracranial vessels assessed by quantitative magnetic resonance angiography with noninvasive optimal vessel analysis.	At randomization and twelve months after randomization.
Secondary	The Changes of White Matter Hyperintensities.	The changes of white matter hyperintensities, assessed by the Fazekas scale using brain magnetic resonance imaging. The Fazekas scale is a 4 point white matter disease severity scale with values ranging from 0 to 3. It quantifies the amount of white matter T2 hyperintense lesions each in periventricular white matter and deep white matter. Higher scales mean a worse white matter status. In the region of the periventricular white matter, 0 means absence of the lesion; 1, caps or pencil-thin lining lesion; 2, smooth halo lesion; 3, irregular high intense signal extending into the deep shite matter. In the region of the deep white matter, 0 means absence of the lesion; 1, punctate foci lesions; 2, beginning confluence; 3, large confluent hyperintense areas.	At randomization and twelve months after randomization.
Secondary	Number of Participants With Changes of Parenchymal Ischemic Lesions	The changes of ischemic parenchymal lesions, assessed by brain magnetic resonance images acquired at randomization and twelve months after randomization. We counted the number of participants who had new ischemic parenchymal lesions at twelve months after randomization.	At randomization and twelve months after randomization.