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Poster Abstract Presentations
Session Title: Poster Session 2

Abstract 366: Beta-1,3 / 1,6-D-Glucan Chemical Structure Characterization of Indonesian Ganoderma lucidum Mycelium Extract

Originally publishedArteriosclerosis, Thrombosis, and Vascular Biology. 2019;39:A366

    Introduction: β-1,3/1,6-D-Glucan may act as an anti-inflammatory and oxidative stress suppressor which may result in the repair of cardiomyocytes and prevent ischemia.

    Aim: To characterize the chemical structure and examine the biological activity of β-1,3/1,6-D-Glucan extracted from Indonesian Ganoderma lucidum Mycelium.

    Result: Chemical structure characterization analysis of β-1,3/1,6-D-Glucan from Ganoderma lucidum demonstrates that: (1) 1-D NMR spectroscopic profile is very similar to the Beta-Glucan of United States Pharmacopoeia (USP) with reference standard for Beta Glucan: Cat.Number 1048288, Lot.Number FOK129, (2) has a molecular weight > 3,755 kDa, with 54% purity (3) complex branching with a 2:1 bond ratio between β-1,3 main chain and β-1,6 branching. The structural characterization of our β-1,3/1,6-D-Glucan from Ganoderma lucidum proves to be in accordance with the β-1,3/1,6-D-Glucan characterization that has a high potency as a strong immunomodulator, such as large molecular weight, complex branching structure and triple helix solution conformation. Through a study on the effect of our β-1,3/1,6-D-Glucan on Stable Angina Pectoris and High-Risk Heart Disease patients at Saiful Anwar Hospital, Malang - East Java (Indonesia), it is demonstrated that the biomarker levels of IL-6, TNF-α, CRP, MDA and CEC decrease significantly (p<0.05) after the consumption of our β-1,3/1,6-D-Glucan as adjuvant therapy with a dose of 540 mg daily for 90 days.

    Conclusion: The structural chemical characterization of our β-1,3/1,6-D-Glucan from Ganoderma lucidum is accordance with the reference standard of β-1,3/1,6-D-Glucan of USP. Similar to the reference standard, adjuvant therapy of β-1,3/1,6-D-Glucan from Ganoderma lucidum may inhibit the progress of cardiovascular damage and prevent the ischemia in cardiomyocytes.


    Author Disclosures: P. Sugita: None. D. Sargowo: None.