Abstract
The medicinal fungus Ganoderma lucidum contains many bioactive triterpenoids, ganoderic acid A (GAA) being one of the major ones. The present study explored the microbial biotransformation of GAA, isolating 283 strains of soil actinomycetes and determining their abilities to biotransform GAA with ultra-performance liquid chromatography analysis. One positive strain, AI 045, was selected to validate the biotransformation activity. The strain was identified as Streptomyces sp. based on the sequenced 16S rRNA gene. The produced compound obtained from the biotransformation of GAA was purified with the preparative high-performance liquid chromatography method and identified as 3-O-acetyl GAA based on mass and nuclear magnetic resonance spectral data. The present study is the first report that bacteria have the novel ability to biotransform the triterpenoids of fungus G. lucidum. Moreover, the identified 3-O-acetyl GAA is a new triterpenoid product discovered in microbes.
Highlights
Ganoderma lucidum has been used as a nutritional supplement in immunomodulatory and antitumor activities [1]
Many Ganoderma triterpenoids have been isolated and studied; few studies have been published on the microbial biotransformation of Ganoderma triterpenoids
To analyze their ability to biotransform Ganoderma triterpenoid ganoderic acid A (GAA), soil actinomycetes were isolated on Actinomycete isolation (AI) agar and cultivated in AI broth with GAA
Summary
Ganoderma lucidum (in Chinese, “Lingzhi”) has been used as a nutritional supplement in immunomodulatory and antitumor activities [1]. The quantity of Ganoderma triterpenoids obtained from the fermentation process varied dramatically based on fermentation parameters, such as pH and dissolved oxygen [4]. Some bioactivities of GAA have been proven [5,6,7,8,9,10]. GAA was proven to play a role in antitumor activity in highly invasive human breast cancer cells [5], human liver cancer cells [6], and human hepatocellular carcinoma [7]. GAA was found to suppress the growth and invasiveness of human breast cancer cells by inhibiting transcription factor activator protein-1 (AP-1) and nuclear factor-κB (NF-κB), resulting in the down-regulation of cyclin-dependent kinase 4 (Cdk4) expression and the suppression of the secretion of urokinase-type plasminogen activator (uPA), respectively [5]
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