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Diosbulbin B


  • Brand : BIOFRON

  • Catalogue Number : BD-P0273

  • Specification : 98.0%(HPLC)

  • CAS number : 20086-06-0

  • Formula : C19H20O6

  • Molecular Weight : 344.4

  • PUBCHEM ID : 177107

  • Volume : 25mg

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Catalogue Number


Analysis Method





Molecular Weight




Botanical Source

This product is isolated and purified from the roots of Dioscorea bulbifera

Structure Type





Hexaaethoxy-aethan/diorthooxalic acid hexaethyl ester/Hexaaethoxy-aethan [German]/(1S,3R,5S,6R,8R,11R,12S,13S)-3-(3-Furyl)-5-methyl-2,9,14-trioxapentacyclo[]heptadecane-10,15-dione/Hexaethoxyethane/Ethane,hexaethoxy/Diorthooxalsaeure-hexaaethylester/Diosbulbin-B/Hexaethoxy-ethan4H-3a,6:7,10-Dimethanofuro[2,3-c]oxepino[4,5-e]oxepin-4,8(6H)-dione, 2-(3-furanyl)octahydro-11b-methyl-, (2R,3aS,6S,6aS,7R,10R,11aR,11bS)-




1.4±0.1 g/cm3


Acetone; Dichloromethane; DMF

Flash Point

301.4±30.1 °C

Boiling Point

574.8±50.0 °C at 760 mmHg

Melting Point


InChl Key


WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:20086-06-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Aim: Diosbulbin B (DB) is a major diterpenoid compound found in Dioscorea bulbifera L, a traditional medicinal herb in China. Clinical reports have confirmed that Dioscorea bulbifera L. can induce significant hepatotoxicity. In this study, we showed that DB can induce mitochondria-dependent apoptosis and investigated the role of autophagy in DB-induced hepatotoxicity in L-02 hepatocytes. Methods: L-02 hepatocytes were treated with different concentrations of DB for 48 h, after which indicators of autophagy and apoptosis were measured. 3-Methyladenine (3-MA) and rapamycin (Rapa) were used as inhibitor and agonist of autophagy, respectively. Furthermore, the reactive oxygen species (ROS) scavenger N-acetyl-l-cysteine (NAC) was used in combination with DB to evaluate the relationship between ROS and autophagy. Results: L-02 cell viability was significantly decreased after treatment with DB for 48 h. Additionally, DB induced concentration-dependent apoptosis and autophagy and increased the activities of caspase-3, caspase-9, alanine aminotransferase (ALT), and aspartate transaminase (AST), and induced excessive leakage of lactate dehydrogenase (LDH). Inhibition of autophagy by 3-MA increased DB-induced apoptosis, resulting in aggravation of hepatotoxicity. Conversely, treatment with Rapa increased malondialdehyde (MDA) content and reduced superoxide dismutase (SOD) activity. Moreover, we found that DB treatment increased the level of intracellular ROS, decreased the mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) production, and caused abnormal opening of the mitochondrial permeability transition pore (mPTP), which were finally restored by the ROS scavenger NAC. Conclusions: Accumulation of ROS can induce mitochondria-dependent apoptosis and likely to play a key role in DB-induced hepatocellular injury. Activation of autophagy may inhibit apoptosis, but also reduces antioxidant capacity.


apoptosis; autophagy; diosbulbin B; hepatocytes; mitochondrial dysfunction.


Diosbulbin B-Induced Mitochondria-Dependent Apoptosis in L-02 Hepatocytes Is Regulated by Reactive Oxygen Species-Mediated Autophagy


Jing Ye 1 , Mei Xue 2 , Yamin Liu 3 , Sirui Zhu 1 , Yu Li 1 , Xiaoli Liu 1 , Danhong Cai 1 , Jia Rui 1 , Liang Zhang 1

Publish date

2019 Jun 19




The rhizome of Dioscorea bulbifera Linn, traditionally used to treat thyroid disease and cancer in China, is reported to induce serious liver injury during clinical practice. Diosbulbin B (DB), a diterpene lactone, has been found to be the main toxic compound in D. bulbifera. The present study aims to investigate the protection of ferulic acid (FA) against DB-induced acute liver injury and its engaged mechanism. Mice were orally administered FA (20, 40, 80 mg/kg) once daily for 6 consecutive days; and then orally given DB (250 mg/kg) on the last day. Daily FA (40, 80 mg/kg) decreased DB (250 mg/kg)-induced increase in serum levels of alanine/aspartate aminotransferase (ALT/AST) and alkaline phosphatase (ALP). Histological evaluation showed that FA (80 mg/kg) ameliorated DB-induced hepatocellular degeneration and lymphocyte infiltration. Results of terminal dUTP nick-end labeling (TUNEL) staining assay showed that FA (80 mg/kg) decreased the DB-increased number of apoptotic hepatocytes. FA (40, 80 mg/kg) reduced DB-increased liver malondialdehyde (MDA) amount. FA (40, 80 mg/kg) decreased DB-increased serum levels of tumor necrosis factor alpha (TNF-α) and interferon-γ (IFN-γ), and liver myeloperoxidase (MPO) activity. FA (80 mg/kg) reversed the DB-induced decrease in expression of inhibitor of kappa B (IκB) and the increase in nuclear translocation of the p65 subunit of nuclear factor kappa B (NFκBp65). Taken together, our results demonstrate that FA prevents DB-induced acute liver injury via inhibiting intrahepatic inflammation and liver apoptosis.


apoptosis; autophagy; diosbulbin B; hepatocytes; mitochondrial dysfunction.


Ferulic Acid Prevents Liver Injury Induced by Diosbulbin B and Its Mechanism


Chengwei Niu 1 , Yuchen Sheng, Enyuan Zhu, Lili Ji, Zhengtao Wang

Publish date

2016 Nov 15




Diosbulbin B (DB) is the main hepatotoxic compound in Airpotato yam, which is traditionally used for treating thyroid disease and cancer in China, and its hepatotoxic mechanism still remains unclear. This study aims to investigate its hepatotoxic mechanism by focusing on regulating microRNA (miRNA). DB induced hepatotoxicity both in vivo and in vitro. Results of miRNA chip analysis showed that the expression of eleven miRNAs was up-regulated and twelve miRNAs was down-regulated in livers from DB-treated mice. The altered expression of seven miRNAs was further validated by using real-time polymerase chain reaction (RT-PCR) assay. DB induced G2/M arrest in L-02/cytochrome P450 3A4 (CYP3A4) cells in both concentration- and time-dependent manner. A total of eleven predicted target genes was related with cell cycle regulation of those above seven miRNAs, among which the mRNA and protein expression of cyclin-dependent kinase 1 (CDK1) decreased both in vivo and in vitro. Both miR-378a-5p and miR-186-3p have binding sites in the 3′-untranslated region (UTR) of CDK1. With the use of CDK1 3′-UTR luciferase reporter assay, miR-378a-5p and miR-186-3p was found to down-regulate the luciferase activity. The mimics of miR-378a-5p or miR-186-3p reduced CDK1 expression in L-02/CYP3A4 cells, but their inhibitors reversed the decreased CDK1 expression induced by DB. Moreover, overexpression of miR-186-3p inhibitor reversed the G2/M cell cycle arrest induced by DB in L-02/CYP3A4 cells. Taken together, our results showed that DB induced hepatotoxicity by inducing G2/M cell cycle arrest in hepatocytes via miR-186-3p or miR-378a-5p-mediated the reduced CDK1 expression.


CDK1; Cell Cycle Arrest; DB; Hepatotoxicity; miRNA.


Diosbulbin B Induced G 2/M Cell Cycle Arrest in Hepatocytes by miRNA-186-3p and miRNA-378a-5p-mediated the Decreased Expression of CDK1


Rui Yang 1 , Mengjuan Wei 2 , Fan Yang 3 , Yuchen Sheng 4 , Lili Ji 5

Publish date

2018 Oct 15