White crystalline powder
4H-1-Benzopyran-4-one, 2,3-dihydro-7-hydroxy-2-(4-hydroxyphenyl)-6-(3-methyl-2-buten-1-yl)-, (2S)-/(2S)-7-Hydroxy-2-(4-hydroxyphenyl)-6-(3-methyl-2-buten-1-yl)-2,3-dihydro-4H-chromen-4-one/7-Hydroxy-2-(4-hydroxyphenyl)-6-(3-methylbut-2-en-1-yl)-2,3-dihydro-4H-chromen-4-one/7-Hydroxy-2-(4-hydroxyphenyl)-6-(3-methyl-2-buten-1-yl)-2,3-dihydro-4H-chromen-4-one/4H-1-Benzopyran-4-one, 2,3-dihydro-7-hydroxy-2-(4-hydroxyphenyl)-6-(3-methyl-2-buten-1-yl)-/Bavachin
Methanol; Acetontrile; DMSO
558.3±50.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:19879-32-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Background: Bavachin is a natural product isolated from Psoralea corylifolia L. that has been applied as a traditional medicine in Asian countries. However, the anti-inflammatory effects of bavachin on LPS-induced inflammation and NLRP3 inflammasome activation by macrophages remain unclear.
Purpose: We investigated the anti-inflammatory effects of bavachin on LPS-activated murine macrophage cell line J774A.1 cells and murine peritoneal macrophages.
Methods: J774A.1 cells and murine peritoneal macrophages were pre-treated with bavachin following LPS treatment. The concentrations of NO, PGE2, IL-6 and IL-12p40 in cell culture supernatant were analyzed. The expressions of iNOS, COX-2, mPGES-1 and MAPKs were analyzed using Western blotting, while NF-κB activity was detected using promoter reporter assay. To examine the activation of NLRP3 inflammasome, J774A.1 cells were incubated with LPS, and then treated with bavachin following treatment with ATP. The concentration of IL-1β in the cell culture supernatant was measured. The expressions of NLRP3, ASC, caspase-1 and IL-1β were analyzed using Western blotting. The formation of inflammasome complex was observed by immunofluorescence microscopy.
Results: Bavachin suppressed LPS-induced NO and PGE2 production, and decreased iNOS and mPGES-1 expression. Bavachin also reduced LPS-induced IL-6 and IL-12p40 production and decreased the activation of MAPKs and NF-κB. Additionally, bavachin suppressed NLRP3 inflammasome-derived IL-1β secretion, decreased caspase-1 activation, repressed mature IL-1β expression, and inhibited inflammasome complex formation. Furthermore, bavachin also suppressed the production of NO, IL-6 and IL-12p40 by LPS-stimulated murine peritoneal macrophages.
Conclusion: Our experimental results indicated anti-inflammatory effects of bavachin exhibit attenuation of LPS-induced inflammation and inhibit activation of NLRP3 inflammasome in macrophages. These results suggest that bavachin might have potential in treating inflammatory and autoimmune diseases.
Bavachin; Inflammation; Macrophage; NLRP3 inflammasome; mPGES-1.
Bavachin Attenuates LPS-induced Inflammatory Response and Inhibits the Activation of NLRP3 Inflammasome in Macrophages
Yung-Li Hung 1 , Shu-Chi Wang 2 , Katsuhiko Suzuki 3 , Shih-Hua Fang 4 , Chi-Shuo Chen 5 , Wei-Chung Cheng 6 , Chia-Cheng Su 7 , Hsin-Chih Yeh 8 , Hung-Pin Tu 9 , Po-Len Liu 10 , Ming-Yii Huang 11 , Chia-Yang Li 12
As a traditional herbal medicine, the fruits of Psoralea corylifolia L. (Fructus Psoraleae (FP)) have been widely used for the treatment of various skin diseases for hundred years. Recently, the emerging FP-induced toxic effects, especially hepatotoxicity, in clinic are getting the public’s attention. However, its exact toxic components and mechanisms underlying remain unclear. Bavachin, one of flavonoids in FP, has been documented as a hepatotoxic substance, and the present study aimed to determine the toxicity caused by bavachin and the possible toxic mechanisms involved using human hepatocellular carcinoma (HepG2) cells. Our results showed that bavachin could significantly inhibited cell proliferation and trigger the endoplasmic reticulum (ER) stress in a dose dependent manner. Downregulating ER stress using tauroursodeoxycholic acid (TUDCA) obvious attenuated bavachin-triggerd cell apoptosis. Then, small interfering RNA (siRNA) knock-down of Mitofusion2 (Mfn2) resulted in a remarkable aggravation of ER stress through the inhibition of the phosphorylation of protein kinase B (Akt). Additionally, suppression of reactive oxygen species (ROS) by ROS Scavenger (N-acetyl-l-cystein (NAC)) also reduced bavachin-induced ER stress. Taken together, our study demonstrated that bavachin-induced ER stress caused cell apoptosis by Mfn2-Akt pathway, and that ROS may participate upstream in this mechanism. Here, we not only provide a new understanding of ROS/Mfn2/Akt pathway in bavachin-induced cytotoxicity via the ER stress, but also identify a new specific intervention to prevent FP-induced hepatotoxicity in the future.
Bavachin; Inflammation; Macrophage; NLRP3 inflammasome; mPGES-1.
Bavachin Induces Apoptosis Through Mitochondrial Regulated ER Stress Pathway in HepG2 Cells
Ying Yang 1 2 , Xianglin Tang 2 , Feiran Hao 2 , Zengchun Ma 2 , Yuguang Wang 2 , Lili Wang 3 , Yue Gao 1
2018 Feb 1
Vascular calcification is a major complication of cardiovascular disease and chronic renal failure. Autophagy help to maintain a stable internal and external environment that is important for modulating arteriosclerosis, but its pathogenic mechanism is far from clear. Here, we aimed to identify the bioactive compounds from traditional Chinese medicines (TCM) that exhibit an anti-arteriosclerosis effect. In β-glycerophosphate (β-GP)-stimulated human aortic smooth muscle cells (HASMCs), the calcium level was increased and the expression of the calcification-related proteins OPG, OPN, Runx2, and BMP2 were all up-regulated, followed by autophagy induction and apoptosis. Meanwhile, we further revealed that β-GP induced apoptosis of human osteoblasts and promoted differentiation of osteoblasts through Wnt/β-catenin signaling. Bavachin, a natural compound from Psoralea corylifolia, dose-dependently reduced the level of intracellular calcium and the expression of calcification-related proteins OPG, OPN, Runx2 and BMP2, thus inhibiting cell apoptosis. In addition, bavachin increased LC3-II and beclin1 expression, along with intracellular LC3-II puncta formation, which autophagy induction is Atg7-dependent and is regulated by suppression of mTOR signaling. Furthermore, addition of autophagy inhibitor, wortmannin (WM) attenuated the inhibitory effect of bavachin on β-GP-induced calcification and apoptosis in HASMCs. Collectively, the present study revealed that bavachin protects HASMCs against apoptosis and calcification by activation of the Atg7/mTOR-autophagy pathway and suppression of the β-catenin signaling, our findings provide a potential clinical application for bavachin in the therapy of cardiovascular disease.
poptosis; Atg7; Wnt/β-catenin; autophagy; vascular calcification.
Bavachin Protects Human Aortic Smooth Muscle Cells Against β-Glycerophosphate-Mediated Vascular Calcification and Apoptosis via Activation of mTOR-Dependent Autophagy and Suppression of β-Catenin Signaling
Hu-Qiang He 1 2 3 , Betty Yuen Kwan Law 1 2 , Ni Zhang 1 2 , Cong-Ling Qiu 1 2 , Yuan-Qing Qu 1 2 , An-Guo Wu 4 5 , Yu Han 1 2 , Qi Song 1 2 6 , Wen-Lu Zheng 1 2 7 8 , Yong Liu 3 , Yan-Zheng He 3 , Vincent Kam Wai Wong 1 2
2019 Dec 19
Bavachin, a flavonoid first isolated from seeds of P. corylifolia, acts as a phytoestrogen that activates the estrogen receptors ERα and ERβ with EC50s of 320 and 680 nM, respectively.