White crystalline powder
Ginkgo biloba,Physalis philadelphica
(1R,3R,6R,7S,8S,10R,11R,12R,13S,16S,17R)-6,12,17-Trihydroxy-16-methyl-8-(2-methyl-2-propanyl)-2,4,14,19-tetraoxahexacyclo[126.96.36.199.0.0.0]nonadecane-5,15,18-trione/ginkgolide b from ginkgo biloba leaves/6H-9,4a-(Epoxymethano)-3aH,9H-cyclopenta[c]furo[2,3-b]furo[3',2':3,4]cyclopenta[1,2-d]furan-2,6,13(1H)-trione, 11-(1,1-dimethylethyl)hexahydro-1,4b,8-trihydroxy-5-methyl-, (1R,3aR,4aR,4bR,5S,8R,8aS,9R,11S,11aS)-/7-DEOXYGINKGOLIDE C/6H-9,4a-(Epoxymethano)-3aH,9H-cyclopenta[c]furo[2,3-b]furo[3',2':3,4]cyclopenta[1,2-d]furan-2,6,13(1H)-trione, 11-(1,1-dimethylethyl)hexahydro-1,4b,8-trihydroxy-5-methyl-, (1R,3aR,4aR,4bR,5S,7aS,8R,8aR,9R,11S,11aS)-/6H-9,4a-(epoxymethano)-3aH,9H-cyclopenta[c]furo[2,3-b]furo[3',2':3,4]cyclopenta[1,2-d]furan-2,6,13(1H)-trione, 11-(1,1-dimethylethyl)hexahydro-1,4b,8-trihydroxy-5-methyl-, (1R,3aR,4aR,4bR,5S,7aS,8aR,9R,11aS)-/(1R,3R,6R,7S,8S,10R,11R,12R,13S,16S,17R)-8-tert-Butyl-6,12,17-trihydroxy-16-methyl-2,4,14,19-tetraoxahexacyclo[188.8.131.52.0.0.0]nonadecane-5,15,18-trione/3-tert-butyl hexahydro-4,-7b-11 hydroxy-8-methyl/(1R,3R,7S,8S,10R,11R,12R,13S,16S,17R)-8-tert-Butyl-6,12,17-trihydroxy-16-methyl-2,4,14,19-tetraoxahexacyclo[184.108.40.206.0.0.0]nonadecane-5,15,18-trione/(1R,3R,6R,7S,8S,10R,11S,12R,16S,17R)-6,12,17-Trihydroxy-16-methyl-8-(2-methyl-2-propanyl)-2,4,14,19-tetraoxahexacyclo[220.127.116.11.0.0.0]nonadecane-5,15,18-trione/ginkgolide B from ginkgo leaves/GinkgolideB
Methanol; Ethyl Acetate; Water
762.4±60.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:15291-77-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Chinese herbal medicines (CHMs) have been used to treat human diseases for thousands of years. Among them, Ginkgo biloba is reported to be beneficial to the nervous system and a potential treatment of neurological disorders. Since the presence of adult neural stem cells (NSCs) brings hope that the brain may heal itself, whether the effect of Ginkgo biloba is on NSCs remains elusive. In this study, we found that Ginkgo biloba extract (GBE) and one of its main ingredients, ginkgolide B (GB) promoted cell cycle exit and neuronal differentiation in NSCs derived from the postnatal subventricular zone (SVZ) of the mouse lateral ventricle. Furthermore, the administration of GB increased the nuclear level of β-catenin and activated the canonical Wnt pathway. Knockdown of β-catenin blocked the neurogenic effect of GB, suggesting that GB promotes neuronal differentiation through the Wnt/β-catenin pathway. Thus, our data provide a potential mechanism underlying the therapeutic effect of GBE or GB on brain injuries and neurodegenerative disorders.
Ginkgolide B Promotes Neuronal Differentiation Through the Wnt/β-catenin Pathway in Neural Stem Cells of the Postnatal Mammalian Subventricular Zone
Ming-Yang Li 1 , Chia-Ting Chang 1 , Yueh-Ting Han 1 , Chien-Po Liao 1 , Jenn-Yah Yu 2 3 , Tsu-Wei Wang 4
Purpose: Ginkgolide B (GB) is a terpene lactone component found in Ginkgo biloba, which has a protective role on ischemia reperfusion (I/R) injury. This study was aimed at exploring the protective mechanism of GB on the myocardial I/R.
Patients and methods: Myocardial I/R model was established on Sprague Dawley rats. The levels of cardiac troponin I, cardiac troponin T, lactic dehydrogenase, and myoglobin were determined by a 200FR NEO automatic biochemical analyzer. Histological examination was performed through HE and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. The expression levels of p-PERK, p-IRE1α, ATF6, p-AKT, and mTOR were detected by Western blot.
Results: The results exhibited that GB treatment suppressed the high levels of cardiac troponin I, cardiac troponin T, lactic dehydrogenase, and myoglobin and ameliorated the damaged and irregularly arranged myocardial cells induced by I/R injury significantly, indicating that GB could ameliorate myocardial I/R injury. Moreover, the high expression levels of endoplasmic reticulum (ER) stress key proteins caused by I/R injury were suppressed significantly by GB treatment, including p-PERK, p-IRE1α, and ATF6. GB treatment also decreased the number of apoptotic cells compared with I/R group. In addition, activation of ER stress by Tunicamycin treatment could counteract the protective effects of GB on I/R injury, suggesting that GB ameliorated myocardial I/R injury through inhibition of ER stress-induced apoptosis. Finally, the decreased p-AKT and p-mTOR expressions caused by I/R injury were upregulated by GB and inhibition of PI3K/AKT/mTOR pathway by LY294002 abolished the protective effects of GB on I/R injury, indicating that GB activated PI3K/AKT/mTOR pathway during I/R injury.
Conclusion: GB protected against myocardial I/R injury through inhibiting ER stress-induced apoptosis via PI3K/AKT/mTOR signaling pathway.
Ginkgolide B; apoptosis PI3K/AKT/mTOR pathway; endoplasmic reticulum stress; myocardial injury.
Ginkgolide B Ameliorates Myocardial Ischemia Reperfusion Injury in Rats via Inhibiting Endoplasmic Reticulum Stress
Changlei Guo 1 , Junbiao Zhang 1 , Peiyong Zhang 1 , Aoyang Si 1 , Zhenling Zhang 1 , Liangping Zhao 1 , Fenghua Lv 1 , Guoan Zhao 1
2019 Feb 26
Background: Osteoarthritis (OA) is one of degenerative and chronic diseases of articular joints. Articular cartilage is an avascular tissue, and its primary cellular component is chondrocytes. The main characteristic of OA is non-classic inflammation and cartilage degeneration. Ginkgolide B (GB) is a component of Ginkgo biloba which has diverse bioactivities.
Objectives: The present study uses an in vitro experimental model to detect the underlying anti-inflammatory and chondroprotective effects of GB and provides a new way for future clinical therapy of OA.
Material and methods: Rat chondrocytes were isolated, cultured and treated with 1 μg/mL lipopolysaccharide (LPS) and/or different concentrations of GB. Cell Counting Kit-8 (CCK-8) was used to test the cell viability of chondrocytes, and chondrocytes apoptosis was detected using a cell apoptosis kit. Collagen-II and aggrecan expression were detected by immunohistochemistry. Relative expression of genes was detected by real-time PCR and western blot.
Results: Ginkolide B did not inhibit chondrocyte proliferation, and ginkgolide B inhibited LPS induced matrixdegradation in chondrocytes. Ginkgolide B also reversed LPS-induced collagen-II and aggrecan decreased in chondrocytes via upregulated synthesis-related gene expression and downregulated matrix-degrading enzyme gene expression. Furthermore, we found that ginkgolide B significantly inhibited LPS-induced MAPK pathway activation.
Conclusions: The results of our study suggest that ginkgolide B exerted anti-inflammatory and chondroprotective effects in LPS-induced chondrocytes, and might be an underlying therapy for OA afterwards.
anti-inflammatory; chondrocyte; ginkgolide B; osteoarthritis.
Ginkgolide B Exerts Anti-Inflammatory and Chondroprotective Activity in LPS-induced Chondrocytes
Hejia Hu 1 , Yan Li 1 , Zengfeng Xin 1 , Xiangfeng Zhanga 1