Ginkgolid A/(1R,3R,7S,8S,10R,11S,13S,16S,17R)-8-tert-Butyl-6,17-dihydroxy-16-methyl-2,4,14,19-tetraoxahexacyclo[126.96.36.199.0.0.0]nonadecane-5,15,18-trione/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-dihydroxy-5-methyl-,(3aR,4aR,4bR,5S,7aS,8aS,9R,11S,11aS)-/BN 5202/GINKGOLIDE A,GINKGO BILOBA L/PRIMULIC ACID 1/gingkolide A/ginkolide A/GINKGOBILOBAP.E./1,7-DIDEOXYGINKGOLIDE C/ginkgolide a from ginkgo biloba leaves/GINKGOLIDE A FROM GINKGO LEAVES/GinkgolideA/(1R,3R,7S,8S,10R,11S,13S,16S,17R)-6,17-Dihydroxy-16-methyl-8-(2-methyl-2-propanyl)-2,4,14,19-tetraoxahexacyclo[188.8.131.52.0.0.0]nonadecane-5,15,18-trione
Methanol; Ethyl Acetate
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provides coniferyl ferulate(CAS#:15291-75-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Utilizing the N-methyl-d-aspartate (NMDA) receptor antagonist as a strategy, memantine is the only agent available for clinically treating mild to severe Alzheimer’s disease (AD). Our aim was to develop novel similar herb-based drugs. Using a screening platform, ginkgolide A (GA), a pure compound extracted from Ginkgo biloba, was found to attenuate amyloid β (Aβ)-induced abnormal depolarization in mouse primary cortical neurons. Using receptor agonists, it was determined that GA inhibits both NMDA receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. Furthermore, the Aβ-induced increase in c-Jun N-terminal kinase phosphorylation in neurons was prevented by GA. Body weight, glutamate oxaloacetate transaminase, glutamic-pyruvic transaminase, liver histology, and kidney histology were similar when the wild-type/AD animal model mice with and without GA treatment were compared. This pure compound improves the memory of wild-type mice. Our findings indicate that GA has great potential clinically for the treatment of AD because it might target NMDA receptors just like memantine.
Alzheimer’s disease; amyloid β; ginkgolide A; glutamate receptors; herbal medicines; memantine.
Ginkgolide A Prevents the Amyloid-β-Induced Depolarization of Cortical Neurons
Li-Chen Kuo 1 , Yan-Qing Song 1 , Chien-An Yao 1 2 , Irene H Cheng 3 , Chiang-Ting Chien 1 , Guan-Chiun Lee 1 , Wen-Chin Yang 4 , Yenshou Lin 1
2019 Jan 9
Ginkgolide A (GA) is a natural compound isolated from Ginkgo biloba and has been used to treat cardiovascular diseases and diabetic vascular complications. However, only a few studies have been conducted on the anti-inflammatory effects of GA. In particular, no related reports have been published in a common inflammation model of lipopolysaccharide (LPS)-stimulated macrophages, and the anti-inflammatory mechanisms of GA have not been fully elucidated. In the present study, we extensively investigated the anti-inflammatory potential of GA in vitro and in vivo. We showed that GA could suppress the expression of pro-inflammatory mediators (cyclooxygenase-2 (COX-2) and nitric oxide (NO) and pro-inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β) in LPS-treated mouse peritoneal macrophages, mouse macrophage RAW264.7 cells, and differentiated human monocytes (dTHP-1) in vitro. These effects were partially carried out via downregulating Nuclear factor kappa-B (NF-κB), Mitogen-activated protein kinases (MAPKs) (p38 mitogen-activated protein kinase and extracellular signal-regulated kinase (ERK), but not c-Jun N-terminal kinase (JNK), and activating the AMP-activated protein kinase (AMPK) signaling pathway also seems to be important. Consistently, GA was also shown to inhibit the LPS-stimulated release of TNF-α and IL-6 in mice. Taken together, these findings suggest that GA can serve as an effective inflammatory inhibitor in vitro and in vivo.
AMPK; Ginkgolide A; MAPKs; NF-κB; inflammation
Ginkgolide A Ameliorates LPS-Induced Inflammatory Responses In Vitro and In Vivo
Yan Li 1 , Yannan Wu 2 , Xinlei Yao 3 , Fang Hao 4 , Chunlei Yu 5 , Yongli Bao 6 , Yin Wu 7 , Zhenbo Song 8 , Ying Sun 9 , Lihua Zheng 10 , Guannan Wang 11 , Yanxin Huang 12 , Luguo Sun 13 , Yuxin Li 14
2017 Apr 10
Non-alcoholic fatty liver disease (NAFLD) is one of the most common diseases worldwide and has continuously increased. NAFLD refers to a spectrum of diseases ranging from fatty liver to steatohepatitis, cirrhosis, and even to hepatocyte carcinoma. Excessive fatty acid enters the cell and the mitochondria undergo stress and unremoved ROS can trigger a form of cell apoptosis known as ‘lipoapoptosis’. NASH arises from damaged liver hepatocytes due to lipotoxicity. NASH not only involves lipid accumulation and apoptosis but also inflammation. Ginkgo biloba has been tested clinical trials as a traditional medicine for asthma, bronchitis and cardiovascular disease. The effects of Ginkgolide A (GA), derived from the ginkgo biloba leaf, are still unknown in NAFLD. To determine the protective effects of GA in NAFLD, we examined the fatty liver disease condition in the non-esterified fatty acid (NEFA)-induced HepG2 cell line and in a high fat diet mouse model. The findings of this study suggest that GA is non-toxic at high concentrations in hepatocytes. Moreover, GA was found to inhibit cellular lipogenesis and lipid accumulation by causing mitochondrial oxidative stress. GA showed hepatoprotective efficacy by inducing cellular lipoapoptosis and by inhibiting cellular inflammation. The results demonstrated that GA may be feasible as a therapeutic agent for NAFLD patients.
Ginkgolide A; Inflammation; Lipogenesis; NAFLD; Therapeutic agent.
Ginkgolide A Ameliorates Non-Alcoholic Fatty Liver Diseases on High Fat Diet Mice
Hyeon-Soo Jeong 1 , Kang-Hoon Kim 1 , In-Seung Lee 1 , Ji Young Park 1 , Yumi Kim 1 , Ki-Suk Kim 2 , Hyeung-Jin Jang 3
Ginkgolide A is an extract from in Ginkgo biloba and a g-aminobutyric acid (GABA) antagonist.Target: GABA ReceptorGinkgolide A is a highly active PAF antagonist cage molecule that is isolated from the leaves of the Ginkgo biloba tree. Shows potential in a wide variety of inflammatory and immunological disorders. Ginkgolide A significantly shortened the sleeping time induced by anesthetics in mice . Ginkgolide A failed to affect apoptotic damage neither in serum-deprived nor in staurosporine-treated neurons .