7,4'-di-O-methylamentoflavone/Amentoflavone 7,4'-dimethyl ether/4H-1-Benzopyran-4-one, 5,7-dihydroxy-8-[5-(5-hydroxy-7-methoxy-4-oxo-4H-1-benzopyran-2-yl)-2-methoxyphenyl]-2-(4-hydroxyphenyl)-/5,7-Dihydroxy-8-[5-(5-hydroxy-7-methoxy-4-oxo-4H-chromen-2-yl)-2-methoxyphenyl]-2-(4-hydroxyphenyl)-4H-chromen-4-one/4H-1-Benzopyran-4-one, 5,7-dihydroxy-8-(5-(5-hydroxy-7-methoxy-4-oxo-4H-1-benzopyran-2-yl)-2-methoxyphenyl)-2-(4-hydroxyphenyl)-/ginkgetin/5,7-dihydroxy-8-[5-(5-hydroxy-7-methoxy-4-oxochromen-2-yl)-2-methoxyphenyl]-2-(4-hydroxyphenyl)chromen-4-one
Ginkgetin is a natural biflavonoid isolated from leaves of Ginkgo biloba L; effects of anti-inflammation and anticancer have been reported.IC50 value:Target:in vitro: Ginkgetin inhibits COX-2 dependent phases of prostaglandin D(2) (PGD(2)) generation in bone marrow-derived mast cells (BMMC) in a concentration-dependent manner with IC(50) values of 0.75 microM. Ginkgetin consistently inhibited the production of leukotriene C(4) (LTC(4)) in a dose dependent manner, with an IC(50) value of 0.33 microM. Ginkgetin also inhibited degranulation reaction in a dose dependent manner, with an IC(50) value of 6.52 microM . Ginkgetin inhibited both inducible and constitutively activated STAT3 and blocked the nuclear translocation of p-STAT3 in DU-145 prostate cancer cells. Furthermore, ginkgetin selectively inhibited the growth of prostate tumor cells stimulated with activated STAT3. Ginkgetin induced STAT3 dephosphorylation at Try705 and inhibited its localization to the nucleus, leading to the inhibition of expression of STAT3 target genes such as cell survival-related genes (cyclin D1 and survivin) and anti-apoptotic proteins (Bcl-2 and Bcl-xL) . Ginkgetin suppressed the viability of PC-3 cells in a concentration-dependent manner and also significantly increased the sub-G1 DNA contents of cell cycle in PC-3 cells. Ginkgetin activated caspase-3 and attenuated the expression of survival genes such as Bcl-2, Bcl-xL, survivin and Cyclin D1 at protein and mRNA levels . Ginkgetin (1 - 10 microM) and the biflavonoid mixture (10 - 50 microg/ml), mainly a 1 : 1 mixture of ginkgetin and isoginkgetin, from G. biloba leaves, inhibited production of prostaglandin E2 from lipopolysaccharide-induced RAW 264.7 cells .in vivo: Ginkgetin inhibited tumor growth in xenografted nude mice and down-regulated p-STAT3Tyr705 and survivin in tumor tissues . At total doses of 1,000 microg/site on the dorsal skin (15 mm x 15 mm), ginkgetin inhibited prostaglandin E2 production by 65.6 % along with a marked suppression of COX-2 induction. In addition, ginkgetin and the biflavonoid mixture (100 - 1,000 microg/ear) dose-dependently inhibited skin inflammation of croton oil induced ear edema in mice by topical application .
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Suilysin (SLY), a crucial virulence-related factor, has multiple cytotoxicities that are regarded as playing a key role in several diseases induced by Streptococcus suis. The aim of this study was to identify an effective inhibitor of SLY and to evaluate the potential inhibitory effect of the inhibitor against S. suis virulence.
METHODS AND RESULTS:
Antibacterial activity experiments and haemolysis tests were used to identify the SLY inhibitor ginkgetin, and Western blot analysis and oligomerization inhibition tests were employed to determine the potential mechanism for its inhibition effect. The potential inhibitory effect of ginkgetin against S. suis virulence was then assessed through a cytotoxicity test and a mouse infection model. In this study, we demonstrated that the natural ingredient ginkgetin can significantly reduce the haemolytic activity of SLY to protect against S. suis-mediated cell injury in vitro by directly binding to SLY to block the oligomerization of the protein and reducing the bacterial burden in vivo.
The results suggest that ginkgetin can start being used as a potential lead drug for the treatment of S. suis infections.
SIGNIFICANCE AND IMPACT OF THE STUDY:
The prevention and treatment of S. suis infection might be possible through the targeting of SLY by ginkgetin.
© 2019 The Society for Applied Microbiology.
Streptococcus suis ; antiinfection; antivirulence; ginkgetin; suilysin
Ginkgetin in vitro and in vivo reduces Streptococcus suis virulence by inhibiting suilysin activity.
Li G1,2, Wang G1,2, Wang S3, Deng Y1,2
Effect of ginkgetin on proliferation of human cervical cancer (HeLa) cells and the underlying mechanism were investigated. Human cervical cancer (HeLa) cells were cultured at 37 °C in 10 % fetal bovine serum (FBS) supplemented RPMI 1640 medium in a humidified incubator containing 5 % CO2. Cell proliferation was determined using MTT assay, while real-time quantitative polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to determine the levels of expression of interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin 8 (IL-8). The expressions of p38 mitogen-activated protein kinases (p38 MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF- κB) were determined using Western blotting. Treatment of HeLa cells with ginkgetin significantly and time- and dose-dependently inhibited their proliferation (p < 0.05). The invasion of the cells were also significantly and dose-dependently decreased, when compared with control cells (p < 0.05). The expressions of p-p38 and p-NF-κB were significantly and dose-dependently down-regulated, relative to control group (p < 0.05). However, the expressions of p38 and NF-κB in ginkgetin-treated cells were not significantly different from those of control group (p > 0.05). The results of qRT-PCR and ELISA showed that the levels of expression of TNF-α, IL-1β and IL-8 mRNAs were significantly and dose-dependently reduced in HeLa cells after 48 h of treatment with ginkgetin, when compared with the control group (p < 0.05). The anti-proliferative effect of ginkgetin on HeLa cells is exerted via a mechanism involving the p38/NF-κB pathway.
Cervical cancer; Expression.; Ginkgetin; Inflammatory cytokines; Proliferation
Ginkgetin inhibits proliferation of HeLa cells via activation of p38/NF-κB pathway.
Cheng J1, Li Y1, Kong J1.
2019 Apr 30
The present investigation evaluates the protective effect of Ginkgetin aglycone (GA) against ischemic stroke-induced neuronal injury. Ischemic stroke was produced by the middle cerebral artery occlusion (MCAO) model and animals were a group that received GA 100 and 200 mg/kg, i.p. five days before the induction of MCAO. The effect of GA against stroke was determined by estimating the neurological deficit score and brain water content was also observed. Moreover terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay was done for determining the neuronal apoptosis and Western blot assay also performed for estimating the expression of several proteins. Results of the study suggest that the neurological deficit score and brain water content was found to be lower in the GA treated group than the ischemia/reperfusion (I/R) group of rats. Moreover the number of TUNEL positive cells was found to be lower in the GA treated group than in the I/R group of rats. There was a significant (p < 0.01) decrease in the oxidative stress parameters and cytokine in the tissue homogenate of the GA treated group compared to the I/R group of rats. Further treatment with GA attenuates altered expression of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), protein kinase B (Akt), B-cell lymphoma 2 (Bcl-2), signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa light chain enhancer of activated B cells (NF-B), toll-like receptor 4 (TLR-4), Janus kinase 2 (JAK-2) and sirtuin-1 (SIRT-1) protein in the brain tissues of stroke rats. In conclusion, data of the report reveal that treatment with Ginkgetin aglycone protects the neuronal injury against stroke in rats by reducing oxidative stress and inflammation.
ischemic stroke; neuroinflammation; neuronal injury; oxidative stress; ginkgetin aglycone
Ginkgetin aglycone attenuates neuroinflammation and neuronal injury in the rats with ischemic stroke by modulating STAT3/JAK2/SIRT1.
Xu B, He X, Sui Y, Wang X, Wang X, Ren L, Zhai YX.