Imbalanced inflammatory response in subchronic arsenic‐induced liver injury and the protective effects of Ginkgo biloba extract in rats: Potential role of cytokines mediated cell–cell interactions

2021 ◽  
Author(s):  
Ling Dong ◽  
Yonglian Liu ◽  
Dapeng Wang ◽  
Kai Zhu ◽  
Zhonglan Zou ◽  
...  
Keyword(s):  
Liver Injury ◽  
Inflammatory Response ◽  
Ginkgo Biloba ◽  
Potential Role ◽  
Ginkgo Biloba Extract ◽  
Cell Interactions ◽  
Protective Effects ◽  
Cell Cell

Inflammation response after the cessation of chronic arsenic exposure and post-treatment of natural astaxanthin in liver: potential role of cytokine-mediated cell–cell interactions

2020 ◽  
Vol 11 (10) ◽  
pp. 9252-9262 ◽  
Author(s):  
Zhigang Zhang ◽  
Changming Guo ◽  
Huijie Jiang ◽  
Bing Han ◽  
Xiaoqiao Wang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Rat Liver ◽  
Potential Role ◽  
Arsenic Exposure ◽  
Post Treatment ◽  
Cell Interactions ◽  
Schematic Diagram ◽  
Inflammation Response ◽  
Chronic Arsenic Exposure

Schematic diagram of the mechanism of post treatment with natural astaxanthin attenuating arsenic-induced inflammatory response in rat liver.

Effect of Ginkgo biloba extract on rat hepatic microsomal CYP1A activity: role of ginkgolides, bilobalide, and flavonols

2004 ◽  
Vol 82 (1) ◽  
pp. 57-64 ◽  
Author(s):  
I fan Kuo ◽  
Jie Chen ◽  
Thomas K.H Chang
Keyword(s):  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Inhibitory Potency ◽  
Hepatic Microsomes ◽  
Cyp1a Activity ◽  
Ginkgo Biloba Extracts ◽  
The Individual ◽  
Vitro Effect

The present study investigated the in vitro effect of Ginkgo biloba extracts and some of the individual constituents (ginkgolides, bilobalide, and flavonols such as kaempferol, quercetin, isorhamnetin, and their glycosides) on CYP1A-mediated 7-ethoxyresorufin O-dealkylation in hepatic microsomes isolated from rats induced with β-naphthoflavone. G. biloba extract competitively inhibited CYP1A activity, with an apparent Ki value of 1.6 ± 0.4 µg/mL (mean ± SE). At the concentrations present in the G. biloba extracts, ginkgolides A, B, C, and J and bilobalide did not affect CYP1A activity, whereas kaempferol (IC50 = 0.006 ± 0.001 µg/mL, mean ± SE), isorhamnetin (0.007 ± 0.001 µg/mL), and quercetin (0.050 ± 0.003 µg/mL) decreased this activity. The monoglycosides (1 and 10 µg/mL) and diglycosides (10 µg/mL) of kaempferol and quercetin but not those of isorhamnetin also inhibited CYP1A activity. The order of inhibitory potency was kaempferol ~ isorhamnetin > quercetin, and for each of these flavonols the order of potency was aglycone >> monoglycoside > diglycoside. In summary, G. biloba extract competitively inhibited rat hepatic microsomal CYP1A activity, but the effect was not due to ginkgolides A, B, C, or J, bilobalide, kaempferol, quercetin, isorhamnetin, or the respective flavonol monoglycosides or diglycosides.Key words: bilobalide, CYP1A, cytochrome P450, Ginkgo biloba, ginkgolide, flavonol.

Low-affinity LFA-1/ICAM-3 interactions augment LFA-1/ICAM-1-mediated T cell adhesion and signaling by redistribution of LFA-1

2000 ◽  
Vol 113 (3) ◽  
pp. 391-400 ◽  
Author(s):  
D.A. Bleijs ◽  
M.E. Binnerts ◽  
S.J. van Vliet ◽  
C.G. Figdor ◽  
Y. van Kooyk
Keyword(s):  
T Cell ◽  
Cell Interactions ◽  
T Cell Proliferation ◽  
Cell Contact ◽  
Surface Distribution ◽  
Affinity Ligand ◽  
Large Clusters ◽  
High Affinity Ligand ◽  
Cell Cell

Although ICAM-3 is implicated in both adhesion and signal transduction events of leukocytes, its low affinity for LFA-1 compared to other ligands of LFA-1 has puzzled many investigators. Here we investigated the role of ICAM-3 in supporting LFA-1-mediated ICAM-1 binding and subsequently cell signaling. We observed that although ICAM-3 binds poorly to LFA-1 expressed on resting T cells, it specifically facilitates and increases LFA-1-mediated adhesion to the high affinity ligand of LFA-1, ICAM-1. We demonstrate that low-affinity binding of LFA-1 to ICAM-3 together with ICAM-1 alters the cell surface distribution of LFA-1 dramatically, inducing large clusters of LFA-1 that facilitate ICAM-1 binding after LFA-1 activation. We found that LFA-1-mediated ICAM-1 cell-cell interactions such as T cell proliferation greatly depend on low affinity LFA-1/ICAM-3 interactions that enhance stable LFA-1/ICAM-1 cell-cell contact. Taken together, these data demonstrate that low affinity LFA-1 binding to ICAM-3 regulates strong LFA-1/ICAM-1-mediated adhesion by driving LFA-1 into clusters to facilitate cell-cell interactions that take place in the immune system.

Downregulation of Agonist-Induced Nitric Oxide Synthesis and Cell-Cell Adhesion by Ginkgo biloba Extract EGb 761

1999 ◽  
pp. 359-370
Author(s):  
Sashwati Roy ◽  
Hirotsugu Kobuchi ◽  
Chandan K. Sen ◽  
Marie-Thérèse Droy-Lefaix ◽  
Lester Packer
Keyword(s):  
Nitric Oxide ◽  
Cell Adhesion ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Egb 761 ◽  
Nitric Oxide Synthesis ◽  
Cell Cell
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