In vitro effect of prion peptide PrP 106–126 on mouse macrophages: Possible role of macrophages in transport and proliferation for prion protein

2008 ◽  
Vol 44 (2) ◽  
pp. 129-134 ◽  
Author(s):  
X.M. Zhou ◽  
G.X. Xu ◽  
D.M. Zhao
Keyword(s):  
Prion Protein ◽  
Mouse Macrophages ◽  
Vitro Effect

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.

scholarly journals The role of chondroprotectors in the pharmacological treatment of osteoarthritis

2019 ◽  
pp. 100-109
Author(s):  
L. K. Peshekhonova ◽  
P. A. Krasyukov
Keyword(s):  
Drug Therapy ◽  
Musculoskeletal System ◽  
Evidence Based Medicine ◽  
Cartilage Tissue ◽  
Evidence Based ◽  
Third Generation ◽  
Based Medicine ◽  
Vitro Effect

The article is devoted to third-generation slow-modifying chondroprotective drug therapy including Alflutop. The evidence-based  medicine showed and substantiated in vitro effect of the drug on the pathogenetic processes in the cartilage tissue, its promotion  of the inflammation regression in the musculoskeletal system. The authors present a series of clinical studies of top osteoarthritis doctors, which showed that Alflutop had an anti-inflammatory, chondroprotective, analgesic effect, and that the administration of  the drug allowed patients to reduce the doses of NSAIDs, and it could be used in patients with comorbid diseases. 

scholarly journals Cellular Prion Protein Participates in Amyloid-β Transcytosis across the Blood—Brain Barrier

2012 ◽  
Vol 32 (4) ◽  
pp. 628-632 ◽  
Author(s):  
Thorsten Pflanzner ◽  
Benjamin Petsch ◽  
Bettina André-Dohmen ◽  
Andreas Müller-Schiffmann ◽  
Sabrina Tschickardt ◽  
...  
Keyword(s):  
Prion Protein ◽  
Blood Brain Barrier ◽  
Amyloid Β ◽  
Cellular Prion Protein ◽  
Brain Barrier ◽  
Putative Receptor ◽  
Blood Brain ◽  
In Vitro Bbb Model

The blood—brain barrier (BBB) facilitates amyloid-β (Aβ) exchange between the blood and the brain. Here, we found that the cellular prion protein (PrPc), a putative receptor implicated in mediating Aβ neurotoxicity in Alzheimer's disease (AD), participates in Aβ transcytosis across the BBB. Using an in vitro BBB model, [125I]-Aβ1–40 transcytosis was reduced by genetic knockout of PrPc or after addition of a competing PrPc-specific antibody. Furthermore, we provide evidence that PrPc is expressed in endothelial cells and, that monomeric Aβ1–40 binds to PrPc. These observations provide new mechanistic insights into the role of PrPc in AD.

scholarly journals Autoamplification of NFATc1 expression determines its essential role in bone homeostasis

2005 ◽  
Vol 202 (9) ◽  
pp. 1261-1269 ◽  
Author(s):  
Masataka Asagiri ◽  
Kojiro Sato ◽  
Takako Usami ◽  
Sae Ochi ◽  
Hiroshi Nishina ◽  
...  
Keyword(s):  
Essential Role ◽  
Osteoclast Differentiation ◽  
Ectopic Expression ◽  
Epigenetic Mechanism ◽  
Bone Homeostasis ◽  
Hematopoietic Stem ◽  
Vitro Effect

NFATc1 and NFATc2 are functionally redundant in the immune system, but it was suggested that NFATc1 is required exclusively for differentiation of osteoclasts in the skeletal system. Here we provide genetic evidence that NFATc1 is essential for osteoclast differentiation in vivo by adoptive transfer of NFATc1−/− hematopoietic stem cells to osteoclast-deficient Fos−/− mice, and by Fos−/− blastocyst complementation, thus avoiding the embryonic lethality of NFATc1−/− mice. However, in vitro osteoclastogenesis in NFATc1-deficient cells was rescued by ectopic expression of NFATc2. The discrepancy between the in vivo essential role of NFATc1 and the in vitro effect of NFATc2 was attributed to selective autoregulation of the NFATc1 gene by NFAT through its promoter region. This suggested that an epigenetic mechanism contributes to the essential function of NFATc1 in cell lineage commitment. Thus, this study establishes that NFATc1 represents a potential therapeutic target for bone disease and reveals a mechanism that underlies the essential role of NFATc1 in bone homeostasis.

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