During sensitization of BALB/c mice to protein antigen, spontaneous and acetylcholine-induced mobility of spleen lymphocytes increased, the maximum being reached on days 1-3 from the sensitization commencement. The acetylcholine-induced mobility of lymphocytes was reduced if the lymphocytes had been preexposed to the antigen. The data obtained attest to the same cellular substrate of antigen and acetylcholine effects.
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Chin J Nat Med
April 2024
School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 211198, China. Electronic address:
Icariin, a flavonoid glycoside, is extracted from Epimedium. This study aimed to investigate the vascular protective effects of icariin in type 1 diabetic rats by inhibiting high-mobility group box 1 (HMGB1)-related inflammation and exploring its potential mechanisms. The impact of icariin on vascular dysfunction was assessed in streptozotocin (STZ)-induced diabetic rats through vascular reactivity studies.
View Article and Find Full Text PDFZh Vyssh Nerv Deiat Im I P Pavlova
August 2013
Effects of some inhibitors of serine/threonine and tyrosine protein phosphatases on the depression and spontaneous recovery of the acetylcholine-induced inward current (ACh-current) in command Helix neurons of defensive behavior at the cellular correlate of habituation were investigated. The following drugs were used: okadaic acid (reduces activity ofphosphatases PP1 and PP2A), endothall (PP2A), cyclosporine A and cypermethrin (PP2B), CCT007093 (PPM1D), dephostatin (blocks tyrosine phosphatases). All used inhibitors modify the depression flow, and endothall reduces spontaneous recovery of ACh-current also.
View Article and Find Full Text PDFInvert Neurosci
December 2013
Department of Higher Nervous Activity, Biological Faculty, Lomonosov State University, Moscow, 119991, Russia,
We investigated the role of the mobility of acetylcholine receptors in the depression of an acetylcholine-induced inward current (ACh-current) of Helix lucorum (a land snail) command neurons of defensive behavior in a cellular analog of habituation. The inhibitors of endocytosis and exocytosis, actin microfilaments and cytoskeleton microtubules, serine/threonine protein kinases (PKA, PKG, calcium calmodulin-dependent PK II, p38 mitogen-activated PK), tyrosine kinases (including Src-family kinases), serine/threonine phosphatases (PP1, PP2A, PP2B, PPM1D), and tyrosine protein phosphatases altered the depression of the ACh-current. A comparison of experimentally calculated curves of the ACh-current of these neurons and those obtained by mathematical modeling revealed the following: (a) ACh-current depression is caused by the reduction in the number of membranous ACh-receptors, which results from the shift in the balance of multidirectional transport processes of receptors toward the predominance of ACh-receptor internalization over their recycling; (b) depression of ACh-current depends on the activity of serine/threonine and tyrosine protein kinases and protein phosphatases, whose one of the main targets is the neuron transport system-actin microfilaments and microtubules of cytoskeleton, as well as motor proteins.
View Article and Find Full Text PDFAtherosclerosis
May 1998
Department of Medicine, University Hospital of Würzburg, Germany.
Hypercholesterolemia is associated with impairment of endothelial function due to increased levels of LDL. In diabetic patients, however, attenuation of endothelial function occurs even under normocholesterolemic conditions. Here we assessed whether glycation of LDL potentiates their influence on endothelial function, with particular emphasis on the oxidizability of LDL and the role of O2-.
View Article and Find Full Text PDFJ Biochem
December 1997
Department of Biochemistry and Pharmacology, Kaohsiung Medical College, Taiwan.
A novel neurotoxin, cobrotoxin b, was isolated from Naja naja atra (Taiwan cobra) venom by successive chromatographies on gel filtration and SP-Sephadex C-25 columns. The yield of this novel toxin was 5% of that of cobrotoxin from the same venom. Its neurotoxicity determined as the inhibition of acetylcholine-induced muscle contractions was approximately 50% of that of cobrotoxin.
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