Disease relevance of beta-Aescin

• 2. In the homogenate of the beta-escin-skinned arterial strip, C3 exoenzyme of Clostridium botulinum catalyzed the [32P]-ADP-ribosylation of only one protein that had the same molecular mass as the protein detected in Western blots with anti-rho p21 antibody [1].
• In beta-escin skinned pulmonary arterial strips, hypoxia had no effect on the calcium concentration-tension relationship [2].
• We investigated the saponin beta-escin as a putative ionophore for perforated patch I(Ca) recordings in acutely dissociated, rat dorsal root ganglion neurons [3].
• Pretreatment by 1 microM okadaic acid in the absence of Ca(2+) suppressed subsequent submaximal Ca(2+)-induced contraction in preparations permeabilized with Staphylococcus aureus alpha-toxin or beta-escin, but not in those treated with saponin or Triton X-100 [4].
• Effects of beta-aescin on apoptosis induced by transient focal cerebral ischemia in rats [5].

High impact information on beta-Aescin

• In beta-escin permeabilized coronary arteries in which the receptor effector coupling is still intact, 5-HT enhanced force at constant submaximal (Ca2+) (pCa 6.38) to a greater extent in SHRSP [6].
• In beta-escin-skinned smooth muscle strips, 0.1 microM NKH477 shifted the pCa-force relation to the right but had no effects on Ca(2+)-independent contraction [7].
• In vascular smooth-muscle cells reversibly permeabilized with beta-escin and treated with alkaline phosphatase, norepinephrine failed to cause cytosolic phospholipase A(2) phosphorylation and translocation to the nuclear envelope; these effects of norepinephrine were minimized by the phosphatase inhibitor okadaic acid [8].
• To calibrate the indicator's fluorescence signal in terms of cytoplasmic [Ca2+], we applied beta-escin to permeabilize the cell membrane of the fibers injected with fura dextran [9].
• Arteries permeabilized with beta-escin developed maximum force in response to free Ca(2+) (6.6 microm), concomitant with a parallel increase in myosin regulatory light chain phosphorylation (MRLC-P(i)), from 0.183 +/- 0.023 to 0.353 +/- 0.019 MRLC-P(i) (total light chain)(-1) [10].

Chemical compound and disease context of beta-Aescin

• CONCLUSION: Sodium beta-aescin can attenuate brain injury, down-regulate the protein expressions of ICAM-1 and E-selectin, and reduce the migration of neutrophils after cerebral I/R [11].

Biological context of beta-Aescin

• Measurements of contractile properties of beta-escin permeabilized smooth muscle strips revealed that the upregulation of Rnd3 correlated with an inhibition of RhoA-Rho kinase-mediated Ca2+ sensitization at mid-pregnancy [12].
• In conclusion, permeabilization with beta-escin allows the transmembrane passage of 150 kD proteins under our experimental conditions that also retain receptor-coupled signal transduction [13].
• 2. This study investigated the mechanism of action of hydralazine on rabbit aorta and pulmonary artery by comparing its effects on the tension generated by intact and beta-escin permeabilized vessels and on the cytoplasmic Ca(2+) concentration, membrane potential and K(+) currents of isolated vascular smooth muscle cells [14].
• In beta-escin-treated skinned myometrial strips from late gestation, 0.3 mumol/L Ca++ evoked contractions [15].
• In order to clarify the role of intracellular second messenger systems in the cortisol secretion from bovine adrenocortical (BAC) cells, the cells were permeabilized with beta-escin and stimulated intracellularly with various compounds [16].

Anatomical context of beta-Aescin

• 1. Fluo-3 fluorescence measurements were made in isolated beta-escin permeablised rat cardiac myocytes using confocal microscopy [17].
• 1. Effects of cyclopiazonic acid (CPA), a specific inhibitor of the Ca(2+)-ATPase in sarcoplasmic reticulum (SR) of skeletal and cardiac muscles, on contractile responses induced by Ca(2+)-release from intracellular storage sites were examined in the longitudinal smooth muscle strip of the guinea-pig ileum skinned with beta-escin [18].
• 5. These results suggest that rho p21 predominantly mediates GTP(gamma)S-induced Ca2+ sensitization of beta-escin-skinned smooth muscle of rabbit mesenteric artery, while the Ca2+ sensitizing actions of heterotrimeric G protein-coupled receptor agonists do not involve this small G protein [1].
• In beta-escin permeabilized myometrium, galanin enhanced the contraction induced by 0.3 microM Ca2+ in the presence of GTP [19].
• The effect of diosmin, a flavone derivative, on the Ca2+ sensitivity of the venous contractile apparatus was investigated in chemically (beta-escin) skinned strips from the rat isolated femoral vein [20].

Associations of beta-Aescin with other chemical compounds

• 5. In smooth muscle preparations that were permeabilized with beta-escin after treatment with toxin B, carbachol-and GTP gamma S-induced Ca2+ sensitization was significantly inhibited [21].
• Involvement of Rho kinase and protein kinase C in carbachol-induced calcium sensitization in beta-escin skinned rat and guinea-pig bladders [22].
• However, (+/-)-kavain had no effect on the caffeine-induced (20 mM) contractions of ileum strips, which were permeabilized with digitonin or beta-escin [23].
• To determine if activation of protein kinase C (PKC) participates in the molecular mechanism for agonist induced force enhancement, force was measured in single beta-escin skinned smooth muscle cells stimulated to contract with Ca2+, myosin light chain (MLC) kinase, PKC and microcystin-LR [24].
• In order to study the intracellular events leading to histamine release, rat peritoneal mast cells were permeabilized using beta-escin, a triterpenoid [25].

Gene context of beta-Aescin

• Beta-escin inhibits colonic aberrant crypt foci formation in rats and regulates the cell cycle growth by inducing p21(waf1/cip1) in colon cancer cells [26].
• Results also indicate that beta-escin inhibited growth of colon cancer cells with either wild-type or mutant p53 [26].
• Beta-escin treatment in HT-29 cells induced growth arrest at the G1-S phase, which was associated with the induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), and this correlated with reduced phosphorylation of retinoblastoma protein [26].
• The mechanical effects of KCl, oxytocin and endothelin-1 on pregnant rat myometrium were examined using intact strips and beta-escin-treated skinned strips [27].
• In smooth muscle permeabilized with alpha-toxin or beta-escin, the increase in force elicited by different agonists at fixed [Ca2+] (Ca(2+)-sensitization) can be inhibited by bacterial toxins (EDIN, and exoenzyme C3) which ADP-ribosylate and inactivate Rho proteins [28].

Analytical, diagnostic and therapeutic context of beta-Aescin

• After treatment with 5 microM beta-escin for 30-35 min, the cell membrane was permeable to small molecules (e.g., Ca2+, ATP), whereas the 10-kD fura dextran only slowly leaked out of the fiber [9].
• The possibility that the inhibition of STOCs was due to direct channel inhibition by PKC was addressed using inside-out or open-cell-attached patch-clamp techniques, the latter established using beta-escin [29].
• METHODS: Rats were pretreated with sodium beta-aescin for 7 d and then subjected to cerebral ischemia/reperfusion (I/R) injury induced by an MCAO [11].
• For the determination of beta-escin serum concentrations, a highly specific radioimmunoassay (RIA) was used [30].
• This novel feature of beta-escin, a triterpene saponin, may be a useful candidate agent for colon cancer chemoprevention and treatment [26].

References