Escin IIB
Escin IIB has positive effects on acute inflammation in animals, it can inhibit the induced by serotonin in rats, the hind paw edema induced by carrageenin, and the scratching behavior induced by compound 48/80 in mice. Escin IIB shows gastroprotection on ethanol-induced gastric mucosal lesions, whereas endogenous prostaglandins, NO, capsaicin-sensitive afferent neurons, and the sympathetic nervous system participate; it also enhances Mg(2+) absorption from the digestive tract in mice, in which the constitutive, but not the inducible, NO synthase plays an important role.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Eur J Pharmacol. 2000 Jan 17;387(3):337-42.
Enhancement by escins Ib and IIb of Mg(2+) absorption from digestive tract in mice: role of nitric oxide.[Pubmed:
10650180]
The effects of escin Ib and Escin IIB isolated from horse chestnuts on Mg(2+) absorption from the digestive tract and the role of endogenous nitric oxide (NO) were investigated in mice.
METHODS AND RESULTS:
Test samples were given orally to fasted mice 30, 120, 180, 240 and 300 min before administration of 0.5 M MgSO(4) (10 ml/kg, p.o.). The serum Mg(2+) levels were determined 30, 60, 120 and 180 min after administration of MgSO(4). Escin Ib and Escin IIB (12.5 and 25 mg/kg) significantly increased the serum Mg(2+) by 10.0-27.3%, 30, 120 and 180 min after administration of the samples, and 30, 60, 120 and 180 min after administration of MgSO(4). Escin Ib and Escin IIB(12.5 mg/kg) significantly decreased the Mg(2+) content in the small intestinal fluid in MgSO(4)-loaded mice, but did not increase the serum Mg(2+) levels in normal mice. The effects of Escin Ib and Escin IIB (12.5 mg/kg) on serum Mg(2+) levels were attenuated in a dose-related manner by the pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 3-20 mg/kg, i.p., an inhibitor of constitutive and inducible NO synthase), but not with D-NAME (10 mg/kg, i.p., the inactive enantiomer of L-NAME) or dexamethasone (0.05 and 0.5 mg/kg, s.c., an inhibitor of inducible NO synthase). The effect of L-NAME was reversed by L-arginine (600 mg/kg, i.p., a substrate of NO synthase), but not by D-arginine (900 mg/kg, i.p., the enantiomer of L-arginine).
CONCLUSIONS:
These results suggest that Escin Ib and Escin IIB enhance Mg(2+) absorption from the digestive tract in mice, in which the constitutive, but not the inducible, NO synthase plays an important role.
Biol Pharm Bull. 1997 Oct;20(10):1092-5.
Effects of escins Ia, Ib, IIa, and IIb from horse chestnut, the seeds of Aesculus hippocastanum L., on acute inflammation in animals.[Pubmed:
9353571]
We investigated the effects of escins Ia, Ib, and IIb isolated from horse chestnut, the seeds of Aesculus hippocastanum L., and desacylescins I and II obtained by alkaline hydrolysis of escins on acute inflammation in animals (p.o.).
METHODS AND RESULTS:
Escins Ia, Ib, IIa, and IIb (50-200 mg/kg) inhibited the increase of vascular permeability induced by both acetic acid in mice and histamine in rats. Escin Ib, Escin IIa, and Escin IIB (50-200 mg/kg) also inhibited that induced by serotonin in rats, but escin Ia didn't. Escin Ib, Escin Ia, Escin IIa, and Escin IIB (200 mg/kg) inhibited the hind paw edema induced by carrageenin at the first phase in rats. Escin Ia (200 mg/kg) and Escin Ib, Escin IIa, and Escin IIB(50-200 mg/kg) inhibited the scratching behavior induced by compound 48/80 in mice, but escin Ia was weakest. Desacylescins I and II (200 mg/kg) showed no effect.
CONCLUSIONS:
With regard to the relationship between their chemical structures and activities, the acyl groups in escins were essential.
Escin Ib, Escin IIa, and Escin IIB with either the 21-angeloyl group or the 2'-O-xylopyranosyl moiety showed more potent activities than escin Ia which had both the 21-tigloyl group and the 2'-O-glucopyranosyl moiety.
Eur J Pharmacol. 1999 May 28;373(1):63-70.
Gastroprotections of escins Ia, Ib, IIa, and IIb on ethanol-induced gastric mucosal lesions in rats.[Pubmed:
10408252]
Effects of escin Ia, escin Ib, escin IIa, and Escin IIB isolated from horse chestnuts on ethanol-induced gastric mucosal lesions and the roles of capsaicin-sensitive afferent neurons, endogenous nitric oxide (NO), sulfhydryls, prostaglandins, as well as gastric secretion and the sympathetic nervous system, were investigated in rats.
METHODS AND RESULTS:
Test samples were given orally to fasted rats 1 h before ethanol (1.5 ml/rat, p.o.) treatment or ligation of the pylorus. Escins Ia–IIb (10–50 mg/kg) potently inhibited ethanol-induced gastric mucosal lesions, whereas desacylescins I and II (50 mg/kg) showed no such effect. These active saponins (10 and 20 mg/kg) did not decrease the gastric secretion. The gastroprotections of escins Ia–IIb were attenuated by the pretreatment with capsaicin, N G -nitro- l -arginine methyl ester, and indomethacin, but not by N -ethylmaleimide. The effects of escins Ia–IIb were also attenuated in streptozotocin-induced diabetic rats, in which the activity of the sympathetic nervous system was abnormal.
CONCLUSIONS:
These results suggest that the gastroprotections of escins Ia–IIb on ethanol-induced gastric mucosal lesions are acid-independent, whereas endogenous prostaglandins, NO, capsaicin-sensitive afferent neurons, and the sympathetic nervous system participate.
