beta-escin has been researched along with Ischemia* in 4 studies
4 other study(ies) available for beta-escin and Ischemia
Article | Year |
---|---|
Synergistic protective effects of escin and low‑dose glucocorticoids on blood‑retinal barrier breakdown in a rat model of retinal ischemia.
Escin, a natural mixture of triterpenoid saponins isolated from the seed of the horse chestnut (Aesculus hippocastanum), has been demonstrated to possess glucocorticoid (GC)‑like anti‑edematous and anti‑inflammatory effects. The aim of the present study was to investigate whether escin exhibits synergistic protective effects on blood‑retinal barrier (BRB) breakdown when combined with GCs in a rat model of retinal ischemia. Low concentrations of escin and triamcinolone acetonide (TA) alone did not affect BRB permeability. However, when administered together, low‑dose escin and TA significantly reduced BRB permeability following ischemia. Furthermore, low‑dose escin and TA alone did not affect the expression of occludin in the ischemic retina; however, when administered together, they significantly increased occludin expression in the ganglion cell layer of the ischemic retina. This indicates that escin and GCs have synergistic protective effects on BRB breakdown and the molecular mechanisms may be correlated with the upregulation of occludin. Therefore, the administration of escin may allow a reduction in the dose of GCs for the treatment of macular edema. The combination of escin with GCs is potentially a beneficial treatment method for BRB breakdown and warrants further investigation. Topics: Animals; Blood-Retinal Barrier; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Synergism; Escin; Glucocorticoids; Ischemia; Male; Occludin; Permeability; Protective Agents; Rats; Rats, Sprague-Dawley; Retinal Vessels; Triamcinolone Acetonide | 2013 |
[Effects of sodium aescinate on the apoptosis-related genes in lung injury induced by intestinal ischemia reperfusion in rats].
To investigate the relationship between apoptosis-related genes and lung injury induced by intestinal ischemia reperfusion and to explore the effects and its possible mechanism of sodium aescinate.. Rat model of intestinal I/R injury was established with clamping of the superior mesenteric artery for 60 min and then clamping was relieved for 60 min. Twenty-four SD rats were randomly divided into three groups with eight rats in each: sham group, intestinal ischemia/reperfusion group (I/R group) and sodium aescinate group (SA + I/R group). Lung wet/dry weight ratio, lung coefficient and Superoxide dismutase (SOD), malondialdehyde (MDA) in plasma and lung tissue were measured, as well as the expression levels of Bcl-2 and Bax proteins in lung tissue were examined using immunohistochemical method.. Compared with sham group, lung wet/dry weight ratio, lung coefficient and MDA in plasma and lung tissue were significantly increased, and while the activity of SOD in plasma and lung tissue were decreased significantly in I/R group. At the same time, the protein expression level of Bcl-2 and Bax were significantly increased. But Bax protein expression was much greater than that of Bcl-2, the ratio of Bcl-2 to Bax was decreased significantly in I/R group than that in sham group. Compared with I/R group, lung wet/dry weight ratio, lung coefficient and MDA in plasma and lung tissue were significantly decreased, and while the activity of SOD in serum and lung tissue were significantly increased in SA + I/R group. At the same time, Bax protein expression was significantly decreased, both Bcl-2 protein expression and the ratio of Bcl-2 to Bax were significantly increased in SA + I/R group than that in I/R group.. Lung injury induced by intestinal ischemia reperfusion is correlated with abnormal expression levels of Bcl-2 and Bax protein which is caused by oxidative injury. Sodium aescinate can protect the lung injury induced by intestinal ischemia/reperfusion (I/R), which may be mediated by inhibiting lipid peroxidation, upregulating Bcl-2 gene protein expression, improving the ratio of Bcl-2/ Bax to inhibit lung apoptosis. Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Escin; Female; Intestines; Ischemia; Lung Injury; Male; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Saponins | 2012 |
Sodium beta-aescin may be an effective therapeutic agent for Bell's palsy.
Although Bell's palsy is the most common acute facial paralysis, the cause of it is still unknown. This made the treatment for it remain very limited. Many methods are simply symptomatic treatment. Up to now we have known that Bell's palsy is related to viral infection and the pathomechanism of Bell's palsy involves inflammatory oedema and entrapment neuropathy in the narrow bony facial canal. So treatment plans for Bell's palsy mainly focus on antiviral therapy, relieving inflammatory oedema and accelerating facial nerve recovery. Sodium beta-aescin is derived from horse chestnut and its major constituent is aescigenin which has been approved by China national drug standard. The pharmacologic action of sodium beta-aescin is to relieve tissue oedema, recover vasopermeability and eliminate pressure caused by oedema. Nowadays sodium beta-aescin has been widely used clinically for encephaledema or tumefaction caused by trauma or operation. It also can be used for treating disease of digestive system and increasing intravenous tension and improving microcirculation. Although many papers had been published on the anti-edema effects of sodium beta-aescin, little was known about the effects in treating oedema complicated by Bell's palsy. Topics: Bell Palsy; Cardiovascular Agents; Chemistry, Pharmaceutical; Drug Design; Edema; Escin; Facial Paralysis; Humans; Inflammation; Ischemia; Models, Biological; Models, Theoretical; Pharmaceutical Preparations; Sodium | 2008 |
[Possible therapeutic influences on experimentally induced edemas (author's transl)].
In pathogenetically different models the antiedemic effect of extractum hippocastani semen (EHS) for intravenous and oral use was to be demonstrated. The histamine-induced edema of the skin, the postischemic edema of muscle and the cerebral edema provoked by cold injury were used. In all the models tested, it was possible to obtain reproducible numerical results which made statistical evaluation of the experiments possible. Antiedemic protective effects could be demonstrated in all investigations, whereas in one model a curative effect could be proved, too. Topics: Brain Edema; Cold Temperature; Disease Models, Animal; Edema; Escin; Histamine; Ischemia; Muscles; Muscular Diseases; Plant Extracts; Plants, Medicinal; Skin Diseases | 1976 |