The anti-inflammatory effect of Escin is similar to that of dexamethasone, but its action time is longer, and it has an effect on the spleen index (SI), thymus index (TI), splenocyte proliferation ability (PS), lymphocyte count (LC) of experimental animals. , Serum tumor necrosis factor-α (TNF-α) level had no significant effect. Aescin does not significantly increase the secretion of corticosteroids in serum, nor does it promote the apoptosis of immune cells in the spleen and thymus, so its anti-inflammatory effect does not depend on the secretion of corticosteroids.
When studying the effect of aescin on the survival rate of lipopolysaccharide-induced endotoxemia mice, it was found that Escin can inhibit the release of high mobility group box B1 (HMGB1) from macrophages, and reduce the levels of TNF-α and IL in macrophages. -1β, IL-6 levels, inhibit the activation of NF-κB, and improve the survival rate of mice. In addition, the antioxidant activity of aescin can enhance its anti-inflammatory ability. Aescin can increase the activity of myeloperoxidase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and reduce serum NO, TNF-α and IL-1β inflammatory factors Increase the expression and function of glucocorticoid receptor, greatly reduce the degree of lung injury in endotoxemia mice, and prolong their survival time. External application of aescin can significantly inhibit carrageenan-induced paw edema in rats, and the effect is more obvious after pretreatment with dexamethasone; it can significantly inhibit xylene-induced ear edema in mice, and the curative effect is better than that of dexamethasone alone; it can inhibit The improvement of skin vascular permeability caused by histamine, but the curative effect is worse than that of dexamethasone; the subacute granulomatous inflammation induced by cotton balls is obviously inhibited, and the curative effect is better than that of dexamethasone. Experiments show that aescin can significantly inhibit PGE2, The increase of TNF-α and IL-1β inflammatory factors may be related to the participation of glucocorticoid receptors.
Escin can significantly inhibit the exudation of inflammatory tissue, reduce its permeability, and has a significant effect on the edema and damage of various tissues. Studies have confirmed that large doses of aescin can significantly inhibit the increase in blood-retinal barrier permeability caused by ischemia/reperfusion in rats, reduce retinal edema, and effectively inhibit retinal edema and vision loss; the combination of aescin and triamcinolone acetonide The application has a synergistic protective effect on the blood-retinal barrier ischemia/reperfusion injury, and the combined use of the two can significantly reduce the permeability of the blood-retinal barrier after ischemia, while a small dose of aescin or triamcinolone acetonide alone has no such effect In addition, the combined application can promote the expression of the tight junction protein occludin, resist the damage of the blood-retinal barrier, and significantly improve the curative effect.
In the treatment of allergic inflammation, the experiment found that the treatment of small doses of prednisone combined with aescin can significantly reduce paw swelling in animal models of arthritis, reduce synovial inflammatory cell infiltration, inhibit synovial hyperplasia and bone erosion, and reduce serum TNF-α, IL-1β and IL-6 levels, and reduce the side effects of high-dose hormones. Aescin can inhibit the skin allergic reaction in a dose-dependent manner. The allergic skin reaction of experimental animals administered orally at 5 mg/kg aescin was significantly inhibited on the second day, and the range of skin redness and swelling was significantly reduced. Its anti-allergic effect may be Associated with the glucocorticoid receptor pathway. In terms of airway allergic inflammation, β-escin sodium can inhibit the activation and degranulation of mouse mast cells in the skin, prevent fluid from penetrating into tissues, and reduce type I hypersensitivity reactions; inhibit lung tissue inflammation and reduce white blood cells , eosinophils, IL-5 and IL-13 in the alveolar accumulation, reduce airway inflammation, reduce the intensity of delayed type Ⅰ hypersensitivity.