Sodium Aescinate
Sodium aescinate has immunity enhancing,anti-inflammatory and antioxidant activities, may effectively control and improve wound healing in diabetic rats. It has obvious antiangiogenic effect, the initiation of angiogenesis and proliferation of endothelial cell are inhibited and the secretion of VEGF is also decreased. 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.;it also can protect against liver injury induced by methyl parathion.
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Chinese Journal of New Drugs, 2007, 16(17):1357- 60.
Antiangiogenic effect and possible mechanism of sodium aescinate.[Reference:
WebLink]
To investigate the antiangiogenic effect and possible mechanism of Sodium Aescinate.
METHODS AND RESULTS:
Rat aortic disks were cultured in 96-well plate to test if Sodium Aescinate could inhibit the initiation and growth of aortic disks' outgrowths.MTT method was used to test if Sodium Aescinate could affect the proliferation of ECV-304 cell.Immunohistochemistry was performed to test if Sodium Aescinate could affect the secretion of VEGF in S180 sarcoma. Sodium Aescinate(50 μg·mL-1)could obviously inhibit the initiation of rat aortic disks from the first to the fifth day,the inhibition rates were more than 39.0%;and from the second to the sixth day,it could obviously inhibit the growth of aortic disks' outgrowths,the inhibition rates were all more than 68.9%.The proliferation of ECV-304 was obviously inhibited,the inhibition rate was 70.3%and 53.6% for 100 and 50 μg·mL-1,respectively.The secretion of VEGF in S180 sarcoma of mouse were obviously decreased by Sodium Aescinate at the dose of 1.4 and 2.8 mg·kg-1.
CONCLUSIONS:
Sodium Aescinate has obvious antiangiogenic effect.The initiation of angiogenesis and proliferation of endothelial cell are inhibited and the secretion of VEGF is also decreased.
Exp Ther Med. 2012 May;3(5):818-822. Epub 2012 Feb 13.
Sodium aescinate ameliorates liver injury induced by methyl parathion in rats.[Pubmed:
22969975]
Methyl parathion, a highly cytotoxic insecticide, has been used in agricultural pest control for several years. The present study investigated the protective effect of Sodium Aescinate (SA, the sodium salt of aescin) against liver injury induced by methyl parathion.
METHODS AND RESULTS:
Forty male Sprague-Dawley rats were randomly divided into 5 groups of 8 animals: the control group; the methyl parathion (15 mg/kg) poisoning (MP) group; and the MP plus SA at doses of 0.45, 0.9 and 1.8 mg/kg groups. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and acetylcholinesterase (AChE) in the plasma were assayed. Nitric oxide (NO) and antioxidative parameters were measured. Histopathological examination of the liver was also performed. The results revealed that SA had no effect on AChE. Treatment with SA decreased the activities of ALT and AST, and the levels of malondialdehyde and NO. Treatment with SA also increased the level of glutathione and the activities of superoxide dismutase and glutathione peroxidase. SA administration also ameliorated liver injury induced by methyl parathion poisoning.
CONCLUSIONS:
The findings indicate that SA protects against liver injury induced by methyl parathion and that the mechanism of action is related to the antioxidative and anti-inflammatory effects of SA.
Inflammation. 2015 Apr 24.
The Efficacy of Sodium Aescinate on Cutaneous Wound Healing in Diabetic Rats.[Pubmed:
25903967]
This study is aimed to evaluate the potential effects of Sodium Aescinate (SA, the sodium salt of aescin) on wound healing in streptozotocin-induced diabetic rats.
METHODS AND RESULTS:
An excision skin wound was created in diabetic rats, and the wounded rats were divided into three groups: I) control group, II) gel-treated group, and III) Sodium Aescinate -treated group. The control group wounds received topically normal saline once daily for 19 days. The gel-treated and Sodium Aescinate -treated wounds received topically 400 μl of pluronic F-127 gel (25 %) and 400 μl of Sodium Aescinate (0.3 %) in pluronic gel, respectively, once daily for 19 days. Sodium Aescinate application in diabetic rats increased the wound contraction and significantly decreased the level of the inflammatory cytokine tumor necrosis factor-alpha (TNF-α) in comparison to the gel-treated group and control group. Sodium Aescinate application in diabetic rats also resulted in a marked increase in the level of anti-inflammatory cytokine interleukin-10 (IL-10) and activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) compared to the other groups. Histopathologically, Sodium Aescinate -treated wounds showed better granulation tissue dominated by marked fibroblast proliferation, and wounds were covered by thick regenerated epithelial layer. Additionally, the application of only pluronic gel produced some beneficial effects in some parameters in comparison to control group, but most of them were not significantly different.
CONCLUSIONS:
These findings demonstrated that Sodium Aescinate may effectively control and improve wound healing in diabetic rats via its anti-inflammatory and antioxidant activities.
Molecules. 2012 Aug 27;17(9):10267-75.
Evaluation of in vivo antioxidant and immunity enhancing activities of sodium aescinate injection liquid.[Pubmed:
22926307]
Oxidative stress is involved in the development and progression of disease. Because Sodium Aescinate has been reported to have immunity enhancing and antioxidative effects, we investigated its activity by employing a hepatocellular carcinoma (HCC) mouse model.
METHODS AND RESULTS:
Sixty BALB/c mice were randomly divided into four groups, including a 1.4 mg/kg treated group (n = 15), a 2.8 mg/kg treated group (n = 15), an untreated hepatocellular carcinoma control group (n = 15) and a normal control group (n = 15). After H22 cells were cultured for one week, we collected 2 × 10⁶ cells and injected them subcutaneously as 0.2 mL cell suspensions in sterile saline into the right shoulder region of every mouse. The animals were monitored for changes in activity, physical condition and body weight during the experiment. The next day after injection of H22 cells, animals in these test groups received one intraperitoneal injection of drug or physiological saline for 13 days. Results showed that in the Sodium Aescinate injection liquid (SAIL)-treated HCC mice, serum interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), Gamma-glutamyltransferase (γ-GT), alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) levels were significantly decreased compared with normal control mice. In addition, treatment with Sodium Aescinate injection liquid significantly decreased blood and liver malondialdehyde (MDA) levels, increased glutathione (GSH) levels, and antioxidant enzyme [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activities in a dose-dependent manner.
CONCLUSIONS:
We conclude that Sodium Aescinate injection liquid can decrease oxidative injury and enhance immunity functions in HCC mice.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2012 Mar;43(2):170-3.
[Effects of sodium aescinate on the apoptosis-related genes in lung injury induced by intestinal ischemia reperfusion in rats].[Pubmed:
22650024]
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.
METHODS AND RESULTS:
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 Sodium Aescinate + 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 Sodium Aescinate + I/R group than that in I/R group.
CONCLUSIONS:
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.
