| 规格: | 98% |
| 分子量: | 254.69 |
| 包装 | 价格(元) |
| 50mg | 电议 |
| 250mg | 电议 |
Background:
Astragalus polysaccharide are active components of the polysaccharides extract of Astragulus, attenuates TNF-α-induced insulin resistance by suppressing miR-721 and activating PPAR-γ and PI3K/Akt in 3T3-L1 adipocytes.
Astragalus Polysaccharides (APS) are active components of the polysaccharides extract of Astragulus, which has important antioxidant, anti-hypertensive, and immunomodulatory roles. Astragalus Polysaccharides (APS) attenuates TNF-α-induced insulin resistance by suppressing miR-721 and activating PPAR-γ and PI3K/Akt in 3T3-L1 adipocytes. Astragalus Polysaccharides (APS) has a strong anti-inflammatory effect, and enhances the gene expression of an inflammatory marker peroxisome proliferator-activated receptor gamma (PPAR-γ) in a time- and dose-dependent manner. Astragalus Polysaccharides (APS) reverses the PPAR-mediated suppression of genes involved in glucose utilization. The expression of miR-721 is suppressed by Astragalus Polysaccharides (APS) in a dose-dependent manner. Also, the expression of PPAR-γ was increased in a dose-dependent manner. Treatment with Astragalus Polysaccharides (APS) attenuates the miR-721-inhibited expressions of PPAR-γ, p-Akt, and GLUT4. In the presence of insulin, Astragalus Polysaccharides (APS) upregulates the expression of PPAR-γ, p-Akt, PI3K, and GLUT4 in the miR-721 mimics. The expression levels of PPAR-γ, p-Akt, PI3K, and GLUT4 in miR-721+Astragalus Polysaccharides (APS)+insulin group are lower than that in the Astragalus Polysaccharides (APS)+insulin group[1].
To determine whether Astragalus Polysaccharides (APS) could preserve heart function in vivo, a heart failure model is generated using Doxorubicin-treated C57BL/6 mice. As shown by H&E staining, Doxorubicin-induced heart failure is associated with decreased thickening of the left ventricular wall and ventricular dilation. The number of apoptotic cells is dramatically higher in hearts of Doxorubicin-treated C57BL/6 mice (26.44±7.72%) compared with hearts from control mice (2.55±0.65%) as demonstrated by TUNEL staining. Importantly, pretreatment with Astragalus Polysaccharides (APS) attenuates Doxorubicin-induced cardiomyocyte apoptosis (15.54±6.06%). Moreover, Western blot analysis reveals that Astragalus Polysaccharides (APS) suppresses Doxorubicin-induced caspase 3 and caspase 9 activation. In addition, Bcl2 protein expression is dramatically upregulated in Astragalus Polysaccharides (APS) pretreated mice[2].
[1]. Ke B, et al. Astragalus polysaccharides attenuates TNF-α-induced insulin resistance via suppression of miR-721 and activation of PPAR-γ and PI3K/AKT in 3T3-L1 adipocytes. Am J Transl Res. 2017 May 15;9(5):2195-2206. eCollection 2017. [2]. Cao Y, et al. Astragalus polysaccharide suppresses doxorubicin-induced cardiotoxicity by regulating the PI3k/Akt and p38MAPK pathways. Oxid Med Cell Longev. 2014;2014:674219.
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