Astragaloside

[Role of BCL-2, caspase-3 and NF-kappaB in astragaloside inducing apoptosis of human NB4 cells].[Pubmed:24989280]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2014 Jun;22(3):703-6.

This study was purposed to investigate the apoptosis-inducing effect of Astragalosides on acute promyelocytic leukemia(APL) cell line NB4 and its mechanism. NB4 cells were treated with different concentrations (200, 300, 400 microg /ml) of Astragalosides for 48 h. The cell proliferation was assayed by using CCK-8 method; the cell apoptosis was analyzed by flow cytometry with Annexin V-FITE/PI double staining. The mRNA expression of BCL-2 and the relative activity of BCL-2, NF-kappaB and caspase-3 were detected by RT-PCR and Western blot, respectively. The results showed that after treated with Astragalosides for 48 h, Astragalosides inhibited NB4 cell proliferation in concentration-dependent way, the apoptosis rate of NB4 cells gradually elevated from 4.69% to 40.85% with the increasing of Astragalosides concentration. Simultaneously, the mRNA expression of BCL-2 was down-regulated, Western blot analysis showed that the protein expression levels of BCL-2 and NF-kappaB decreased after Astragalosides treatment, while caspase-3 protein expression level increased. It is concluded that the molecular mechanism of the Astragalosides-induced apoptosis in NB4 cells may be associated with down-regulation of the expression of BCL-2 and NF-kappaB, finally the relative activity of caspase-3 activated.

Protective effect of astragaloside on focal cerebral ischemia/reperfusion injury in rats.[Pubmed:20503469]

Am J Chin Med. 2010;38(3):517-27.

This study was to observe the neurological protective effects of Astragalosides (AST) on focal cerebral ischemia-reperfusion (I/R) injury in rats and to explore its possible mechanism. Male SD rats received right middle cerebral artery occlusion for 120 min and AST (40 mg/kg) was orally administered. The rats were decapitated 1, 3, 7, and 14 days after reperfusion. The neurological deficit score, infarct volume and water content of brain were measured; the activity of superoxide dismutase (SOD), lactate dehydrogenase (LDH) and nitric oxide synthase (NOS), and the content of malondialdehyde (MDA), lactate (LD) and nitric oxide (NO) of brain tissue were detected too. The expression of inducible nitric synthase (iNOS), nerve growth factor (NGF) and tropomyosin receptor kinase A (TrkA) mRNA were measured by RT-PCR or real-time PCR. AST could significantly reduce the neurological deficit score; infract volume and water content, increase SOD and LDH activities, decrease NOS activity and MDA, LD and NO content. AST treatment could down-regulate expression of iNOS mRNA, while, NGF and TrkA mRNA were up-regulated. Our data suggest that AST have the protective effects on focal cerebral ischemia in rats at the different reperfusion time points, the mechanism may be related to the antioxidation, regulated the expressions of iNOS, NGF and TrkA mRNA.

Astragaloside improves outcomes of traumatic brain injury in rats by reducing microglia activation.[Pubmed:25384449]

Am J Chin Med. 2014;42(6):1357-70.

Astragaloside (AST) is traditionally prescribed for the prevention and treatment of cerebrovascular diseases. We directly tested the therapeutic effects of AST in a rat model of traumatic brain injury (TBI). One hour after the onset of TBI rats were given Saline (1 ml/kg) or AST (20-80 mg/kg) via i.p. injection. AST causes the attenuation of TBI-induced cerebral contusion, neuronal apoptosis, and neurological motor dysfunction. TBI-induced microglial activation evidenced by the morphological transformation of microglia (or ameboid microglia) and the microglial overexpression of tumor necrosis factor-alpha was reduced by AST. Our results indicate that AST may protect against brain contusion and neuronal apoptosis after TBI by attenuating microglia activation in male rats.