Aim To investigate the effects of astragalus polysaccharide (APS) on renal TGF-β1/Smads signa-ling pathway in rats with diabetes mellitus(DM). Methods Wistar rats were randomly divided into nor-mal group,DM group,APS low dose (APS-low) group and APS high dose (APS-high) group. Rats in APS-low group and APS-high group respectively received 200 and 400 mg·kg-1·d-1APS for 8 weeks. Con-centrations of fasting blood-glucose(FBG),blood urea nitrogen and creatinine,as well as urinary kidney injury molecule-1 (KIM-1) and osteopontin (OPN) were measured. Levels of TGF-β1,Smad2,phosphorylated Smad2 (p-Smad2),Smad3,phosphorylated Smad3 (p-Smad3),Smad7,matrix metalloproteinase (MMP) 2,MMP-9,tissue inhibitor of matrix metalloproteinases (TIMP)-1 and TIMP-2 were investigated. Results Compared to control group,DM group had higher levels of FBG,blood urea nitrogen,creatinine KIM-1,OPN, TGF-β1,Smad2,p-Smad2,Smad3,p-Smad3,TIMP-1 and TIMP-2,but lower levels of Smad7,MMP-2 and MMP-9. APS significantly decreased the levels of FBG,blood urea nitrogen,creatinine KIM-1 and OPN, as well as inhibited the activity of TGF-β1/Smads sig-naling pathway. Conclusion The renoprotective effects of APS might be associated with the inhibition of TGF-β1/Smads signaling pathway.

Aim To investigate the effects of astragalus polysaccharide ( APS ) on depressive behaviors and hippocampal NF-κB signaling in rats with depression. Methods Wistar rats were randomly divided into con-trol group, depressive group, APS-low (200 mg·kg-1 ·d-1 ) group and APS-high ( 400 mg · kg-1 · d-1 ) group. Depressive behaviors were induced by chronic unpredictable mild stress ( CUMS) in rats. After trea-ted with APS, depressive behaviors were valuated by open field test, forced swim test and sucrose preference test. Levels of NF-κB p65, phosphorylated NF-κB p65 ( p-NF-κB p65 ) , phosphorylated IκBα ( p-IκBα) , NF-κB p65 DNA binding activity, TNF-α, IL-1β and IL-6 were measured to assess the activity of NF-κB sig-naling pathways. Results Compared to control group, rats in depressive group had less sucrose intake in su-crose preference and longer immobility time in forced swim test, as well as increased hippocampal NF-κB signaling activity. However, APS treatment dose-de-pendently alleviated depressive-like behaviors and in-hibited the activation of NF-κB signaling induced by UCMS. Conclusion The antidepressant effects of APS might be associated with the inhibition of hipp-ocampal NF-κB signaling pathway.

Astragalus polysaccharide (APS) is a natural compound extracted from astragalus membranaceus which has an antidepressant activity. Initially APS was studied for its immunomodulatory potential, and later was found to exhibit multiple pharmacological effects, including anti-inflammatory activity. More recently APS was shown to attenuate the lipopolysaccharide (LPS) induced neuroinflammation and improve the learning and memory ability of rats. The major objectives of this study were to investigate whether APS would exhibit antidepressant effects in an animal model of depression induced by LPS, and whether this effect might be associated with regulating nuclear factor-kappaB (NF-kappa B) and mitogen-activated protein kinase (MAPK) signaling pathways. Three groups of Wistar rats were injected LPS (i.p.), two groups of which were pretreated with APS (200 mg or 400 mg, i.p.). Behaviors were evaluated by forced swim test, saccharin preference test and open field test. Levels of NF-kappa B p65, phospho-NF-kappa B p65, phospho-I kappa B alpha, ERK1/2, JNK, p38 MAPK, phospho-ERK1/2, phospho-JNK and phospho-p38 MAPK in hippocampus and hypothalamus were measured to assess the activities of NF-kappa B and MAPK signaling pathways. In addition, levels of TNF-alpha, IL-1 beta and IL-6 (both protein and mRNA levels) in hippocampus and hypothalamus were determined. Results showed LPS induced depressive behaviors, as well as activated the NF-kappa B and MAPK signaling pathways in rats. APS treatment dose-dependently alleviated depressive-like symptoms and inhibited the activation of NF-kappa B and MAPK signaling pathways induced by LPS. The data indicate an antidepressant-like activity of APS in a LPS-induced animal model of depression possibly via inhibition of NF-kappa B and MAPK signaling pathways.