Angelica Polysaccharide Research Articles

Leukemia cells apoptosis by a newly discovered heterogeneous polysaccharide from Angelica sinensis (Oliv.) Diels

Galectin-3 (Gal-3) is a potential target for acute myeloid leukemia therapeutics which contains a carbohydrate-recognition domain. However, the development of polysaccharide inhibitors against Gal-3 is insufficient. In this research, we found a polysaccharide from Angelica sinensis (Oliv.) Diels, named APS-2I, that can bind to Gal-3 with dissociation constant (Kd) of 9.35 ± 0.3 μM and activate the intrinsic apoptosis pathways to induce leukemia cells apoptosis. APS-2I is a homogeneous polysaccharide with a molecular weight of 7.2 × 105 Da, that composes of mannose, rhamnose, galacturonic acid, glucose, galactose and arabinose with a ratio of 4:5:1:10:23:39. In addition, a galactosidase digested fraction of APS-2I named G-4 showed higher affinity to Gal-3 with the Kd of 1.97 ± 0.7 μM and higher apoptosis inducing effect on leukemia cells, which demonstrated that G-4 contains the bio-active structural region of APS-2I. This study provides effective basis for structural analysis and the anti-leukemia mechanism of Angelica polysaccharide APS-2I.

Effects of Angelica Polysaccharide on telomere length in mice with benzene-induced aplastic anemia

Effects of Angelica Polysaccharide on telomere length in mice with benzene-induced aplastic anemia

Angelica polysaccharide ameliorates memory impairment in Alzheimer's disease rat through activating BDNF/TrkB/CREB pathway.

This study aimed to investigate the effect of Angelica sinensis polysaccharides (ASP) on Alzheimer’s disease (AD) and its underlying mechanisms. In our study, we build the AD model by injecting Aβ25–35. Morris water maze (MWM) was applied to investigate learning and memory. Moreover, neurotransmitters, free radical, and inflammatory factors were also measured. Pathological change and neuronal death in hippocampus CA1, CA3, and DG region were detected by HE staining and Nissl staining. The neuronal apoptosis was detected by TUNEL. The expressions of caspase-3, Bcl-2 and Bax were measured by immunohistochemistry and Western blot. The expressions of BDNF, TrkB, p-Akt, Akt, p-CREB, and CREB were measured by Western blot. Our results showed that ASP could ameliorate spatial learning and memory deficiency in AD rats. ASP decreased AchE level and increased the levels of Ach and chAT in AD rats. ASP could increase the activity of SOD and CAT, decrease MDA activity, and inhibit the expression levels of inflammatory factors and neurons apoptosis in AD rats. Pathological change of hippocampus CA1, CA3, and DG region was ameliorated by ASP. In addition, the effects of ASP were reversed by K252a (TrkB inhibitor). Our study demonstrated that ASP could ameliorate memory impairment in AD rat through activating BDNF/TrkB/CREB pathway. Impact statement The present study demonstrated that ASP could ameliorate memory impairment through regulation of the balance of neurotransmitters, free radical metabolism, inflammation, and neurons apoptosis. Moreover, the mechanism of ASP on memory impairment may be related to BDNF/TrkB/CREB pathway in AD. Our research provides an innovatively regulatory mechanism about the ASP in AD rat and points a new way to the treatment of AD.

Retraction.

Yang J, Shao X, Wang L, et al. Angelica polysaccharide exhibits antitumor effect in neuroblastoma cell line SH-SY5Y by up-regulation of miR-205. BioFactors. 2023;49:201. https://doi.org/10.1002/biof.1586 This article, published online on 23 November 2019 in Wiley Online Library, has been retracted by agreement between the International Union of Biochemistry and Molecular Biology, the Editor in Chief (Dr. Angelo Azzi), and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Evidence for image manipulation was found in figures 1, 2, 3, 4, 5 and 6. As a result, the conclusions of this article are considered to be invalid.

Retraction.

Zhao Y, Liu C, Zhang X, Yan X. Angelica polysaccharide alleviates TNF-α-induced MIN6 cell damage a through the up-regulation microRNA-143. BioFactors. 2022;49:200. https://doi.org/10.1002/biof.1588 This article, published online on 20 November 2019 in Wiley Online Library, has been retracted by agreement between the International Union of Biochemistry and Molecular Biology, the Editor in Chief (Dr. Angelo Azzi), and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Evidence for image manipulation was found in figures 1, 2, 4, and 5. As a result, the conclusions of this article are considered to be invalid.

Angelica Polysaccharide Resists Platelets Apoptosis Induced by LY294002

To investigate the anti-apoptotic effect of Angelica polysaccharide (APS) on cryopreservated platelets and its mechanism. The platelets were divided into 4 group: control group(4 ℃ stored platelets),APS group (APS-treated platelets stored at 4 ℃), LY294002 group (LY294002-treated platelets stored at 4 ℃) and LY294002+APS group(LY294002+APS treated platelets stored at 4 ℃ ). The expression of platelet membrane glycoprotein CD41 and CD61, as well as the platelet apoptotic rate, Caspase 3 expression and mitochondrial membrane potential (MMP) were detected by flow cytometry; the anti-apoptotic mechanism of APS by PI3K /AKT signaling pathway was analyzed by Western blot assay. The apoptosis rate of platelets in LY294002 group obviously increased, the activity of CD41 and CD61 expression gradually decreased along with the enhancement of LY294002 concentrations (r=-0.953)； compared with control group, the apoptosis rate of platelets in LY294002 group was enhanced significantly(P<0.05)，while the apoptosis rate of platelets in LY294002+APS group significantly was reduced(P<0.05) as compare with LY294002 group, which suggest that APS has an anti-apoptotic effect on the cryopreserved platelets. APS decreased the expression of Caspase-3 and inhibited the reduction of mitochondrial membrane potential induced by LY294002, moreover, APS could increase the activation of PI3K /AKT pathway in Plt. APS has an anti-apoptotic effect on the cryopreserved platelets through activating the PI3K /AKT pathway, decreasing the expression of apoptosis protease Caspase-3 and inhibiting the reduction of MMP.

Angelica polysaccharide mitigates lipopolysaccharide-evoked inflammatory injury by regulating microRNA-10a in neuronal cell line HT22

Background Angelica polysaccharide (AP) is disengaged from the roots of Angelica sinensis. The extensive pathological activities of AP have been discovered in disparate diseases. Nevertheless, the impression of AP in epilepsy (EP) remains unaware. The research attempted to probe the impact of AP on lipopolysaccharide (LPS)-evoked inflammatory injury in HT22 cells. Methods AP were exploited to stimulate HT22 cells, cell cytotoxicity was monitored by CCK-8 assay. LPS was utilized to administrate HT22 cells to evoke inflammatory injury, meanwhile the involvements of AP in cell proliferation, apoptosis and inflammatory cytokines productions were examined. MicroRNA-10a (miR-10a) inhibitor and its negative control were one by one transfected into HT22 cells, the effect of miR-10a inhibition on LPS- and AP-treated cells was determined. NF-κB and JAK2/STAT3 pathways were ultimately detected. Results AP promoted cell proliferation, inhibited apoptosis and suppressed IL-1β, TNF-α and IL-6 productions in LPS-stimulated HT22 cells. Additionally, AP raised miR-10a expression in HT22 cells administration with LPS. These functions of AP in LPS-disposed cells were conversed by miR-10a suppression. Further, AP interdicted NF-κB and JAK2/STAT3 pathways via enhancing miR-10a. Conclusions Data corroboarted that AP mitigated LPS-evoked inflammatory injury through repression of NF-κB and JAK2/STAT3 pathways by regulating miR-10a in HT22 cells.

Transcriptomic profiles of human HaCaT cells in response to angelica polysaccharide.

The aim of this study was to explore the anti-psoriatic effect and potential mechanism of Angelica polysaccharide (APS) on an in vitro HaCaT cell model. MTS assay was performed to determine whether APS has the ability to inhibit the proliferation of HaCaT cells. RNA-sequencing (RNA-seq) was performed to investigate the underlying mechanism of APS. Quantitative real-time PCR (qRT-PCR) was used to verify the accuracy of RNA-seq data. Our MTS assay results demonstrated that APS time- and concentration-dependently inhibits the proliferation of HaCaT cells. The anti-proliferation property of APS suggests that APS may have anti-psoriatic effect. In the RNA-seq part, comparison between the CK group (i.e., Control group) and ASP groups revealed dramatic differences [468 differentially expressed genes (DEGs) for CK group vs. ASP50 group; 563 DEGs for CK group vs. ASP100 group; 532 DEGs for CK group vs. ASP200 group]. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrich analysis performed on all DEGs failed to find any significant enriched GO terms or KEGG pathways to explain the anti-proliferativeeffect of APS. All DEGs were then classified into 20 expression profiles by trend analysis. Interestingly, cell proliferation-related GO terms were mostly dispersed in the profile 2 and 17. DEGs enriched in these terms were then analyzed. After literature retrieval, DEGs such as SERPINE1, SMAD6, CTGF, and TGF-β were suspected to closely relevant to the anti-proliferation effect of APS. qRT-PCR results showed similar expression trend with RNA-seq data for 8 out of 10 genes, indicating our sequence data are reliable.

RETRACTED: Angelica polysaccharide alleviates oxidative response damage in HaCaT cells through up-regulation of miR-126

Pressure ulcers (PUs) prevalence has been considered as an index for patient safety and cure quality of hospital and community. Skin cellular oxidative response damage is existed in the development of PUs. Angelica polysaccharide (AP) has the anti-oxidation function. Therefore, our goal was to investigate the mechanism of AP in relieving cellular oxidative damage. Transfected HaCaT cells with miR-126 inhibitor, pre-treated by AP, and then treated by H2O2. CCK-8 assay and flow cytometry detection were set to test viability and apoptosis of cells respectively. qRT-PCR and western blot tested levels of miR-126 and oxidative damage relative factors. ROS assay tested the production of ROS in cells. Cellular oxidative response damage was induced by H2O2 at concentration of 300 μM. We found that AP could attenuate cellular oxidative response damage caused by H2O2 that it elevated cell viability, attenuated cell apoptosis and production of ROS and promoted activation of PI3K/AKT and mTOR signal pathways. Further, miR-126 was up-regulated by AP. The up-regulation of miR-126 could activate the PI3K/AKT and mTOR signal pathways. Our study demonstrated that AP attenuated cellular oxidative response damage in HaCaT cells by positively regulated miR-126.

Angelica polysaccharide promotes proliferation and osteoblast differentiation of mesenchymal stem cells by regulation of long non-coding RNA H19: An animal study.

ObjectivesOsteoporosis is a systemic bone metabolic disease, which often occurs among the elderly. Angelica polysaccharide (AP) is the main component of angelica sinensis, and is widely used for treating various diseases. However, the effects of AP on osteoporosis have not been investigated. This study aimed to uncover the functions of AP in mesenchymal stem cell (MSC) proliferation and osteoblast differentiation.MethodsMSCs were treated with different concentrations of AP, and then cell viability, Cyclin D1 protein level, and the osteogenic markers of runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), alkaline phosphatase (ALP), bone morphogenetic protein 2 (BMP-2) were examined by Cell Counting Kit-8 (CCK-8) and western blot assays, respectively. The effect of AP on the main signalling pathways of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and Wnt/β-catenin was determined by western blot. Following this, si-H19#1 and si-H19#2 were transfected into MSCs, and the effects of H19 on cell proliferation and osteoblast differentiation in MSCs were studied. Finally, in vivo experimentation explored bone mineral density, bone mineral content, and the ash weight and dry weight of femoral bone.ResultsThe results revealed that AP significantly promoted cell viability, upregulated cyclin D1 and increased RUNX2, OCN, ALP, and BMP-2 protein levels in MSCs. Moreover, we found that AP notably activated PI3K/AKT and Wnt/β-catenin signalling pathways in MSCs. Additionally, the relative expression level of H19 was upregulated by AP in a dose-dependent manner. The promoting effects of AP on cell proliferation and osteoblast differentiation were reversed by H19 knockdown. Moreover, in vivo experimentation further confirmed the promoting effect of AP on bone formation.ConclusionThese data indicate that AP could promote MSC proliferation and osteoblast differentiation by regulating H19.Cite this article: X. Xie, M. Liu, Q. Meng. Angelica polysaccharide promotes proliferation and osteoblast differentiation of mesenchymal stem cells by regulation of long non-coding RNA H19: An animal study. Bone Joint Res 2019;8:323–332. DOI: 10.1302/2046-3758.87.BJR-2018-0223.R2.

Recovery of Chemotherapy-induced Anemia by Angelica Polysaccharides in C57BL/6N Mice and Elucidation of Underlying Mechanism

Recovery of Chemotherapy-induced Anemia by Angelica Polysaccharides in C57BL/6N Mice and Elucidation of Underlying Mechanism

Angelica polysaccharide moderates hypoxia-evoked apoptosis and autophagy in rat neural stem cells by downregulation of BNIP3

Neonatal hypoxia–ischemia is a troublesome disease. Angelica polysaccharide (AP) is proved to have antioxidant effects. Our study was performed to confirm the effects of AP in hypoxia-exposed neural stem cells (NSCs). NSCs were pre-treated with AP and then stimulated with hypoxia. Viability of NSCs was examined by Cell Counting Kit-8 assay. Hypoxia-introduced apoptosis was observed by flow cytometry. Essential regulators of mTOR and Notch signalling pathways were examined by Western blot. mRNA expression was accessed using qRT-PCR. Bcl2/adenovirus EIB 19kD-interacting protein 3 (BNIP3) was altered by transfection. We noticed that NSCs were sensitive to hypoxia-induced apoptosis and showed decreased viability. Moreover, Beclin and light chain 3-II was upregulated while p62 was downregulated. However, AP reversed all these results. Similarly, hypoxia decreased the phosphorylation of mTOR and p70S6K and Notch1 expression while AP increased the phosphorylation of mTOR and p70S6K as well as the expression of Notch1. BNIP3 was upregulated by hypoxia while downregulated by AP. Further experiments demonstrated that overexpression of BNIP3 broken all the effects induced by AP shown in cell viability, apoptosis, autophagy and signalling pathways. Collectively, AP alleviated hypoxia-introduced NSCs damages by maintaining cell viability, blocking apoptosis and autophagy via downregulation of BNIP3 with the activation of mTOR and Notch signalling pathways.

Possible treatment for cutaneous lichen planus: An in vitro anti-inflammatory role of Angelica polysaccharide in human keratinocytes HaCaT.

Cutaneous lichen planus (CLP) is an autoimmune disease. Angelica polysaccharide (AP) has been found to exert immunomodulation activity. In this study, we explored the roles of AP in lipopolysaccharide (LPS)-induced inflammatory injury of human keratinocytes (HaCaT cells), as well as the underlying mechanisms. LPS-induced cell injury was evaluated by alterations of cell viability, apoptosis, and expressions of proteins associated with apoptosis and inflammatory cytokines. Then, the protective effects of AP on LPS-induced cell injury were assessed. The protein expressions of sirtuin 1 (SIRT1) and key kinases in the Nrf2/HO-1 and nuclear factor κB (NF-κB) pathways were measured using western blotting. SIRT1 knockdown and overexpression were used to analyze whether AP affected HaCaT cells through regulating SIRT1. Finally, the possible inhibitory effects of AP on cell injury after LPS treatment were also evaluated. We found that LPS reduced HaCaT cell viability, enhanced apoptosis, and induced release of inflammatory cytokines. AP alleviated LPS-induced HaCaT cell inflammatory injury. The expression of SIRT1 was enhanced after AP treatment. AP activated Nrf2/HO-1 pathway while inhibited NF-κB pathway in HaCaT cells. The protective effects of AP on LPS-induced HaCaT cell injury were reversed by SIRT1 knockdown. Dysregulation of SIRT1 altered the activation of Nrf2/HO-1 and NF-κB pathways in LPS-treated HaCaT cells. Furthermore, AP also exerted inhibitory effects on HaCaT cell injury after LPS stimulation. In conclusion, AP could alleviate LPS-induced inflammatory injury of HaCaT cells through upregulating SIRT1 expression and then activating Nrf2/HO-1 pathway but inactivating NF-κB pathway. This study provided a possible therapeutic strategy for clinical CLP treatments.

RETRACTED: Angelica polysaccharide protects PC-12 cells from lipopolysaccharide-induced injury via down-regulating microRNA-223.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. Concerns were initially raised regarding the Western Blots from Figures 1C, 1G, 2B, 2D, 4D, 4F, 5 (left panel), 6C and 6E. Given also the comments of Dr Elisabeth Bik regarding this article “… the Western blot bands in all 400+ papers are all very regularly spaced and have a smooth appearance in the shape of a dumbbell or tadpole, without any of the usual smudges or stains. All bands are placed on similar looking backgrounds, suggesting they were copy/pasted from other sources, or computer generated”, the journal requested the authors to provide the raw data. The authors have not provided raw data of sufficient quality and detail to support the authors’™ claim and therefore the Editor-in-Chief decided to retract the article.

Effect of Angelica polysaccharide on brain senescence of Nestin-GFP mice induced by D-galactose

The incidence of neurodegenerative diseases is severely increasing with the aging. It has been proposed that NSCs (neural stem cells) help to control aging, but the mechanisms responsible remain unclear. Angelica polysaccharide is an active ingredient of Angelica sinensis in traditional Chinese medicine, which possesses versatile pharmacological activities including anti-oxidative and anti-aging effects. In this study, D-gal (D-galactose) was used to construct an aging model of Nestin-GFP transgenic mice brain tissues and NSCs. Mouse model was subcutaneously injected with D-gal, as we observed that mice consistently displayed acceleration of aging-like behavior change, energy metabolism decreased, the expression of aging-related genes was up-regulated. Conversely, aging retardation was achieved in Nestin-GFP mice Induced by D-gal that was locally injected with ASP (Angelica polysaccharide). Mechanistically, we isolated and cultured NSCs in vitro. ASP protected NSCs by increasing the cell proliferation; decreasing the number of SA-β-gal stained neurons; increasing the activity of SOD(superoxide dismutase) and T-AOC(total antioxidant capacity), decreasing the content of MDA(malondialdehyde); decreasing the levels of IL-1b,IL-6,TNF-a and ROS; and down-regulated the expression of cellular senescence associated genes p53, p21 in the aging NSCs. In conclusion, ASP can delay aging speed by protecting NSCs and promote neurogenesis by enhancing the antioxidant and anti-inflammatory capacity, up-regulation of p53/p21 signaling pathway. As to provide theoretical basis for treatment for brain aging related diseases, add new scientific connotation for “qi and blood theory” and “supplement blood and delay aging” of Traditional Chinese Medicine.

Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells

Background/Aims: Chinese angelica polysaccharide (CAP) is the main effective ingredient of angelica sinensis and exerts anti-inflammatory and anti-apoptotic effects on many diseases. This study aimed to explore the pharmacological potential of CAP on spinal cord injury (SCI). Methods: PC12 cells were pretreated by CAP and were subjected to LPS. Transfection was performed to alter the expression of COX-1. Cell viability and apoptotic cell rate were measured by CCK-8 and flow cytometry respectively. qRT-PCR and western blot analysis were performed to assess the expression changes of pro-inflammatory cytokines, apoptosis-related factor and core kinases in PI3K/AKT pathway. Results: LPS stimulation induced significant cell damage in PC12 cells as cell viability was repressed, apoptosis was induced and the expression levels of IL-1β, IL-6, IL-8, and TNF-α were increased. CAP pretreatment protected PC12 cells against LPS-induced cell damage. Meanwhile CAP treatment reduced the expression of COX-1 even in LPS-stimulated PC12 cells. More importantly, COX-1 overexpression abolished the protective effects of CAP on LPS-injured PC12 cells. Finally, Western blot analytical results showed that CAP activated PI3K/AKT pathway also in a COX-1-dependent manner. Conclusion: CAP exerted anti-apoptotic and anti-inflammatory effects on LPS-injured PC12 cells via down-regulation of COX-1.

Angelica polysaccharides inhibit the growth and promote the apoptosis of U251 glioma cells in vitro and in vivo

BackgroundAngelica sinensis (Oliv) Diels (Apiaceae) is a traditional medicine that has been used for more than 2000 years in China. It exhibits various therapeutic effects including neuroprotective, anti-oxidant, anti-inflammatory, and immunomodulatory activities. Angelica polysaccharides (APs), bioactive constituents of Angelica have been shown to be responsible for these effects; however, the utility of APs for the treatment of glioma and their mechanism of action remain to be elucidated. PurposeIn this study, we investigated the inhibitory effects of APs on a glioma cell line and their molecular mechanism of action. Study designU251 cells were utilized to confirm the effects of APs on glioma. MethodsThe human glioblastoma cell line U251 was utilized for both in vitro and in vivo models, in which we tested the effects of APs. Flow cytometry, gene expression analysis, western blotting, and MTT assays were used to elucidate the effects of APs on cell proliferation, cell cycle, and apoptosis. ResultsThe results demonstrated that APs significantly inhibited the growth and proliferation of U251 cells and induced their apoptosis. Furthermore, APs effectively reduced the expression of several cell cycle regulators: cyclins D1, B, and E. The apoptosis suppressor protein Bcl-2 was also downregulated, and the expression of pro-apoptotic proteins Bax and cleaved-caspase-3 increased. Additionally, APs inhibited the transforming growth factor (TGF)-β signaling pathway and stimulated the expression of E-cadherin, thus prohibiting cell growth. ConclusionIn conclusion, the results indicate that APs attenuate the tumorigenicity of glioma cells and promote their apoptosis by suppressing the TGF-β signaling pathway. The present study therefore provides evidence of the inhibitory effects of APs against glioma progression, and proposes their potential application as alternative therapeutic agents for glioma.

The antioxidative and hepatoprotective effects comparison of Chinese angelica polysaccharide(CAP)and selenizing CAP (sCAP) in CCl4 induced hepatic injury mice

Chinese angelica polysaccharides (CAP) and selenizing CAP (sCAP) were prepared and identified through FTIR and SEM observation. Their antioxidant activities in vitro and hepatoprotective effects in vivo were compared by free radical-scavenging tests or with CCl4-induced hepatic injury model mice. The results showed that for DPPH radical, superoxide anion and hydroxyl radical, the scavenging capabilities of sCAP were significantly stronger than those of CAP. In hepatic injury model mice, sCAP could significantly reduce ALT, AST and ALP contents and raised TP content in serum, significantly reduce MDA and ROS contents and raised SOD and T-AOC activities in liver homogenate in comparison with CAP; obviously relieve the pathological changes of liver and significantly inhibit the expressions of p-ERK, p-JNK and p-p38 protein as compared with those in model control group. These results indicate that selenylation modification can enhance the antioxidant and hepatoprotective actions of Chinese angelica polysaccharide. A action mechanism of sCAP is suppressing the protein expression of MAPK signaling pathway.

Inhibitory Effects of Angelica Polysaccharide on Activation of Mast Cells.

This study was designed to investigate the inhibitory effects of Angelica polysaccharide (AP) on activation of mast cells and its possible molecular mechanism. In our study, we determined the proinflammatory cytokines and allergic mediators in anti-DNP IgE stimulated RBL-2H3 cells and found that AP (50, 100, and 200 μg/mL) significantly decreased the release of histamine, β-hexosaminidase, leukotrienes C4 (LTC4), IL-1, IL-4, TNF-α, IL-6, and human monocyte chemotactic protein-1 (MCP-1/CCL2) (p < 0.05). In addition, Ca2+ entry was inhibited by treatment with AP. AP also downregulated the protein expressions of p-Fyn, p-Akt, p-P38, IL-4, TNF-α, and NF-κB p65 in both Fyn gene upregulated and normal RBL-2H3 cells (p < 0.05). Collectively, our results showed that AP could inhibit the activation of mast cells via suppressing the releases of proinflammatory cytokines allergic mediators, Gab2/PI3-K/Akt and Fyn/Syk pathways.

Effects of selenizing angelica polysaccharide and selenizing garlic polysaccharide on immune function of murine peritoneal macrophage.

The effects of two selenizing polysaccharides (sCAP2 and sGPS6) on immune function of murine peritoneal macrophages taking two non-selenizing polysaccharides (CAP and GPS) and modifier Na2SeO3 as control. In vitro test, the changes of selenizing polysaccharides, non-selenizing polysaccharides and Na2SeO3 on murine macrophages function were evaluated by phagocytosis and nitric oxide (NO) secretion tests. In vivo test, the mice were injected respectively with 0.2, 0.4 and 0.6 mg of sCAP2, sGPS6, CAP and GPS, or Na2SeO3 80 μg or normal saline 0.4 mL. The peritoneal macrophages were collected and cultured to determine the contents of TNF-α, IL-6 and IL-10 in supernatants by enzyme-linked immunosorbent assay. The results showed that sCAP2 and sGPS6 could significantly promote the phagocytosis and secretion of NO and three cytokines of macrophages in comparison with CAP and GPS. sCAP2 possessed the strongest activity. This indicates that selenylation modification can further improve the immune-enhancing activity of polysaccharide, and sCAP2 could be as a new immunopotentiator.