Astragaloside Ⅳ Protects Against Aβ1-42-induced Oxidative Stress, Neuroinflammation and Cognitive Impairment in Rats

Objective To investigate the neuroprotective action of astragaloside Ⅳ(AS-Ⅳ) on spatial learning and memory impairment induced by amyloid-beta 1-42(Aβ1-42) in rats and elucidate its underlying molecular mechanisms.Methods Adult-male Sprague-Dawley rats(230-250 g) were divided into six groups randomly: control, Aβ1-42, AS-Ⅳ, Aβ1-42 plus 5 mg/kg·d AS-Ⅳ, Aβ1-42 plus 25 mg/kg·d AS-Ⅳ, and Aβ1-42 plus 50 mg/kg·d AS-Ⅳ groups. Aβ1-42 were delivered by intracerebroventricular injection under the guidance of a brain stereotaxic apparatus. The Morris water maze test(hidden platform test, probe trials, visible platform test) was performed one week after Aβ1-42 injection to obtain the ability of rat spatial learning and memory. AS-Ⅳ(5, 25 and 50 mg/kg·d) was administrated intraperitoneally once per day from the 8 th day after Aβ1-42 injection for 5 consecutive days. Average escape latencies, distances for searching for the platform under water and the percentage of total time elapsed and distance swam in the right quadrant after removing platform were determined by behavior softwaresystem. The vision and swim speeds of rats were also determined to exclude the effect of these factors on the parameters of learning and memory. After behavioral tests, the rats were sacrificed immediately by decapitation. Hippocampus were collected. The enzyme activities of superoxide dismutase(SOD), glutathione peroxidase(GSH-px) and catalase(CAT) in the hippocampus obtained from different-treated rat brain were measured by following the manufacturer’s instructions. The levels of interleukin-1 beta(IL-1β) and tumor necrosis factor-alpha(TNF-α) in tissue lysates were assayed with ELISA.Results The water maze test results indicated that chronic treatments with AS-Ⅳ effectively protected the rats from Aβ1-42-induced spatial learning and memory impairment. Furthermore, the activities of SOD, GSH-px and CAT decreased by Aβ1-42 were also restored by AS-Ⅳ treatment in the hippocampus of rats. In addition, AS-Ⅳ significantly decreased the levels of IL-1β and TNF-α in the hippocampus of Aβ1-42-induced amnesia’s rats. Conclusion Our findings suggest that AS-Ⅳ might be a useful chemical in improving the spatial memory and relieving the oxidative stress and neuroinflammation in Alzheimer patients.

Astragaloside Ⅳ inhibits pathological functions of gastric cancer-associated fibroblasts

AIM To investigate the inhibitory effect of astragaloside IV on the pathological functions of cancer-associated fibroblasts,and to explore the underlying mechanism.METHODS Paired gastric normal fibroblast(GNF) and gastric cancer-associated fibroblast(GCAF) cultures were established from resected tissues. GCAFs were treated with vehicle control or different concentrations of astragaloside Ⅳ. Conditioned media were prepared from GNFs,GCAFs,control-treated GCAFs,and astragaloside Ⅳ-treated GCAFs,and used to culture BGC-823 human gastric cancer cells. Proliferation,migration and invasion capacities of BGC-823 cells were determined by MTT,wound healing,and Transwell invasion assays,respectively. The action mechanism of astragaloside Ⅳ was investigated by detecting the expression of micro RNAs and the expression and secretion of the oncogenic factor,macrophage colonystimulating factor(M-CSF),and the tumor suppressive factor,tissue inhibitor of metalloproteinase 2(TIMP2),in different groups of GCAFs. The expression of the oncogenic pluripotency factors SOX2 and NANOG in BGC-823 cells cultured with different conditioned media was also examined.RESULTS GCAFs displayed higher capacities to induce BGC-823 cell proliferation,migration,and invasion than GNFs(P < 0.01). Astragaloside Ⅳ treatment strongly inhibited the proliferation-,migration-and invasion-promoting capacities of GCAFs(P < 0.05 for 10 μmol/L,P < 0.01 for 20 μmol/L and 40 μmol/L). Compared with GNFs,GCAFs expressed a lower level of micro RNA-214(P < 0.01) and a higher level of micro RNA-301 a(P < 0.01). Astragaloside Ⅳ treatment significantly upregulated micro RNA-214 expression(P < 0.01) and down-regulated micro RNA-301 a expression(P < 0.01) in GCAFs. Reestablishing the micro RNA expression balance subsequently suppressed M-CSF production(P < 0.01) and secretion(P < 0.05),and elevated TIMP2 production(P < 0.01) and secretion(P < 0.05). Consequently,the ability of GCAFs to increase SOX2 and NANOG expression in BGC-823 cells was abolished by astragaloside Ⅳ.CONCLUSION Astragaloside Ⅳ can inhibit the pathological functions of GCAFs by correcting their dysregulation of micro RNA expression,and it is promisingly a potent therapeutic agent regulating tumor microenvironment.

Effect of astragaloside Ⅳ on lipid and glucose metabolism in acute myocardial infarction through PPARγ pathway

OBJECTIVE To investigate the effects of astragaloside IV(which can be extracted from the traditional Chinese medicine Astragalus membranaceus)on lipid and glucose metabolism in acute myocardial infarction(AMI).METHODS Model of heart failure(HF)after AMI was established with ligation of left anterior descending artery on Sprague-Dawley(SD)rats.The rats were divided into three groups:sham,model and astragaloside IV treatment group.Twenty-eight days after treatment(astragaloside IV,20 mg·kg-1 daily),hematoxylin-eosin(HE)staining was applied to visualize cardiomyocyte morphological changes.High performance liquid chromatography(HPLC)was performed to assess the contents of adenosine phosphates in heart.Positron emission tomography and computed tomography(PET-CT)was conducted to evaluate the cardiac glucose metabolism.Expressions of key molecules such as peroxisome proliferatoractivated receptor γ(PPARγ),sterol carrier protein 2(SCP2)and long chain acyl CoA dehydrogenase(ACADL)were measured by Western blotting and immunohistochemistry.Oxygen-glucose deprivation-reperfusion(OGD/R)-induced H9C2 injury cardiomyocyte model was adopted for potential mechanism research in vitro.RESULTS Treatment with astragaloside Ⅳ rescued hearts from structural and functional damages as well as inflammatory infiltration.Levels of adenosine triphosphate(ATP)and energy charge(EC)in astragaloside IV group were also up-regulated compared to model group.Further results demonstrated that critical enzymes both in lipid metabolism and glucose metabolism compro mised in model group compared to sham group.Intriguingly,astragalosideⅣcould up-regulate critical enzymes including ACADL and SCP2 in lipid metabolism accompanying with promoting effect on molecules in glycolysis simultaneously.Results on upstreaming signaling pathway demonstrated that astragaloside Ⅳ could dramatically increase the expres sions of PPARγ.In vitro study suggested the efficacy of astragalosideⅣcould be blocked by T0070907,a selective PPARγ inhibitor.CONCLUSION Astragaloside IV has cardioprotective effect in improving cardiac function and energy metabolism through regulating lipid and glucose metabolism.The effects may be mediated by PPARγ pathway.

The mechanism of astragaloside Ⅳ promoting sciatic nerve regeneration

3-O-beta-D-xylopyranosyl-6-O-beta-D-glucopyranosyl-cycloastragenol （astragaloside IV）, the main active component of the traditional Chinese medicine astragalus membranaceus, has been shown to be neuroprotective. This study investigated whether astragaloside IV could promote the repair of injured sciatic nerve. Denervated sciatic nerve of mice was subjected to anastomosis. The mice were intraperitoneally injected with 10, 5, 2.5 mg/kg astragaloside IV per day for 8 consecutive days Western blot assay and real-time PCR results demonstrated that growth-associated protein-43 ex- pression was upregulated in mouse spinal cord segments L4-6 after intervention with 10, 5, 2.5 mg/kg astragaloside IV per day in a dose-dependent manner. Luxol fast blue staining and elec- trophysiological detection suggested that astragaloside IV elevated the number and diameter of myelinated nerve fibers, and simultaneously increased motor nerve conduction velocity and action potential amplitude in the sciatic nerve of mice. These results indicated that astragaloside IV con- tributed to sciatic nerve regeneration and functional recovery in mice. The mechanism underlying this effect may be associated with the upregulation of growth-associated protein-43 expression.

Content Determination of Astragaloside Ⅳ in Astragalus from Three Different Regions by HPLC

[Objectives] The content of astragaloside in Astragalus membranaceus(Fisch.) Bge.var.mongholicus(Bge.) Hisao from three different regions was determined.[Methods] Referring to the method recorded in the Chinese Pharmacopoeia(2015 edition),the content of astragaloside IV in A.membranaceus was determined by HPLC.[Results] There were great differences in the astragaloside IV content of A.membranaceus among different regions.The content of astragaloside IV in A.membranaceus cultivated in Inner Mongolia was highest(0.155%),followed by that(0.143%) in A.membranaceus cultivated in Gansu,and the content of astragaloside IV in A.membranaceus cultivated in Shanxi was lowest(0.080%).The contents of astragaloside IV in A.membranaceus from different regions were all in line with the standard(not less than 0.040%) of Chinese Pharmacopoeia(2015 edition).[Conclusions]The content of astragaloside IV in A.membranaceus cultivated in three different regions met the medicinal standards.

An updated role of astragaloside Ⅳ in heart failure

Heart failure has become a global public health problem that seriously threatens human health.Due to "multi-target" effect,traditional Chinese medicine has unique advantages in the treat.ment of heart failure.Astragaloside Ⅳ is one of the main active ingredients of astragalus membrana.ceus.It has the functions of protecting the heart and neovascularization,anti-inflammation,anti-oxida.tion,regulating energy metabolism,neuroprotection and anti-cancer effects.This article reviews the recent progresses of astragaloside Ⅳ in the treatment of heart failure.Data show that astragaloside Ⅳ can inhibit heart fibrosis,attenuate excessively activation of renin-angiotensin system,increase energy metabolism,promote positive inotropic action,inhibit myocardial cell apoptosis,etc,which are all involved in the protective role of astragalosideⅣ in rodents or cellular models of heart failure.Astragalo.side Ⅳ may be a potential active ingredient in traditional Chinese medicine for the treatment of heart failure.

Angiogenesis function of astragaloside Ⅳ in rats with myocardial infarction via PKD1-HDAC5-VEGF pathway

OBJECTⅣE This study aimed to investigate the role and mechanism of Astragaloside Ⅳ(AS-Ⅳ) in rats with myocardial infarction.METHODS The myocardial infarction model was established by ligation of the left anterior descending artery.The rats were randomly divided into sham,DMSO,model group,AS-Ⅳ and CID755673 groups.The rats were sacrificed 4 weeks later,and segmental heart samples were used for hematoxylin and eosin staining and masson staining.The expression of PKD1,HDAC5 and VEGF were analyzed using immunohistochemistry,reverse transcription poly.merase chain reaction and western blot.RESULTS Compared with the sham operation and DMSO groups,morphology of myocardium in model group was disordered,accompanied with necrotic myocar.dial cells and obvious collagen tissues.After treatment with AS-Ⅳ,the morphology of myocardium was obviously improved,and the number of new blood vessels increased significantly.However,after treatment with CID755673,the myocardial tissue of rats became disordered again,the necrotic cells increased,and some vessels closed.The expression levels of PKD1,HDAC5 and VEGF mRNA and protein in myocardial tissue of model group were significantly lower than the other four groups(P<0.05),whereas these levels in the AS-Ⅳ group were significantly higher than those in the other four groups(P<0.01).Additionally,the CID755673 group had significantly higher levels of PKD1,HDAC5 and VEGF mRNA and protein than the sham group,DMSO group and model group(P<0.05).CONCLUSION AS-Ⅳ may partly promote the angiogenesis of myocardial tissue in rats with myocardial infarction via the PKD1-HDAC5-VEGF pathway.

Study on mechanism of astragaloside Ⅳ in treatment of pulmonary fibrosis with epithelial-mesenchymal transition

OBJECTIVE Currently discussing the clinical treatment of pulmonary fibrosis commonly used drugs astragalus main active ingredient astragalosideⅣ(ASTⅣ) in vitro after transforming growth factor-β1 induced lung adenocarcinoma A549 epithelial cells after epithelial cell interstitial EpithelialMesenchymal Transition(EMT).METHODS The effect of astragalosideIV on the proliferation of A549 cells was detected by MTT assay for the first time.No significant effect of astragaloside on the prolifera.tion of A549 cells was found in the range of 1.25-20 μmol/L.A549 cells in vitro were divided into 5 groups:normal group,control group,low,medium and high experimental groups,which were treated for 72 hours,and the morphological changes of cells in each group were observed by light microscope.Real-time quantitative PCR(qPCR) and Western blotting were performed.Detection of gene and protein expression levels.RESULTS The results of real-time fluorescence quantitative PCR showed that the quantitative analysis of high-dose astragalosideⅣ in the experimental group was lower than that of the control group in the α-SMA analysis,and the difference was statistically significant(P<0.05).The dose of Astragaloside Ⅳ in the experimental group was higher than that of the control group in the E-Cad analysis,and the difference was statistically significant(P<0.05).Western Blot results showed that the expression of α-SMA antibody in the high-dose and low-dose experimental group was lower than that in the control group,the difference was statistically significant(P<0.05).The high-dose experimental group had a significantly higher expression of E-Cad antibody than the control group,the difference was statistically significant(P<0.01).CONCLUSION This study uses A549 epithelial cells as a model,A549 cells were modeled and confirmed that Astragaloside can effectively inhibit TGF-β1-induced epithelialmesenchymal transition(EMT) and provide a new basis for the treatment of pulmonary fibrosis.

Review of the pharmacological effects of astragalosideⅣand its autophagic mechanism in association with inflammation

Astragalus membranaceus Bunge,known as Huangqi,has been used to treat various diseases for a long time.AstragalosideⅣ(AS-Ⅳ)is one of the primary active ingredients of the aqueous Huangqi extract.Many experimental models have shown that AS-Ⅳexerts broad beneficial effects on cardiovascular disease,nervous system diseases,lung disease,diabetes,organ injury,kidney disease,and gynaecological diseases.This review demonstrates and summarizes the structure,solubility,pharmacokinetics,toxicity,pharmacological effects,and autophagic mechanism of AS-Ⅳ.The autophagic effects are associated with multiple signalling pathways in experimental models,including the PI3KI/Akt/m TOR,PI3KⅢ/Beclin-1/Bcl-2,PI3K/Akt,AMPK/m TOR,PI3K/Akt/m TOR,SIRT1–NF-κB,PI3K/AKT/AS160,and TGF-β/Smad signalling pathways.Based on this evidence,AS-Ⅳcould be used as a replacement therapy for treating the multiple diseases referenced above.

Astragaloside Ⅳ suppresses post-ischemic natural killer cell infiltration and activation in the brain:involvement of histone deacetylase inhibition

Natural killer(NK)cells,a type of cytotoxic lymphocytes,can infiltrate into ischemic brain and exacerbate neuronal cell death.Astragaloside Ⅳ(ASIV)is the major bioactive ingredient of Astragalus membranaceus,a Chinese herbal medicine,and possesses potent immunomodulatory and neuroprotective properties.This study investigated the effects of ASIV on post-ischemic brain infiltration and activation of NK cells.ASIV reduced brain infarction and alleviated functional deficits in MCAO rats,and these beneficial effects persisted for at least 7 days.Abundant NK cells infiltrated into the ischemic hemisphere on day 1 after brain ischemia,and this infiltration was suppressed by ASIV.Strikingly,ASIV reversed NK cell deficiency in the spleen and blood after brain ischemia.ASIV inhibited astrocyte-derived CCL2 upregulation and reduced CCR2+NK cell levels in the ischemic brain.Meanwhile,ASIV attenuated NK cell activating receptor NKG2D levels and reduced interferon-γproduction.ASIV restored acetylation of histone H3 and the p65 subunit of nuclear factor-κB in the ischemic brain,suggesting inhibition of histone deacetylase(HDAC).Simultaneously,ASIV prevented p65 nuclear translocation.The effects of ASIV on reducing CCL2 production,restoring acetylated p65 levels and preventing p65 nuclear translocation were mimicked by valproate,an HDAC inhibitor,in astrocytes subjected to oxygen-glucose deprivation.Our findings suggest that ASIV inhibits post-ischemic NK cell brain infiltration and activation and reverses NK cell deficiency in the periphery,which together contribute to the beneficial effects of ASIV against brain ischemia.Furthermore,ASIV’s effects on suppressing NK cell brain infiltration and activation may involve HDAC inhibition.

Effects of Astragaloside Ⅳ Derivative on Heart Failure in Rats

Objective Astragaloside Ⅳ derivative(ASId) is one of Astragaloside Ⅳ(ASI) derivatives with higher water-solubility and may have more druggability than ASI.The present study aims at observing the effects of ASId on cardiovascular parameters in chronic heart failure in rats.Methods Using echocardiographic and haemodynamic measurements,the effects of ASId on congestive heart failure(CHF) induced by ligation of the left coronary artery in rats were investigated.Results ASId iv 0.5,1.0,and 2.0 mg/(kg·d) attenuated the decline of ejection fraction.The peak derivatives of the left ventricle(LV) pressure(dp/dt) in ASId treated groups were significantly increased.Both LV volumes in diastole and in systole were decreased significantly after ASId treatment,accompanied with a trend towards normalization of relative wall thickness at end-systole.ASId 0.5,1.0,and 2.0 mg/(kg·d) attenuated the increase of LV systolic and diastolic wall stress.ASId treatment also inhibited compensatory hypertrophy of depressed heart.Conclusion ASId could improve cardiac functions and inhibite compensatory hypertrophy and LV remodelling,which suggests the possibility of ASId as a new therapeutic drug for the treatment of CHF.

Anti-inflammatory and DNA Repair Effects of Astragaloside IV on PC12 Cells Damaged by Lipopolysaccharide

Objective This study aimed to establish a neural cell injury model in vitro by stimulating PC12 cells with lipopolysaccharide(LPS)and to examine the effects of astragaloside IV on key targets using high-throughput sequence technology and bioinformatics analyses.Methods PC12 cells in the logarithmic growth phase were treated with LPS at final concentrations of 0.25,0.5,0.75,1,and 1.25 mg/mL for 24 h.Cell morphology was evaluated,and cell survival rates were calculated.A neurocyte inflammatory model was established with LPS treatment,which reached a 50%cell survival rate.PC12 cells were treated with 0.01,0.1,1,10,or 100µmol/L astragaloside IV for 24 h.The concentration of astragaloside IV that did not affect the cell survival rate was selected as the treatment group for subsequent experiments.NOS activity was detected by colorimetry;the expression levels of ERCC2,XRCC4,XRCC2,TNF-α,IL-1β,TLR4,NOS and COX-2 mRNA and protein were detected by RT-qPCR and Western blotting.The differentially expressed genes(DEGs)between the groups were screened using a second-generation sequence(fold change>2,P<0.05)with the following KEGG enrichment analysis,RT-qPCR and Western blotting were used to detect the mRNA and protein expression of DEGs related to the IL-17 pathway in different groups of PC12 cells.Results The viability of PC12 cells was not altered by treatment with 0.01,0.1,or 1µmol/L astragaloside IV for 24 h(P>0.05).However,after treatment with 0.5,0.75,1,or 1.25 mg/mL LPS for 24 h,the viability steadily decreased(P<0.01).The mRNA and protein expression levels of ERCC2,XRCC4,XRCC2,TNF-α,IL-1β,TLR4,NOS,and COX-2 were significantly increased after PC12 cells were treated with 1 mg/mL LPS for 24 h(P<0.01);however,these changes were reversed when PC12 cells were pretreated with 0.01,0.1,or 1µmol/L astragaloside IV in PC12 cells and then treated with 1 mg/mL LPS for 24 h(P<0.05).Second-generation sequencing revealed that 1026 genes were upregulated,while 1287 genes were downregulated.The DEGs were associated with autophagy,TNF-α,interleukin-17,MAPK,P53,Toll-like receptor,and NOD-like receptor signaling pathways.Furthermore,PC12 cells treated with a 1 mg/mL LPS for 24 h exhibited increased mRNA and protein expression of CCL2,CCL11,CCL7,MMP3,and MMP10,which are associated with the IL-17 pathway.RT-qPCR and Western blotting analyses confirmed that the DEGs listed above corresponded to the sequence assay results.Conclusion LPS can damage PC12 cells and cause inflammatory reactions in nerve cells and DNA damage.astragaloside IV plays an anti-inflammatory and DNA damage protective role and inhibits the IL-17 signaling pathway to exert a neuroprotective effect in vitro.

Effect of astragaloside Ⅳ on the immunoregulatory function of adipose-derived mesenchymal stem cells from patients with psoriasis vulgaris

OBJECTⅣE:To compare the phenotype and adipogenic and osteogenic differentiation capacities of adiposederived mesenchymal stem cells(AMSCs)isolated from patients with psoriasis vulgaris and healthy donors,and to explore the effects of astragalosideⅣ,a Traditional Chinese Medicine,on the immunoregulatory function of AMSCs.METHODS:AMSCs were isolated from human adipose tissue and cultured for three generations in vitro.Cell phenotype and cell cycle analysis were performed by flow cytometry.Adipogenic and osteogenic differentiation of AMSCs was examined by lipid(oil red O)and alkaline phosphatase staining,respectively.Expression of inflammatory mediators was examined by real-time quantitative polymerase chain reaction analysis,and proliferation was quantified using the cell counting kit-8 assay.RESULTS:Expression of CD29,CD44,and CD73 was higher in AMSCs from healthy donors than psoriasis patients,while the reverse was true for expression of CD45,CD31,and HLA-DR.AMSCs from psoriasis patients had a greater ability to undergo adipogenic differentiation than cells from healthy donors,whereas there was no significant difference in osteogenic differentiation between AMSCs from the two sources.Compared with AMSCs from healthy donors,psoriasis patient-derived AMSCs expressed lower levels of the anti-inflammatory cytokines interleukin-10 and transforming growth factor-β(TGF-β)and the immune checkpoint ligand programmed cell death 1 ligand 1(PDL1)(P<0.05)and higher levels of the pro-inflammatory cytokines tumor necrosis factor-α(TNF-α)and interferon-γ(IFN-γ).Incubation of AMSCs from psoriasis patients with astragalosideⅣhad no significant effect on proliferation but increased the expression of TGF-βand PDL1 and decreased the expression of IFN-γand TNF-α.CONCLUSION:AMSCs from patients with psoriasis vulgaris display abnormal proliferation and adipogenesis and an enhanced pro-inflammatory phenotype.These defects were normalized by treatment with astragalosideⅣ,suggesting that this Traditional Chinese Medicine may be useful for restoring the immunoregulatory function of AMSCs and immune homeostasis in patients with psoriasis vulgaris.

Astragaloside Ⅳ for Heart Failure: Preclinical Evidence and Possible Mechanisms, A Systematic Review and Meta-Analysis

Objective:To explore the cardioprotective effects of astragaloside Ⅳ(AS-Ⅳ) in heart failure(HF).Methods:PubMed,Excerpta Medica Database(EMBASE),Cochrane Library,Web of Science,Wanfang Database,Chinese Bio-medical Literature and Retrieval System(SinoMed),China Science and Technology Journal Database(VIP),and China National Knowledge Infrastructure(CNKI) were searched from inception to November 1,2021for animal experiments to explore AS-Ⅳ in treating HF in rats or mice. The left ventricular ejection fraction(LVEF),left ventricular fractional shortening(LVFS),left ventricular end-diastolic dimension(LVEDD),left ventricular endsystolic dimension(LVESD),left ventricular weight-to-body weight(LVW/BW) and B-type brain natriuretic peptide(BNP) were recorded.The qualities of included studies were assessed by the risk of bias according to the Cochrane handbook.Meta-analysis was performed using Stata 13.0.Results:Twenty-one articles involving 558 animals were considered.Compared with the control group,AS-Ⅳ improved cardiac function,specifically by increasing LVEF(mean difference(MD)=6.97,95% confidence interval(CI)=5.92 to 8.03,P<0.05;fixed effects model) and LVFS(MD=7.01,95% CI=5.84 to 8.81,P<0.05;fixed effects model),and decreasing LVEDD(MD=-4.24,95% CI=-4.74to-3.76,P<0.05;random effects model) and LVESD(MD-4.18,95% CI=-5.26 to-3.10,P<0.05;fixed effects model).In addition,the BNP and LVW/BW levels were decreased in the AS-Ⅳ treatment group(MD=-9.18,95%CI=-14.13 to-4.22,P<0.05;random effects model;MD=-1.91,95% CI=-2.42 to-1.39,P<0.05;random effects model).Conclusions:AS-Ⅳ is a promising therapeutic agent for HF.However,this conclusion needs to be clinically validated in the future.

Determination of Astragaloside IV in Yupingfeng Oral Solution by HPLC-ELSD Method

[Objective] This study aimed to establish a method for determining the content of Astragaloside IV in Yupingfeng oral solution.[Method] The HPLC-ELSD method was adopted.The chromatographic column was Venusil MP（4.6 mm × 150 mm,5 μm）.The mobile phase was acetonitrile-water（35∶65）.The ELSD evaporator tube temperature was 65 ℃.N2 was used as the carrier gas（pressure,30 psi）.[Result] When the content of Astragaloside IV ranged from 0.5 to 5.0 μg,the Astragaloside IV content showed a good linear relationship with peak area（r=0.999,n=6）.The average recovery was 96.36%,and the RSD was 2.46%.[Conclusion] This method is accurate and reliable,and can be applied in the quality control of Yupingfeng oral solution.

Astragaloside 对实验性自身免疫性脑脊髓炎小鼠的防治作用研究

目的:探讨Astragaloside对实验性自身免疫性脑脊髓炎(EAE)小鼠的保护作用及机制。方法:采用髓鞘MOG 35-55诱导C57BL/6雌性小鼠建立EAE模型,随机分为EAE对照组、Astragaloside高、低剂量组。造模的第3天起,采用腹腔注射给药,持续25 d。EAE对照组给予PBS;Astragaloside高、低剂量组分别给予Astragaloside溶液30 mg/(kg·d),15 mg/(kg·d);各组小鼠给药0.2 ml/(次·只),每天记录小鼠症状、体征、体重变化和临床评分。HE染色检测脊髓炎细胞浸润。ELISA法检测外周血中IL-1β、IL-17、TNF-α、IL-10的表达量。Western blot法检测脊髓组织中ROCKⅡ、P-MYPT1、p-NF-κB/p65的表达变化。结果:与EAE对照组比较,Astragaloside高、低剂量组均可明显降低平均最高临床评分,减轻EAE临床症状(P<0.01,P<0.05),高剂量组治疗效果优于低剂量组;Astragaloside可抑制中枢神经系统炎症细胞浸润,显著降低血清中IL-1β、IL-17的表达(P<0.05,P<0.001),增加血清IL-10水平(P<0.05),明显抑制ROCKⅡ、P-MYPT1、p-NF-κB/p65的表达(P<0.05)。结论:Astragaloside可通过抑制Rock通路和调节细胞因子的表达改善EAE的临床症状。

CroweⅢ-Ⅳ型DDH患者全髋关节置换术后不满意及相关因素分析

目的:探讨全髋关节置换术的CroweⅢ-Ⅳ型发育性髋关节发育不良(developmental dysplasia of the hip,DDH)患者的满意度及造成不满意的相关因素。方法:回顾性分析2013年3月至2018年3月行全髋关节置换术的169例CroweⅢ-Ⅳ型DDH患者,通过微信进行调查问卷,调查患者对手术总体满意度、10项日常功能满意度和患者认为对自己日常生活影响比较大的前5个问题。手术前后采用髋关节Harris评分进行功能评价。结果:收到完整调查问卷145份,所有患者获随访,时间1~5(3.23±1.22)年。145例患者分成两组,其中对手术疗效满意的118例,不满意的27例,手术总体满意率81.38%(118/145)。患者认为对生活影响比较大的前5个问题分别是术后髋部疼痛,肢体明显不等长、行走、上下楼梯、蹲起。两组术前Harris评分比较,差异无统计学意义(P>0.05),不满意组术后Harris评分较低。术后髋关节疼痛、肢体不等长是影响手术不满意的直接因素。结论:采用全髋关节置换术治疗CroweⅢ-Ⅳ型DDH患者手术难度大;术后髋关节疼痛(轻度以上),肢体不等长(>2 cm)是术后不满意的独立危险因素。

辽宁第Ⅳ金刚石成矿带东部潘家沟辉绿岩中铬铁矿的矿物化学特征及其意义

辽宁省永宁地区因发现原生金刚石而被划分为辽宁第Ⅳ金刚石成矿带,但尚未厘定出金刚石的来源,有必要加强对与金刚石伴生的指示矿物的研究。对该成矿带东部潘家沟地区辉绿岩中选获的铬铁矿开展电子探针成分分析,并与辽宁典型金伯利岩管中的铬铁矿成分进行对比,以探讨该地区铬铁矿的成因及其与金刚石的关系。根据铬铁矿样品电子探针背散射图像显示的粒径、形态及熔蚀特征,以及铬铁矿电子探针成分测试显示的高Cr、富Mg、低Al及贫Ti的特征,推测该地区的铬铁矿来自地幔捕掳晶,属于镁铬铁矿亚类,主要为镁铁-铬铝铁亚种和镁铁-铬铝亚种。计算得到铬铁矿的形成温度为1 252~1 307℃,与前人报道的瓦房店典型金伯利岩中铬铁矿的形成温度基本一致,也接近金刚石的形成温度,表明潘家沟地区辉绿岩中铬铁矿的成因与金刚石关系密切,该地区具有良好的金刚石成矿潜力和找矿前景。研究成果对潘家沟地区金刚石原生矿的勘查及探明该地区金刚石的来源具有指导意义。

腹腔镜下侧腹壁悬吊术与阴道后壁修补术联合治疗POP-QⅢ或Ⅳ期盆腔器官脱垂的效果分析

目的:探究腹腔镜下侧腹壁悬吊术联合阴道后壁修补术在盆腔器官脱垂定量分期法(POP-Q)Ⅲ或Ⅳ期盆腔器官脱垂患者中的应用效果。方法:选择2021年2月—2023年6月厦门市第三医院收治的90例POP-QⅢ或Ⅳ期盆腔器官脱垂患者,根据随机数字表法分为对照组和观察组,各45例。对照组进行阴式子宫切除术联合阴道前后壁修补术治疗,观察组则进行腹腔镜下侧腹壁悬吊术联合阴道后壁修补术治疗。比较两组的治疗总有效率、手术指标(手术时间、术中出血量、排气时间、住院时间)、并发症发生率、手术前后的盆底相关参数[阴道总长度(TVL)、阴道前壁中线离处女膜缘3 cm处(Aa)、前穹隆或阴道顶端到Aa点之间阴道前壁上段中距离处女膜的最远点(Ba)及宫颈或子宫切除后阴道顶端所处的最远端(C)]及盆底功能障碍问卷(PFDI-20)评分。结果:观察组治疗总有效率高于对照组,手术指标均优于对照组,并发症发生率显著低于对照组,差异均有统计学意义(P<0.05)。术后6个月,观察组盆底相关参数及PFDI-20各项评分均显著低于对照组,差异均有统计学意义(P<0.05)。结论:腹腔镜下侧腹壁悬吊术联合阴道后壁修补术在POP-QⅢ或Ⅳ期盆腔器官脱垂患者中的应用效果更好,可显著改善患者的盆底相关参数及盆底功能,且安全性较高。

二肽基肽酶-Ⅳ有机小分子荧光探针的研究进展

二肽基肽酶-IV(DPP-IV)是一种重要的跨膜糖蛋白水解酶,与各种生理过程和疾病密切相关,检测DPP-IV的有机小分子荧光探针被相继报道,是当前研究生物酶检测的热点。首次综述了用于DPP-IV体外和体内检测及成像的3类有机小分子荧光探针,分别是非近红外荧光探针(λ_(em)<650nm)、近红外荧光探针(λ_(em)>650nm)和双光子荧光探针,对比并总结了三种探针的设计原理、结构特点、生物应用情况及其在DPP-IV相关疾病诊断中的应用,并探讨了DPP-IV活性检测在未来发展方向上所面临的挑战。