Puerarin mediated miR-30b-5p targeting fibroblast activation protein against oral submucous fibrosis

Background:Puerarin(Pue)has been reported to be a natural active ingredient with multiple antifibrotic properties.This work aimed at exploring the function of Pue in oral submucousfibrosis(OSF)treatment.Methods:Human oral mucosafibroblasts(hOMF)were induced with transforming growth factor beta1(TGF-β1)and intervened with Pue.Expressions offibrosis-related markers were analyzed by Western blot and IF staining.Cell viability was characterized by the CCK-8 assay.Expressions of miR-30 family members were quantified by qRT-PCR.The correlation betweenfibroblast activation protein(FAP)and miR-30 family expression was evaluated by the Pearson correlation coefficient.Bioinformatics prediction and dual-luciferase reporter assay were employed to verify the regulation between FAP and miR-30b-5p.The specific mechanism of Pue on OSF was explored through the promotion or inhibition of miR-30b-5p.Results:After induction by TGF-β1,hOMF showed upregulated Collagen I,Collagen III,and FAP expressions,while miR-30 family expression was downregulated with miR-30b-5p being the most significant.Pue intervention inhibited the excessive proliferation of TGF-β1-induced hOMF,downregulated FAP,collagen type 3(COL3A1),collagen type 1(COL1A1),matrix metalloproteinase 1(MMP1),and matrix metalloproteinase 3(MMP3)expressions,and restored miR-30 family expression.Bioinformatics prediction and dual-luciferase reporter assay revealed that miR-30b-5p selectively inhibited FAP expression.Mechanistically,miR-30b-5p mimic suppressed the excessive proliferation of TGF-β1-induced hOMF and declinedfibrosis levels.Pue intervention significantly reversed the promotion of TGF-β1-induced OSF by miR-30b-5p inhibition.Conclusion:Pue mediated miR-30b-5p targeting FAP against OSF,which provided a theoretical basis for the pathogenesis research and Pue application in OSF.

Puerarin modulation of CENPA affects downstream PLK1 and CCNB1 expression to inhibit bladder cancer cell proliferation

Background:The treatment alternatives for bladder cancer(BLCA),the 10th most prevalent cancer in the world,need to be further investigated,and many active substances like Puerarin in herbal medicine were found to be effective in treating BLCA.The purpose of this study was to investigate the potential treating mechanisms of Puerarin on BLCA.Methods:The cell counting kit 8 assay and flow cytometry were performed to confirm Puerarin’s ability to suppress BLCA.The differentially expressed proteins(DEPs)were obtained by Tandem Mass Tags technology and functional enrichment analysis performed by R studio.The most enriched pathways were selected for study and the DEPs were screened out.Protein-protein interaction network maps were created using String and Cytoscape and key proteins,which will be analyzed for survival,expression,and upstream transcription factor prediction,were screened out using the cytoHubba plugin.CHEA3 was used to obtain upstream transcription factor validated by molecular docking and western blotting experiments.Results:Cell counting kit 8 showed that Puerarin inhibited BLCA cells,with 50%inhibitory concentration of 218μmol/L in T24 and 198μmol/L in 5637.Flow cytometry reveals that Puerarin blocks T24 and 5637 cells in G1 phase.1,385 DEPs were obtained and the enrichment analysis revealed that cell cycle and DNA replication were the two main areas in which DEPs were enriched.Cyclin-B-cyclin dependent kinase 1(CDK1),cyclin B1(CCNB1),and polo-like kinase 1(PLK1)were identified as key proteins,and their upstream transcription factor was predicted to be centromere protein A(CENPA).Puerarin’s binding energy to CENPA was determined by molecular docking to be−6.3 kcal/mol,indicating a strong binding interaction.Western blot showed that Puerarin significantly reduced the expression of CENPA.Conclusion:We hypothesize that Puerarin may inhibit the proliferation of bladder cancer cells by inhibiting CENPA expression to regulate PLK1 and CCNB1 expression,thereby affecting cell cycle.

Puerarin alleviates sleep disorders in aged mice related to repairing intestinal mucosal barrier

More and more evidence suggests that puerarin,a potential remedy for gut inflammation,may have an ameliorative effect on sleep disturbances.However,the relationship between puerarin and sleep disruption has not been extensively researched.This study aims to explore the role and mechanisms of puerarin in improving sleep disorders.We established a light-induced sleep disorder model in mice and assessed the effects of puerarin on cognitive behavior using open field and water maze tests.Pathological detection demonstrated that sleep disturbances resulted in observable damage to the liver,lung,and kidney.Puerarin reversed multi-organ damage and inflammation.Further,puerarin activated paneth cells,resulting in increased lysozyme and TGF-βproduction,and stimulating intestinal stem cell proliferation.Puerarin also effectively inhibited the expression of F4/80,iNOS,TNF-α,and IL-1βin the small intestine,while it increased Chil3,CD206,and Arg-1 levels.Moreover,puerarin treatment significantly decreased P-P65,TLR4,Bcl-xl,and cleaved caspase-3 protein levels while increasing barrier protein levels,including ZO-1,Occludin,Claudin 1 and E-cadherin suggesting a reduction in inflammation and apoptosis in the gut.Overall,puerarin diminished systemic inflammation,particularly intestinal inflammation,and enhanced intestinal barrier integrity in mice with sleep disorders.Our findings suggest a potential new therapeutic pathway for sleep disorders.

Effect of puerarin on inflammation and alveolar bone resorption in experimental rats with periodontitis

Objective:To investigate the effect of puerarin on inflammation and alveolar bone resorption in rats with experimental periodontitis.Methods:Thirty-six 7-week-old Sprague-Dawley rats were randomly divided into three groups(n=12).Twelve rats as the control group and the remaining rats were to establish a chronic periodontitis model ligated with orthodontic ligature wire on the cervical part of the left maxillary first molar under general anesthesia.All three groups were administered by gavage for 14 days:equal amounts of saline were given to the control and periodontitis groups,and 400 mg/kg concentration of puerarin was given to the puerarin group.All rats were anesthetized after 24 h of the last administration,blood was collected from the abdominal aorta,and the serum was centrifuged for the detection of IL-4,IL-10,IL-6,and IFN-γin peripheral blood,then all rats were executed,some rats separated from the left maxilla,fresh gingival tissue removed from the buccal-palatal side of the left maxillary first molar,and the remaining maxillary bone tissue used for the detection of Micro-CT;some rats subjected to the left maxillary bone specimens taken with the gingival tissues,used for HE staining detection.Results:HE staining showed that inflammatory cell infiltration was significantly reduced in the puerarin group compared to the periodontitis group.ELISA analysis showed that puerarin promoted IL-4 and IL-10 expression and decreased IL-6 and IFN-γexpression levels in serum(P<0.05).Micro-CT showed that puerarin significantly reduced alveolar bone resorption compared to the periodontitis group(P<0.05).Conclusion:Puerarin may inhibit inflammation and alveolar bone resorption in experimental periodontitis rats.

Two new C-glucofuranosyl isoflavones in puerarin injection

Two new C-glucofuranosyl isoflavones of impurities in puerarin injection were isolated. Their structures were detemained to be 8-C-α-glucofuranosyl-7, 4P-dihydroxyisoflavone and 8-C-β-glucofuranosyl-7, 4＇-dihydroxy- isoflavone by chemical and spectral analysis.

Puerarin逆转K562/AO2耐药的分子机制

目的:研究黄酮类化合物puerarin对K562/AO2(人红白血病多药耐药细胞系)细胞耐药逆转作用的分子机制。方法:免疫荧光染色方法检测阿霉素(ADR)和puerarin对K562(人红白血病细胞系)和K562/AO2两种细胞NF-κB活性的影响;免疫细胞化学染色方法检测ADR和puerarin对K562和K562/AO2的survivin表达的影响;流式细胞仪检测ADR和puerarin对K562和K562/AO2的p-gp表达的影响。结果:经ADR处理后的K562细胞和K562/AO2细胞NF-κB的活性明显高于K562细胞空白对照组;经puerarin预处理后再加ADR处理的K562细胞中的NF-κB的活性明显低于只用ADR处理的K562细胞。经puerarin干预后的K562/AO2细胞的NF-κB的活性明显低于未经puerarin干预的K562/AO2细胞;经ADR处理后的K562细胞和K562/AO2细胞的p-gp,survivin表达明显高于K562细胞空白对照组;经puerarin预处理后再加ADR处理的K562细胞中的p-gp,survivin表达明显低于未经pu-erarin预处理的K562细胞;经puerarin干预后的K562/AO2细胞的p-gp,survivin表达明显低于未经puer-arin干预的K562/AO2细胞。p-gp和survivin表达呈正相关。结论:NF-κB的活化使p-gp和survivin表达增多可能是K562细胞多药耐药形成的机制之一。Puerarin能预防和阻止K562细胞耐药形成,并能逆转K562/AO2对ADR的耐药,其机制与抑制NF-κB活性及survivin和p-gp的表达有关。

Inhibition of Excitatory Amino Acid Efflux Contributes to Protective Effects of Puerarin Against Cerebral Ischemia in Rats

To investigate whether the protective effects of puerarine （Pur） against cerebral ischemia is associated with depressing the extracellular levels of amino acid transmitters in brain of rats. Methods Male Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion （MCAO） for 60 min followed by 24 h reperfusion. Put （50, 100 mg/kg, i.p.） was administered at the onset of MCAO. The infarct rate and edema rate were detected on TTC （2,3,5-triphenyltetrazolium chloride）-stained coronal sections. The extracellular levels of amino acid transmitters were monitored in striatum of rats with ischemic/reperfusion injury using in vivo microdialysis technique. Furthermore, the protective effects of Pur against glutamate-induced neurotoxicity were detected. Glutamate-induced apoptotic and necrotic cells in hippocampus were estimated by flow cytometric analysis of Annexin-V and PI labeling cells. Results Pur （100 mg/kg） significantly decreased infarct size by 31.6% （P〈0.05）, reduced edema volume （P〈0.05）, and improved neurological functions （P〈0.05） following MCAO. In these rats, the ischemia-induced extracellular levels of aspartate （Asp）, glutamate （Glu）, γ-aminobutyric acid （GABA）, and taurine （Tau） were significantly reduced in striatum of vehicle-treated animals by 54.7%, 56.7%, 75.8%, and 68.1% （P〈0.01 and P〈0.05）. Pur reduced the peak values of Glu and Asp more obviously than those of GABA and Tau, and the rate of Glu/GABA during MCAO markedly decreased in Pur-treated MCAO rats, compared with the vehicle-treated MCAO rats. Meanwhile, apoptosis and necrosis induced by Glu in cultured hippocampal neurons were significantly reduced after Pur treatment. Conclusion Acute treatment with Put at the onset of occlusion significantly depresses ischemia-induced efflux of amino acids, especially, excitotoxicity in the striatum, a mechanism underlying the neuroprotective effect on cellular survival.

Puerarin enhances superoxide dismutase activity and inhibits RAGE and VEGF expression in retinas of STZ-induced early diabetic rats

Objective:To investigate the effects of puerarin on the activity of superoxide dismutase(SOD), and expressions of advanced glycation end-product(AGE) receptor(RAGE) and vascular endothelial growth factor(VEGF) in retinas of streptozotocin(STZ)-induced early diabetic rats. Methods:Diabetic rat models were established by inducing diabetes via intra-peritoneal injection of STZ.Rats were randomly divided into normal(control),diabetic(DM),and DM+ puerarin groups.After intra-gastric administration of puerarin(500 mg/kg/day for 4 weeks),levels of SOD and malondialdehyde(MDA) were determined in serum and retina.mRNA and protein expression levels of RAGE and VEGF in retinas were determined by real-lime polymerase chain reaction(RT-PCR)(mRNA) and Western blot analysis(protein levels).Results:There was significantly lower SOD activity and significantly higher MDA in serum and retinas of the DM group compared with the two other groups(P【0.05).After treatment with puerarin,SOD activity increased and MDA content decreased in this group(P【0.05).mRNA and protein expression levels of RACE and VECF in the DM group were significantly higher than those of the other groups (P【0.05),and decreased after puerarin treatment(P【0.05).Conclusions:Puerarin is able to enhance SOD activity,and inhibit RAGE and VEGF expressions in retinas of STZ-induced early diabetic ruts.

Puerarin protects rat brain against ischemia/reperfusion injury by suppressing autophagy via the AMPK-mT OR-ULK1 signaling pathway

Puerarin suppresses autophagy to alleviate cerebral ischemia/reperfusion injury, and accumulating evidence indicates that the AMPKm TOR signaling pathway regulates the activation of the autophagy pathway through the coordinated phosphorylation of ULK1. In this study, we investigated the mechanisms underlying the neuroprotective effect of puerarin and its role in modulating autophagy via the AMPK-m TOR-ULK1 signaling pathway in the rat middle cerebral artery occlusion model of cerebral ischemia/reperfusion injury. Rats were intraperitoneally injected with puerarin, 50 or 100 mg/kg, daily for 7 days. Then, 30 minutes after the final administration, rats were subjected to transient middle cerebral artery occlusion for 90 minutes. Then, after 24 hours of reperfusion, the Longa score and infarct volume were evaluated in each group. Autophagosome formation was observed by transmission electron microscopy. LC3, Beclin-1 p62, AMPK, m TOR and ULK1 protein expression levels were examined by immunofluorescence and western blot assay. Puerarin substantially reduced the Longa score and infarct volume, and it lessened autophagosome formation in the hippocampal CA1 area following cerebral ischemia/reperfusion injury in a dose-dependent manner. Pretreatment with puerarin（50 or 100 mg/kg） reduced Beclin-1 expression and the LC3-II/LC3-I ratio, as well as p-AMPK and p S317-ULK1 levels. In comparison, it increased p62 expression. Furthermore, puerarin at 100 mg/kg dramatically increased the levels of p-m TOR and p S757-ULK1 in the hippocampus on the ischemic side. Our findings suggest that puerarin alleviates autophagy by activating the APMK-m TOR-ULK1 signaling pathway. Thus, puerarin might have therapeutic potential for treating cerebral ischemia/reperfusion injury.

Puerarin protects brain tissue against cerebral ischemia/reperfusion injury by inhibiting the inflammatory response

Puerarin, a traditional Chinese medicine, exerts a powerful neuroprotective effect in cerebral ischemia/reperfusion injury, but its mechanism is unknown. Here, we established rat models of middle cerebral artery ischemia/reperfusion injury using the suture method. Puerarin （100 mg/kg） was administered intraperitoneally 30 minutes before middle cerebral artery occlusion and 8 hours after reperfusion. Twenty-four hours after reperfusion, we found that puerarin significantly improved neurological deficit, reduced infarct size and brain water content, and notably diminished the expression of Toll-like receptor-4, myeloid differentiation factor 88, nuclear factor kappa B and tumor necrosis factor-α in the ischemic region. These data indicate that puerarin exerts an anti-inflammatory protective effect on brain tissue with ischemia/reperfusion damage by downregulating the expression of multiple inflammatory factors.

Compound of icariin,astragalus,and puerarin mitigates iron overload in the cerebral cortex of Alzheimer＇s disease mice

Increasing evidence indicates that disruption of normal iron homeostasis may contribute to pathological development of Alzheimer＇s disease.Icariin,astragalus,and puerarin have been shown to suppress iron overload in the cerebral cortex and improve spatial learning and memory disorders in Alzheimer＇s disease mice,although the underlying mechanism remains unclear.In the present study,APPswe/PS1ΔE9 transgenic mice were administered icariin,astragalus,and puerarin（120,80,and 80 mg/kg,respectively,once a day,for 3 months）.Iron levels were detected by flame atomic absorption spectroscopy.Interleukin-1β,interleukin-6,and tumor necrosis factor-α levels were measured in the cerebral cortex by enzyme linked immunosorbent assay.Glutathione peroxidase and superoxide dismutase activity and malondialdehyde content were determined by colorimetry.Our results demonstrate that after treatment,iron levels and malondialdehyde content are decreased,while glutathione peroxidase and superoxide dismutase activities are increased.Further,interleukin-1β,interleukin-6,and tumor necrosis factor-α levels were reduced.These results confirm that compounds of icariin,astragalus,and puerarin may alleviate iron overload by reducing oxidative stress and the inflammatory response.

Mechanism of combined use of vitamin D and puerarin in anti-hepatic fibrosis by regulating the Wnt/β-catenin signalling pathway

AIM To reveal the protective mechanism of the combined use of vitamin D and puerarin in the progression of hepatic fibrosis induced by carbon tetrachloride(CCl4).METHODS Eight-week-old male Wistar rats were randomly divided into a normal control group(C group), a CCl4 group(CCl4 group), a vitamin D group(V group), a puerarin group(P group), and a combined group of vitamin D and puerarin(V + P group), each of which contained ten rats. In this way, we built a rat model of CCl4-induced hepatic fibrosis with intervention by vitamin D, puerarin, or a combination of the two. After eight weeks, the mice were sacrificed to collect serum and liver specimens. Blood was collected to detect the hyaluronic acid(HA). We also measured hydroxyproline(Hyp) and prepared paraffin sections of liver. After Sirius red staining, the liver specimens were observed under a microscope. RT-PCR and western blot analysis were adopted to detect the mRNA and the proteinlevels of Collagen I, Collagen III, Wnt1, and β-catenin in the liver tissues, respectively.RESULTS Hepatic fibrosis was observed in the CCl4 group. In comparison, hepatic fibrosis was attenuated in the V, P, and V + P groups: the HA level in blood and the Hyp level in liver were reduced, and the mRNA levels of Collagen I, Collagen III, Wnt, and β-catenin in liver were also decreased, as well as the protein levels of Wnt1 and β-catenin. Among these groups, the V + P group demonstrated the greatest amelioration of hepatic fibrosis.CONCLUSION The combined application of vitamin D and puerarin is capable of alleviating CCl4-induced hepatic fibrosis of rats. As to the mechanism, it is probably because the combined use is able to silence the Wnt1/β-catenin pathway, suppress the activation of hepatic stellate cells, and reduce the secretion of collagen fibers, therefore improving the anti-hepatic fibrosis effect.

Response surface optimization of microwave-assisted extraction for HPLC-fluorescence determination of puerarin and daidzein in Radix Puerariae thomsonii

Microwave-assisted extraction was optimized with response surface methodology for HPLC-fluorescence determination of puerarin and daidzein in Radix Puerariae thomsonii.The optimized extraction procedure was achieved by soaking the sample with 70% methanol（1∶15,v/v）for 30 min,and then microwave irradiation for 11 min at a power of 600 W.Coupling the extraction process with HPLC-fluorescence presented good recovery,satisfactory precision,and good linear relation.Compared with a method from the Chinese Pharmacopoeia,the proposed method enables higher extraction efficiency and more accurate analytical results.It can be of potential value in quality assessment of Radix Puerariae thomsonii medicinal materials.

Pharmacokinetic and pharmacodynamic analysis of ferulic acidpuerarin-astragaloside in combination with neuroprotective in cerebral ischemia/reperfusion injury in rats

Objective:To investigate the effects of the active ingredients combined therapy on inflammatory factors interleukin 1 beta(IL-1β)and neuropeptide Y(NPY)based on pharmacodynamics in rats.Methods:The animal model was built by transient middle cerebral artery occlusion(MCAO).The method for evaluating the concentrations of the FA-Pr-AI components in rat plasma was established by using HPLC and the expression levels of IL-1βand NPY were determined by ELISA.A new mathematics method of the trend of percentage rate of change(PRC)was used to assess the correlation between pharmacokinetics(PK)and pharmacodynamics(PD).Results:FA-Pr-Al in combination reduced neurological deficits,decreased infarct volume and inhibited the expression levels of IL-1βand NPY(all P<0.05)compared with the model group.FA,Pr and Al all displayed two compartment open models in rats.Clockwise hysteresis loops were obtained by time-concentration-effect curves.IL-1βand NPY level changes in the plasma followed an opposite trend to the plasma concentration tendency after C_(max)was reached.Astragaloside's PRC value was significantly higher than those of FA and puerarin between 120 to 180 min.Conclusions:The pharmacokinetics of FA-PrAl in combination were closely related its pharmacodynamics in treating ischemia/reperfusion injury,and the components of FA-Pr-Al may have a synergistic pharmacological effect.Astragaloside may play a more pronounced role in regulating IL-1βand NPY levels compared with puerarin or FA.

A Novel Conformation Investigation on Newly Synthesized Compound of Diethyl Puerarin-7-yl Phosphate

A novel compound, diethyl puerarin-7-yl phosphate, was synthesized through a simplified Atheron-Todd reaction for the first time. The structure of this compound was elucidated by IR, ESI-MS and NMR. Two conformations of the compound were testified by 2D NMR （HSQC and HMBC） and dynamic NMR. Furthermore, we carried out the conformational analysis using chemical calculation by the Gaussian 03. Finally, we obtained two preferred conformations and energy values.

Puerarin prevents high glucose-induced apoptosis of Schwann cells by inhibiting oxidative stress

Oxidative stress may be the unifying factor for the injury caused by hyperglycemia in diabetic peripheral neuropathy. Puerarin is the major isoflavonoid derived from Radix puerariae and has been shown to be effective in increasing superoxide dismutase activity. This study sought to investigate the neuroprotective effect of puerarin on high glucose-induced oxidative stress and Schwann cell apoptosis in vitro. Intracellular reactive oxygen radicals and mitochondrial transmembrane potential were detected by flow cytometry analysis. Apoptosis was confirmed by TUNEL and oxidative stress was monitored using an enzyme-linked immunosorbent assay for the DNA marker 8-hydroxy-2-deoxyguanosine. The expression levels of bax and bcl-2 were analyzed by quantitative real-time reverse transcriptase-PCR, while protein expression of cleaved caspase-3 and -9 were analyzed by means of western blotting. Results suggested that puerarin treatment inhibited high glucose-induced oxidative stress, mitochondrial depolarization and apoptosis in a dose-dependent manner. Furthermore, puerarin treatment downregulated Bax expression, upregulated bcl-2 expression and attenuated the activation of caspase-3 and -9. Overall, our results indicated that puerarin antagonized high glucose-induced oxidative stress and apoptosis in Schwann cells.

Puerarin ameliorates allodynia and hyperalgesia in rats with peripheral nerve injury

Puerarin is a major active ingredient of the traditional Chinese plant medicine,Radix Puerariae,and commonly used in the treatment of myocardial and cerebral ischemia.However,the effects of puerarin on neuropathic pain are still unclear.In this study,a neuropathic pain animal model was created by partial sciatic nerve ligation.Puerarin（30 or 60 mg/kg） was intraperitoneally injected once a day for 7 days.Mechanical allodynia and thermal hyperalgesia were examined at 1 day after model establishment.Mechanical threshold and paw withdrawal latency markedly increased in a dose-dependent manner in puerarin-treated rats,especially at 7 days after model establishment.At 7 days after model establishment,quantitative real-time reverse transcriptase-polymerase chain reaction results showed that puerarin administration reversed m RNA expression of transient receptor potential vanilloid 1（Trpv1） and transient receptor potential ankyrin 1（Trpa1） in a dose-dependent manner in dorsal root ganglion neurons after peripheral nerve injury.These results suggest that puerarin dose-dependently ameliorates neuropathic pain by suppressing Trpv1 and Trpa1 up-regulation in dorsal root ganglion of neuropathic pain rats.

Puerarin exhibits greater distribution and longer retention time in neurons than astrocytes in a co-cultured system

The phytoestrogen puerarin has been shown to protect neurons and astrocytes in the brain, and is therefore an attractive drug in the treatment of Alzheimer’s disease, Parkinson’s disease and cerebral ischemia. Whether puerarin exhibits the same biological processes in neurons and astro-cytesin vitro has rarely been reported. In this study, cortical neurons and astrocytes of newborn Sprague-Dawley rats were separated, identiifed and co-cultured in a system based on Transwell membranes. The retention time and distribution of puerarin in each cell type was detected by lfuorescence spectrophotometry and lfuorescence microscope. The concentration of puerarin in both co-cultured and separately cultured neurons was greater than that of astrocytes. Puerarin concentration reached a maximum 20 minutes after it was added. At 60 minutes after its addi-tion, a scant amount of drug was detected in astrocytes; however in both separately cultured and co-cultured neurons, the concentration of puerarin achieved a stable level of about 12.8 ng/mL. The results indicate that puerarin had a higher concentration and longer retention time in neu-rons than that observed in astrocytes.

Effect of puerarin on myocardial perfusion and ventricular wall motion in patients with acute coronary syndrome

Objective To investigate the effects of puerarin (Pur) on myocardial perfusion and ventricular wall motion in patients with acute coronary syndrome (ACS).Methods Thirty-seven patients with ACS were randomly divided into two groups:conventional treatment group (n= 17,11 males,range of age:32-80 years,average age:60.9±4.9 years) and Pur treatment group (n=20,12 males,range of age:40-76 years,average age:62.7±3.5 years).Patients in the conventional treatment group received standard treatment according to the current guidelines,while patients in the Pur treatment group received intravenous administration of Pur (500 mg/day) for 10 days plus conventional treatment.Real-time myocardial contrast echocardiography (RT-MCE) was performed to evaluate the change in myocardial perfusion index (MPI) and ventricular wall motion index (VWMI) at admission and 10 days after treatment.Results At 10 days after treatment,MPI was significantly higher (P【0.01) and VWMI significantly lower (P【0.01) in the Pur group comparing with those in the conventional group.Conclusions Puerarin might improve myocardial microcirculation perfusion and ventricular wall motion in patients with ACS.

Restrictive Effect of Puerarin on Myocardial Infarct Area in Dogs and Its Possible Mechanism

Summary: To evaluate the protective effect of puerarin on ischemic myocardium in dogs with acute myocardial infarction (AMI) and to reveal its possible mechanism, 10 dogs were randomly divided into puerarin group (group G) and control group (group C). AMI model was established in all dogs. Puerarin or saline was administered over a period of 21 days. Coronary angiography was performed before and after ligation of coronary artery. Eight hemorheological parameters were examined before and 22 days after the operation. The infarct area and vessel density of myocardium were assessed. The infarct area in group G was smaller than that in group C. Angiography 2 h and 22 d after ligation of coronary artery revealed significant augmentation of collateral vessels in group G as compared with control group. The platelet aggregation and the blood viscosity were in- creased during AMI when compared with control phase, and the increased indexes during AMI would be inhibited when puerarin were given. Capillaries and distribution vessel density in is- chemic zone on day 22 showed statistically significant augmentation in group G as compared with control group. Puerarin might improve the opening and formation of coronary collateral circula- tion, and might inhibit the increase of platelet aggregation and the blood viscosity during AMI, and thereby improve microcirculation and restrict myocardial infarct area.