Neuroprotective effects of G9a inhibition through modulation of peroxisome-proliferator activator receptor gamma-dependent pathways by miR-128

Dysregulation of G9a,a histone-lysine N-methyltransferase,has been observed in Alzheimer’s disease and has been correlated with increased levels of chronic inflammation and oxidative stress.Likewise,microRNAs are involved in many biological processes and diseases playing a key role in pathogenesis,especially in multifactorial diseases such as Alzheimer’s disease.Therefore,our aim has been to provide partial insights into the interconnection between G9a,microRNAs,oxidative stress,and neuroinflammation.To better understand the biology of G9a,we compared the global microRNA expression between senescence-accelerated mouse-prone 8(SAMP8)control mice and SAMP8 treated with G9a inhibitor UNC0642.We found a downregulation of miR-128 after a G9a inhibition treatment,which interestingly binds to the 3′untranslated region(3′-UTR)of peroxisome-proliferator activator receptor γ(PPARG)mRNA.Accordingly,Pparg gene expression levels were higher in the SAMP8 group treated with G9a inhibitor than in the SAMP8 control group.We also observed modulation of oxidative stress responses might be mainly driven Pparg after G9a inhibitor.To confirm these antioxidant effects,we treated primary neuron cell cultures with hydrogen peroxide as an oxidative insult.In this setting,treatment with G9a inhibitor increases both cell survival and antioxidant enzymes.Moreover,up-regulation of PPARγby G9a inhibitor could also increase the expression of genes involved in DNA damage responses and apoptosis.In addition,we also described that the PPARγ/AMPK axis partially explains the regulation of autophagy markers expression.Finally,PPARγ/GADD45αpotentially contributes to enhancing synaptic plasticity and neurogenesis after G9a inhibition.Altogether,we propose that pharmacological inhibition of G9a leads to a neuroprotective effect that could be due,at least in part,by the modulation of PPARγ-dependent pathways by miR-128.

The Magnaporthe oryzae effector Avr-PikD suppresses rice immunity by inhibiting an LSD1-like transcriptional activator

Avirulence effectors(Avrs),encoded by plant pathogens,can be recognized by plants harboring the corresponding resistance proteins,thereby initiating effector-triggered immunity(ETI).In susceptible plants,however,Avrs can function as effectors,facilitating infection via effector-triggered susceptibility(ETS).Mechanisms of Avr-mediated ETS remain largely unexplored.Here we report that the Magnaporthe oryzae effector Avr-PikD enters rice cells via the canonical cytoplasmic secretion pathway and suppresses rice basal defense.Avr-PikD interacts with an LSD1-like transcriptional activator AKIP30 of rice,and AKIP30 is also a positive regulator of rice immunity,whereas Avr-PikD impedes its nuclear localization and suppresses its transcriptional activity.In summary,M.oryzae delivers Avr-PikD into rice cells to facilitate ETS by inhibiting AKIP30-mediated transcriptional regulation of immune response against M.oryzae.

Screening and field application of microbial-flooding activator systems

This study aims to further enhance the oil recovery of reservoirs in the Zhong-2 Block of the Gudao Oilfield by identifying the most effective microbial-flooding activator systems and applying them in the field.We began by analyzing the structure of the reservoirs'endogenous microbial communities to understand the potential impact of microbial flooding.This was followed by determining commonly used activator systems based on their abilities to stimulate oil-displacement functional bacteria.Through laboratory experiments on oil displacement efficiency and sweep characteristics,we determined the optimal activator injection method(injection ratio)and the requisite bacterial concentration for maximal microbial-flooding efficacy.Finally,we selected the optimal activator systems and applied them to field tests.Our findings suggest the target block is highly receptive to microbial-flooding.In terms of performance,the activator systems ranked as No.3>No.4>No.1>No.2.Interestingly,a deep activator system,when compared to the top-performing No.3 system,exhibited a higher bacterial concentration peak and longer peaking duration.Optimal oil displacement effects were observed at a 1:4 vol ratio between the No.3 activator and deep activator systems,with bacterial concentrations of up to 106 cells/mL or above.Field tests with the selected activator systems,following a specific injection protocol,demonstrated a notable increase in oil production and a reduction in water cut.

Effects of interleukin-10 treated macrophages on bone marrow mesenchymal stem cells via signal transducer and activator of transcription 3 pathway

BACKGROUND Alveolar bone defects caused by inflammation are an urgent issue in oral implant surgery that must be solved.Regulating the various phenotypes of macrophages to enhance the inflammatory environment can significantly affect the progression of diseases and tissue engineering repair process.AIM To assess the influence of interleukin-10(IL-10)on the osteogenic differentiation of bone marrow mesenchymal stem cells(BMSCs)following their interaction with macrophages in an inflammatory environment.METHODS IL-10 modulates the differentiation of peritoneal macrophages in Wistar rats in an inflammatory environment.In this study,we investigated its impact on the proliferation,migration,and osteogenesis of BMSCs.The expression levels of signal transducer and activator of transcription 3(STAT3)and its activated form,phos-phorylated-STAT3,were examined in IL-10-stimulated macrophages.Subsequently,a specific STAT3 signaling inhibitor was used to impede STAT3 signal activation to further investigate the role of STAT3 signaling.RESULTS IL-10-stimulated macrophages underwent polarization to the M2 type through substitution,and these M2 macrophages actively facilitated the osteogenic differentiation of BMSCs.Mechanistically,STAT3 signaling plays a crucial role in the process by which IL-10 influences macrophages.Specifically,IL-10 stimulated the activation of the STAT3 signaling pathway and reduced the macrophage inflammatory response,as evidenced by its diminished impact on the osteogenic differentiation of BMSCs.CONCLUSION Stimulating macrophages with IL-10 proved effective in improving the inflammatory environment and promoting the osteogenic differentiation of BMSCs.The IL-10/STAT3 signaling pathway has emerged as a key regulator in the macrophage-mediated control of BMSCs’osteogenic differentiation.

Long noncoding RNA steroid receptor RNA activator 1 inhibits proliferation and glycolysis of esophageal squamous cell carcinoma

BACKGROUND The clinical effects and detailed roles of long non-coding RNA(LncRNA)steroid receptor RNA activator 1(SRA1)in esophageal squamous cell carcinoma(ESCC)remain ambiguous.In the present study,the complementary sites between lncRNA SRA1,miRNA-363-5p,and phospholysine phosphohistidine inorganic pyrophosphate phosphatase(LHPP)predicted via bioinformatics analysis stimulated us to hypothesize that miRNA-363-5p/LHPP axis might be required for SRA1-mediated ESCC progression.AIM To investigate the molecular events of SRA1 in the malignant behavior in ESCC.METHODS Thirty-eight ESCC tissues and paired adjacent normal tissues were acquired.SRA1 expression was detected in ESCC tissues and cell lines using quantitative reverse transcription-polymerase chain reaction.Cell counting Kit-8 assay,transwell invasion assay,glycolysis assay,and xenograft tumor model were performed to address the malignant biological behaviors of ESCC cells after the introduction of SRA1.The t-test and theχ2 test were used for comparison between groups.Survival curve analysis was performed using the Kaplan-Meier method.RESULTS SRA1 downregulation was identified in ESCC.ESCC patients exhibiting a low SRA1 expression faced shorter overall survival than those with a high SRA1 expression.The introduction of SRA1 inhibited cell proliferation,glucose uptake,and lactate production in ESCC.In vivo,the growth of ESCC was hindered by SRA1 overexpression.Then,SRA1 overexpresses the LHPP by inhibiting miRNA-363-5p.Lastly,the introduction of small interfering RNA si-LHPP or miRNA-363-5p mimic could abrogate the inhibition roles triggered by SRA1.CONCLUSION SRA1 inhibits the oncogenicity of ESCC via miRNA-363-5p/LHPP axis.The SRA1/miRNA-363-5p/LHPP pathway may be a therapeutic target for ESCC.

Diagnostic Value of the Padua Score Combined with Thrombotic Biomarker Tissue Plasminogen Activator Inhibitor-1 (tPAI-1) Detection for the Risk of Deep Vein Thrombosis in Patients with Pulmonary Heart Disease

This study explores the diagnostic value of combining the Padua score with the thrombotic biomarker tissue plasminogen activator inhibitor-1(tPAI-1)for assessing the risk of deep vein thrombosis(DVT)in patients with pulmonary heart disease.These patients often exhibit symptoms similar to venous thrombosis,such as dyspnea and bilateral lower limb swelling,complicating differential diagnosis.The Padua Prediction Score assesses the risk of venous thromboembolism(VTE)in hospitalized patients,while tPAI-1,a key fibrinolytic system inhibitor,indicates a hypercoagulable state.Clinical data from hospitalized patients with cor pulmonale were retrospectively analyzed.ROC curves compared the diagnostic value of the Padua score,tPAI-1 levels,and their combined model for predicting DVT risk.Results showed that tPAI-1 levels were significantly higher in DVT patients compared to non-DVT patients.The Padua score demonstrated a sensitivity of 82.61%and a specificity of 55.26%at a cutoff value of 3.The combined model had a significantly higher AUC than the Padua score alone,indicating better discriminatory ability in diagnosing DVT risk.The combination of the Padua score and tPAI-1 detection significantly improves the accuracy of diagnosing DVT risk in patients with pulmonary heart disease,reducing missed and incorrect diagnoses.This study provides a comprehensive assessment tool for clinicians,enhancing the diagnosis and treatment of patients with cor pulmonale complicated by DVT.Future research should validate these findings in larger samples and explore additional thrombotic biomarkers to optimize the predictive model.

Fabrication of pollution-free coal gangue-based catalytic material utilizing ferrous chloride as activator for efficient peroxymonosulfate activation

Novel coal gangue-based persulfate catalyst(CG-FeCl_(2))was successfully synthesized by the means of calcinating under nitrogen atmosphere with the addition of ferrous chloride tetrahydrate(FeCl_(2)·_(4)H_(2)O).The phase transformation of the prepared materials and gas products during the heating process are thoroughly investigated.It is suggested that ferrous chloride participated in the phase transformation and formed Si-O-Fe bonds.And the main gaseous products are H_(2)O,H_(2),and HCl during the heating process.Besides,the ability of CG-FeCl_(2) to activate peroxymonosulfate(PMS)for catalytic degradation of polycyclic aromatic hydrocarbons(PAHs)and phenol was deeply studied.More than 95%of naphthyl,phenanthrene and phenol were removed under optimizied conditions.In addition,1O_(2),·OH,and SO_(4)·−were involved in the CG-FeCl_(2)/PMS system from the free radical scavenging experiment,where 1O_(2) played a major role during the oxidation process.Furthermore,CG-FeCl_(2)/PMS system exhibited superior stability in a relatively wide pH range and the presence of common anion from related degradation experiments.Overall,the novel CG-FeCl_(2) is an efficient and environmentally friendly catalyst,displaying potential application prospect in the field of PAHs and phenol-contaminated wastewater treatment.

18β-glycyrrhetinic acid promotes gastric cancer cell autophagy and inhibits proliferation by regulating miR-328-3p/signal transducer and activator of transcription 3

BACKGROUND Gastric cancer(GC)is one of the most common cancer types worldwide,and its prevention and treatment methods have garnered much attention.As the active ingredient of licorice,18β-glycyrrhetinic acid(18β-GRA)has a variety of pharmacological effects.The aim of this study was to explore the effective target of 18β-GRA in the treatment of GC,in order to provide effective ideas for the clinical prevention and treatment of GC.AIM To investigate the mechanism of 18β-GRA in inhibiting cell proliferation and promoting autophagy flux in GC cells.METHODS Whole transcriptomic analyses were used to analyze and screen differentially expressed microRNAs(miRNAs)in GC cells after 18β-GRA intervention.Lentivirus-transfected GC cells and the Cell Counting Kit-8 were used to detect cell proliferation ability,cell colony formation ability was detected by the clone formation assay,and flow cytometry was used to detect the cell cycle and apoptosis.A nude mouse transplantation tumor model of GC cells was constructed to verify the effect of miR-328-3p overexpression on the tumorigenicity of GC cells.Tumor tissue morphology was observed by hematoxylin and eosin staining,and microtubule-associated protein light chain 3(LC3)expression was detected by immunohistochemistry.TransmiR,STRING,and miRWalk databases were used to predict the relationship between miR-328-3p and signal transducer and activator of transcription 3(STAT3)-related information.Expression of STAT3 mRNA and miR-328-3p was detected by quantitative polymerase chain reaction(qPCR)and the expression levels of STAT3,phosphorylated STAT3(p-STAT3),and LC3 were detected by western blot analysis.The targeted relationship between miR-328-3p and STAT3 was detected using the dual-luciferase reporter gene system.AGS cells were infected with monomeric red fluorescent protein-green fluorescent protein-LC3 adenovirus double label.LC3 was labeled and autophagy flow was observed under a confocal laser microscope.RESULTS The expression of miR-328-3p was significantly upregulated after 18β-GRA intervention in AGS cells(P=4.51E-06).Overexpression of miR-328-3p inhibited GC cell proliferation and colony formation ability,arrested the cell cycle in the G0/G1 phase,promoted cell apoptosis,and inhibited the growth of subcutaneous tumors in BALB/c nude mice(P<0.01).No obvious necrosis was observed in the tumor tissue in the negative control group(no drug intervention or lentivirus transfection)and vector group(the blank vector for lentivirus transfection),and more cells were loose and necrotic in the miR-328-3p group.Bioinformatics tools predicted that miR-328-3p has a targeting relationship with STAT3,and STAT3 was closely related to autophagy markers such as p62.After overexpressing miR-328-3p,the expression level of STAT3 mRNA was significantly decreased(P<0.01)and p-STAT3 was downregulated(P<0.05).The dual-luciferase reporter gene assay showed that the luciferase activity of miR-328-3p and STAT33’untranslated regions of the wild-type reporter vector group was significantly decreased(P<0.001).Overexpressed miR-328-3p combined with bafilomycin A1(Baf A1)was used to detect the expression of LC3 II.Compared with the vector group,the expression level of LC3 II in the overexpressed miR-328-3p group was downregulated(P<0.05),and compared with the Baf A1 group,the expression level of LC3 II in the overexpressed miR-328-3p+Baf A1 group was upregulated(P<0.01).The expression of LC3 II was detected after intervention of 18β-GRA in GC cells,and the results were consistent with the results of miR-328-3p overexpression(P<0.05).Additional studies showed that 18β-GRA promoted autophagy flow by promoting autophagosome synthesis(P<0.001).qPCR showed that the expression of STAT3 mRNA was downregulated after drug intervention(P<0.05).Western blot analysis showed that the expression levels of STAT3 and p-STAT3 were significantly downregulated after drug intervention(P<0.05).CONCLUSION 18β-GRA promotes the synthesis of autophagosomes and inhibits GC cell proliferation by regulating the miR-328-3p/STAT3 signaling pathway.

Activator与Headgear-Activator治疗作用的研究

目的比较Activator与Headgear-Activator的治疗作用,探讨两者的作用机理,并评价其临床应用的综合效果。方法选取36例安氏II类错牙合病例,12例采用Activator治疗,17例采用Headgear-Activator治疗,7例未经治疗作对照。分别摄取治疗前后(对照组采用1年时间间隔)X线头影侧位定位片,用同一参考系统定量分析两种治疗过程中发生的变化。结果两种治疗方法均能有效纠正II类错牙合,但作用机制不同。结论Activator和Headgear-Activator能有效调节上下颌骨发育的不协调,纠正儿童骨性II类错牙合。Headgear-Activator由于使用高位头帽,可以加强对上颌生长发育,特别是垂直方向的生长发育的控制;同时对牙齿牙槽产生作用,一定程度地控制Activator的一些不良反应,有利于患者牙颌面形态的充分改善及变化的表达。

Activator功能矫治对髁突、关节窝和下颌骨生长改形的影响研究——X线头影测量研究

目的探讨去除生长因素Activator的骨骼矫形效果和机理。方法选定40例Angle Ⅱ1随机分为治疗组和对照组,在治疗前后头颅侧位片上选用坐标系,测量固定骨性标志点的垂直向和矢状向改变,并进行影响下颌综合长度的相关因素分析。结果Activator治疗可以明显增加下颌骨垂直向上的生长,使关节窝向前下移位,治疗组的升支高度和下颌骨综合长度在排除正常生长因素下有明显的增加,髁突的垂直生长是引起升支高度和下颌综合长度显著增加的重要因素。结论Activator功能矫治有明显的下颌骨矫形效果,可以促进下颌骨髁突的生长,增加下颌骨的长度。

PancherzⅡ类错矫正分析方法评价Activator的治疗机制

目的 :探讨 Activator对生长发育期 类 1分类患者的牙和颌骨的作用机制。方法 :应用 Pancherz 类错牙合矫正分析法 (Class correction analysis)结合传统测量项目对 2 2例 (男 8例 ,女 14例 ,年龄男 10～ 13岁 ,女 9～ 12岁 ) ANB角大于 5°、前牙覆盖大于 7mm、磨牙完全远中或尖对尖远中关系患者的治疗前后 X线头影测量分析项目进行配对 t检验。结果 :SNA减小 ,Go- Me增大 ,NSL / ML增大 ,ANB角减小 ,前后面高增加 ,下颌位置 Pg/ OL P前移均有显著性差异。上中切牙角变小 ,下切牙角度变大 ,下磨牙前移 ,磨牙关系得到改善。结论 :Activator对下颌骨的矫形作用比较复杂 ,下颌骨的绝对长度增加 ,下颌平面角加大 ,SNB角无变化 ;Activator可以改善前牙的覆盖 ,后牙的 类关系及 类骨关系。

改良型ACTIVATOR矫治反对颅颌面三维结构改变的影响

目的 研究改良型ACTIVATOR矫治早期反对颅颌面三维结构的影响。方法 采用改良型ACTIVATOR矫治乳牙期及替牙期前牙反 80人 ,对治疗前后的模型、薛氏位关节片及头颅侧位片投影测量进行分析。结果 ①上下颌牙弓宽度治疗前后无明显改变 ;②上颌长度及突度增大 ,上切牙唇倾 ;③下颌髁突后退至正常位 ,上下颌基骨关系明显改善 ,乳牙反改变最明显 ,矫治后呈Ⅰ类骨面型 ,替牙期反矫治后仍遗留骨骼异常 ,骨面型仍属Ⅲ类 ;④下切牙舌倾及颏角变小更趋严重。结论 改良型ACTIVATOR矫治反 ,能有效促进上颌生长 ,抑制下颌生长 。

Headgear—activator治疗安氏Ⅱ^1类错（牙合）对鼻唇颏协调性影响的研究

目的研究Headgear-activator矫治器治疗安氏Ⅱ1类患者对鼻唇颏协调性的影响。方法选择自然生长和使用Headgear-activator矫治的38例骨性Ⅱ1类错牙合患者为研究对象,将其分为对照组和Headgear-activator组,每组均为19例患者。对2组患者治疗前后拍摄X线头颅定位侧位片,测量所得角度和线距,采用SPSS 11.0软件包分别计算均值和标准差,利用配对t检验比较测量指标的变化。结果上唇审美平面距、下唇审美平面距、上切牙露齿度、上唇突角、上下唇突角、上唇颏突角减小;上唇长、下唇长、上唇倾角、下唇倾角、下唇突角、鼻唇角、颏唇沟角、软组织面角、Z角、面突角增大,与对照组比较有统计学意义(P<0.05)。结论 Headgear-activator矫治器可显著减小安氏Ⅱ1类错牙合患者上下唇突度,改善开唇露齿,在一定程度上恢复了鼻、唇、颏之间的协调性,使侧貌轮廓变得自然舒缓,软组织侧貌趋于直面型。

同源Activator－Inhibitor模型的整体解

本文证明了同源Ａｃｔｉｖａｔｏｒ—Ｉｎｈｉｂｉｔｏｒ模型：ｕｔ＝ｄ△ｕ─μμ＋μｐ／ｖｑ＋σ整体解的存在性．

Activator矫治安氏Ⅱ类错前后髁突和关节盘位置改变的MRI研究

目的分析Activator功能矫治对髁突、关节盘的位置及盘髁关系的影响。方法选择20个AngleⅡ1错患者,在斜矢状位闭口MRI影像上测量Activator功能矫治前后髁突和关节盘位置的改变。结果在无症状AngleⅡ1错中有40%出现关节盘前移位,功能矫治前后其髁突和关节盘位置没有明显改变。结论Activator治疗不会改变髁突在关节窝中的位置,不会引起正常位置的关节盘前移位,也不会使已经存在的盘前移位复位。

Activator治疗骨性Ⅱ类畸形的临床研究

目的 探讨Activator矫正器的作用机理。方法 应用随机原理 ,将生长发育高峰期骨性Ⅱ类错牙合畸形分为三组 ,一年后评价各组上下颌骨骨性关系。结果 骨性Ⅱ类错牙合畸形在生长发育高峰期上下颌骨均有生长 ,但不足以自行调整至正常。Activator及头帽型Activator可显著改善上下颌骨骨性关系。结论 Activator适合于下颌发育不足或位置后缩者 ,头帽型Activator更适合于下颌发育不足伴上颌发育过度或位置前突者。

改良式Activator矫治Ⅱ类错对颞下颌关节影响的研究

对 2 0例采用改良式 activator矫治的替牙早期安氏 类错牙合病例进行矫治前、后及追踪的薛式位片的测量分析。旨在说明改良式的 activator矫治安氏 类错牙合各个时期颞颌关节的改变。结果发现 :矫治前、后及追踪复查的比较 ,关节前后间隙均有显著性差异 (P<0 .0 1)。而矫治初与后期追踪复查的比较无显著性变化 (P>0 .0 5 )。提示 :替牙早期主要为功能性 类错牙合 ,改良式的 activator可引导后缩的下颌及髁突前移 ,并稳定于正常关节位。对于矫治安氏 类错牙合 ,防止复发均具有重要意义。

Urokinase-type plasminogen activator receptor as a predictor of poor outcome in patients with systemic inflammatory response syndrome

BACKGROUND:Urokinase-type plasminogen activator(uPA) and urokinase-type plasminogen activator receptor(uPAR) are known as important factors,which mediate a variety of functions in terms of vascular homeostasis,inflammation and tissue repair.However,their role in systemic inflammatory response syndrome(SIRS) has been less well studied.This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the patients with SIRS.We therefore analyzed their role and clinicopathological significance in patients with SIRS.METHODS:A case-control study was conducted with 85 patients who were divided into two groups according to the diagnostic criteria of SIRS:SIRS group(n=50) and non-SIRS group(/7=35).The SIRS group was divided into MODS group(n=26) and non-MODS group(n=24) by their severity,and survival group(n=35) and non-survival group(n=15) by their prognosis.Another 30 healthy adults served as normal controls.uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay(ELISA) kits.RESULTS:The plasma level of uPA was lower in the SIRS group than in the non-SIRS group and controls(P<0.001 and P<0.001).It was lower in sepsis patients and the MODS group than in the non-sepsis patients and the non-MODS patients(all P<0.05).However,there was no difference in uPA level between survivors and non-survivors(P>0.05).The plasma level of uPAR increased in the SIRS group compared with the non-SIRS group and controls(P<0.001 and P<0.001).There was a significant elevation of uPAR in sepsis patients,MODS patients and non-survivors as compared with non-sepsis patients,non-MODS patients and survivors respectively(all P<0.05).Plasma uPAR levels were positively correlated with APACHE Ⅱ score(r=0.575,P<0.001) and SOFA score(r=0.349,P=0.013).AUCs for the prediction of SIRS mortality were 0.67 and 0.51,respectively,for uPA and uPAR.CONCLUSION:uPAR could be a predictor of poor outcome in patients with SIRS.

Roles of tissue plasminogen activator and its inhibitor in proliferative diabetic retinopathy

AIMTo investigate the role of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) in proliferative diabetic retinopathy (PDR) and to discuss the correlations among t-PA, PAI and vascular endothelial growth factor (VEGF) expressions.

Diffusion-weighted magnetic resonance imaging reflects activation of signal transducer and activator of transcription 3 during focal cerebral ischemia/reperfusion

Signal transducer and activator of transcription（STAT）is a unique protein family that binds to DNA,coupled with tyrosine phosphorylation signaling pathways,acting as a transcriptional regulator to mediate a variety of biological effects.Cerebral ischemia and reperfusion can activate STATs signaling pathway,but no studies have confirmed whether STAT activation can be verified by diffusion-weighted magnetic resonance imaging（DWI）in rats after cerebral ischemia/reperfusion.Here,we established a rat model of focal cerebral ischemia injury using the modified Longa method.DWI revealed hyperintensity in parts of the left hemisphere before reperfusion and a low apparent diffusion coefficient.STAT3 protein expression showed no significant change after reperfusion,but phosphorylated STAT3 expression began to increase after 30 minutes of reperfusion and peaked at 24 hours.Pearson correlation analysis showed that STAT3 activation was correlated positively with the relative apparent diffusion coefficient and negatively with the DWI abnormal signal area.These results indicate that DWI is a reliable representation of the infarct area and reflects STAT phosphorylation in rat brain following focal cerebral ischemia/reperfusion.