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Background Current treatment for functional dyspepsia (FD) has limited and unsustainable efficacy. Probiotics have the potential to alleviate FD; However, the underlying mechanism remains unclear. This study aimed to evaluate the effect and mechanism of probiotics in alleviating FD. Methods A randomized, positive-drug and placebo-controlled clinical trial was conducted; 200 FD patients were randomly divided into four groups (placebo, positive control [proton pump inhibitors, PPI] or Bifidobacterium lactis BL-99 [low, high doses]). The clinical response rates in 8-week treatment, 2-week follow-up and 6-week questionnaire survey periods were recorded. Faecal microbiota and metabolites were assessed by metagenomics, un-target and target metabolomics technology. Results The clinical response rate for BL-99_high [43 (95.6%) of 45] group was significantly higher than that for placebo [28 (62.2%) of 45, P = 0.001], BL-99_low [36 (76.6%) of 47, P = 0.019] or positive control group [34 (70.8%) of 48, P = 0.006] after an 8-week treatment. In particular, BL-99_high group was still higher than that for placebo or positive control group after 2-week follow-up and 6-week questionnaire survey periods. Further metagenomic and metabolomics studies found that PPI significantly decreased the gut microbiota diversity, induced the cluster of Escherichia enterotype and decreased butyrate contents. Interestingly, BL-99 converted the gut microbiota enterotype from Bacteroidetes (Alistipes finegoldii, Alistipes shahii) to Firmicutesc (Roseburia intestinalis, Roseburia inulinivorans) and Escherichia enterotype was not clustered after 8-week treatment, which activates carbohydrate esterase activity, and increases faecal and serum butyrate levels. Conclusion BL-99 sustainably alleviated FD symptoms by altering the taxonomic composition and functional potential of the FD microbiome. Trial registration Chictr.org.cn ChiCTR2000041430.

Mesenchymal stem cells (MSCs) are the excellent candidates in myocardial regeneration given their easy accessibility, low immunogenicity and high potential for cardiomyocyte differentiation. This work focused on investigating the role of icariin, a main active component of the Traditional Chinese herb epimedium, in human bone marrow-derived MSCs (BMSCs) proliferation and differentiation into cardiomyocytes In Vitro. Human BMSCs were cultivated In Vitro, and MTT assay was conducted to measure their proliferation. On this basis, we selected the optimal icariin dose for promoting the proliferation to induce cardiomyocyte differentiation of MSCs, which were pretreated with or without 5-azacytidine (5-Aza). Cardiac-specific cardiac troponin I (cTnI) and connexin 43 (Cx43)-positive cells were detected by immunofluorescent staining. The differentiation ratio of MSCs was examined by flow cytometry. This study measured early cardiac transcription factors (TFs) Nkx2.5 and GATA4 levels through RT-PCR and Western blotting (WB). As a result, icariin increased MSC proliferation dependent on its dose, and the optimal dose was determined to be 80 μg/l. Furthermore, MSCs showed minimal cardiomyogenic differentiation when induced by icariin alone as confirmed by the expression of cardiac-related markers. Moreover, a synergic interaction was observed when icariin and 5-Aza cooperated to induce cardiomyocyte differentiation of MSCs. In conclusion, Icariin stimulates proliferation and facilitates cardiomyocyte differentiation of MSCs In Vitro and may be potentially used as a new method for enhancing the MSCs efficacy in cardiovascular disease.

Crush syndrome (CS), also known as traumatic rhabdomyolysis, is the leading cause of death following extrication from structural collapse due to earthquakes. Due to the unfeasibility of human studies, animal models are used to study crush syndrome pathophysiology, including biochemistry and treatment regimes. The aim of this systematic literature review was to identify the differences and benefits of various animal models used in the study of CS and provide valuable information for design of future research. A systematic search was conducted in two methods: with the filters "(crush syndrome) AND (crush muscle injury)" and with the keywords "(crush syndrome) AND (animal model)" covering all articles in the PubMed databases. The search generated 378 articles. After screening abstracts, 91 articles were retrieved and read, then 11 repeated articles were removed and 2 reference papers were included. We finally reviewed 82 original articles. There appear to be two primary methods employed for inducing crush syndrome in animal models, which are chemically induced injury and physically induced injury. Chemical method mainly includes intramuscular (IM) injection of tissue extract solution and IM injection of 50% glycerine. Physical method can be classified into invasive and non-invasive physical compression by elasticated material, inflatable band and heavy load. Various species of animals have been used to study CS, including mice (13.4%), rats (68.3%), rabbits (11.0%), canines (4.9%), goats (1.2%), and pigs (1.2%). Small animals are suitable for researches exploring the mechanism of disease or drug efficacy while large animals can work better with clinical application-related researches. In regard to the choice of modeling method, compressing the certain muscle of animals by heavy things is superior to others to cause systemic trauma-related rhabdomyolysis signs. In addition, due to the significant burden of crush injuries on animals, further attention shall be paid to the selection of the most suitable anesthetics and appropriate analgesics.

Background: Lipid droplets (LDs) establish a considerable number of contact sites with mitochondria to enable energy transfer and communication. In this study, we developed a fluorescent biosensor to image LD-mitochondria interactions at the nanoscale and further explored the function of LD-mediated matrix transmission in processes involving multi-organelle interactions. Methods: A fluorescent probe called C-Py (C21H19N3O2, 7-(diethylamino) coumarin-3-vinyl-4-pyridine acetonitrile) was designed and synthesized. Colocalization of C-Py and the commercial LD stain Nile Red was analyzed in HeLa cells. The fluorescence stability and signal to background ratio of C-Py under structured illumination microscopy (SIM) were compared to those of the commercial probe BODIPY493/503. The cytotoxicity of C-Py was assessed using CCK-8 assays. The uptake pattern of C-Py in HeLa cells was then observed under various temperatures, metabolic levels, and endocytosis levels. Contact sites between LDs and various organelles, such as mitochondria, nuclei, and cell membrane, were imaged and quantitated using SIM. Physical changes to the contact sites between LDs and mitochondria were monitored after lipopolysaccharide induction. Results: A LD-targeted fluorescent biosensor, C-Py, with good specificity, low background signal, excellent photostability, low cytotoxicity, and high cellular permeability was developed for tracking LD contact sites with multiple organelles using SIM. Using C-Py, the subcellular distribution and dynamic processes of LDs in living cells were observed under SIM. The formation of contact sites between LDs and multiple organelles was visualized at a resolution below ~200 nm. The number of LD-mitochondria contact sites formed was decreased by lipopolysaccharide treatment inducing an inflammatory environment. Conclusions: C-Py provides strategies for the design of ultra-highly selective biosensors and a new tool for investigating the role and regulation of LDs in living cells at the nanoscale.

ObjectivePatients with renal failure suffer from symptoms caused by uraemic toxins, possibly of gut microbial origin, as deduced from studies in animals. The aim of the study is to characterise relationships between the intestinal microbiome composition, uraemic toxins and renal failure symptoms in human end-stage renal disease (ESRD).DesignCharacterisation of gut microbiome, serum and faecal metabolome and human phenotypes in a cohort of 223 patients with ESRD and 69 healthy controls. Multidimensional data integration to reveal links between these datasets and the use of chronic kidney disease (CKD) rodent models to test the effects of intestinal microbiome on toxin accumulation and disease severity.ResultsA group of microbial species enriched in ESRD correlates tightly to patient clinical variables and encode functions involved in toxin and secondary bile acids synthesis; the relative abundance of the microbial functions correlates with the serum or faecal concentrations of these metabolites. Microbiota from patients transplanted to renal injured germ-free mice or antibiotic-treated rats induce higher production of serum uraemic toxins and aggravated renal fibrosis and oxidative stress more than microbiota from controls. Two of the species, Eggerthella lenta and Fusobacterium nucleatum, increase uraemic toxins production and promote renal disease development in a CKD rat model. A probiotic Bifidobacterium animalis decreases abundance of these species, reduces levels of toxins and the severity of the disease in rats.ConclusionAberrant gut microbiota in patients with ESRD sculpts a detrimental metabolome aggravating clinical outcomes, suggesting that the gut microbiota will be a promising target for diminishing uraemic toxicity in those patients.Trial registration numberThis study was registered at ClinicalTrials.gov (NCT03010696).

Homology of medicine and food-zizyphi spinosi semen (ZSS) exhibits abundant pharmacological activities, such as sedation, hypnosis and anti-depression. In the present study, the water soluble polyphenols extracted from ZSS via the acid digestion method were named ZSSP, and exhibited significant anti-colorectal cancer (CRC) activity, characterized by restraining cell proliferation, promoting cell apoptosis and increasing chemo-sensitivity of CRC cells. The potential of ZSSP in vivo was further evaluated in an AOM/DSS-induced colitis-associated carcinogenesis (CAC) mouse model. Intriguingly, ZSSP diminished the number and volume of CAC polyps in mice in a dose-dependent manner, and effectively limited the damage of mice organs induced by AOM/DSS. The immunohistochemistry result showed that the elevated CRC early markers in CAC mice, such as COX-II, EMR1, and Ki67, were potently prevented by the ZSSP treatment. Further, the component in ZSSP with the anti-CRC activity was identified as spinosin by the macroporous resin of SP207 and RP-HPLC-MS/MS. Interestingly, during the extraction process, sodium ions were introduced forming spinosin·Na+, which had better water solubility and more remarkable anti-CRC activity than the spinosin. This study provides a new pharmacological property of spinosin derived from ZSS, inhibiting the growth of human CRC cells and colitis-associated CRC in mice, which indicates its potential use as a natural agent against CRC.

Doxorubicin (DOXO) can be used to treat a variety of human tumors, but its clinical application is limited due to severe cardiotoxic side effect. Here, we explore the role of

Oncosis, depending on DNA damage and mitochondrial swelling, is an important approach for treating cancer and other diseases. However, little is known about the behavior of mitochondria during oncosis, due to the lack of probes for in situ visual illumination of the mitochondrial membrane and mtDNA. Herein, a mitochondrial lipid and mtDNA dual‐labeled probe, MitoMN, and a continuous add‐on assay, are designed to image the dynamic process of mitochondria in conditions that are unobservable with current mitochondrial probes. Meanwhile, the MitoMN can induce oncosis in a light‐activated manner, which results in the enlargement of mitochondria and the death of cancer cells. Using structured illumination microscopy (SIM), MitoMN‐stained mitochondria with a dual‐color response reveals, for the first time, how swelled mitochondria interacts and fuses with each other for a nonlinear enlargement to accelerate oncosis into an irreversible stage. With this sign of irreversible oncosis revealed by MitoMN, oncosis can be segregated into three stages, including before oncosis, initial oncosis, and accelerated oncosis., A mitochondrial lipids and mtDNA dual‐labeling probe with continuous add‐on assay is designed to induce and image the nonlinear enlargement of mitochondria during oncosis. Together with super‐resolution imaging, it is revealed how swelled mitochondria interact and fuse with each other for a nonlinear enlargement to accelerate oncosis into an irreversible stage, which can be a new landmark for staging oncosis process.

Nonalcoholic fatty liver disease (NAFLD) is the early stage of many metabolic syndromes. The intervention of NAFLD can prevent its further development into severe metabolic syndromes. Given the inefficiency and side effects of chemical drugs for treating NAFLD, the hepatic-targeted nanocarriers loaded with bioactive compounds may offer a more effective and acceptable strategy for eliminating NAFLD. Here we developed hepatic-targeted oxidized starch-lysozyme (OSL) nanocarriers to specifically deliver resveratrol (Res) to liver tissue in order to maximize its therapeutic efficiency. The hepatic targeting was achieved using covalently conjugated galactose (Gal), which is recognized by the asialoglycoprotein receptors specifically expressed in hepatocytes. In steatotic HepG2 cell model, treatment with hepatic-targeted Gal-OSL/Res nanocarriers enhanced the cellular Res uptake and anti-lipogenesis capabilities, and effectively decreased triglyceride accumulation by modulating AMP-activated protein kinase (AMPK)/silent information regulation 2 homolog 1(SIRT1)/fatty acid synthase (FAS)/sterol regulatory element-binding protein-1c (SREBP1c) signaling pathway. In mice, Gal-OSL increased Res delivery into liver tissues and increased their hepatic effective concentration in liver. Most importantly, Gal-OSL/Res nanocarriers effectively reversed NAFLD and recovered hepatic insulin sensitivity of NAFLD mice to the healthy state. Furthermore, Gal-OSL/Res efficiently ameliorated lipid deposition and insulin resistance by modulating AMPK/SIRT1/FAS/SREBP1c signaling pathway and downregulated insulin receptor substrate-1 (IRS-1) phosphorylation at serine 307 in liver. These findings suggested that the hepatic-targeted Gal-OSL nanocarriers delivering Res could potentially serve as a safe and promising platform for NAFLD and other liver related diseases.

Nowadays, the application of lithium-ion batteries in various industries including our daily life is increasing, so the evaluation of the safety and reliability of lithium-ion batteries is essential. Assessing the performance of lithium-ion batteries accurately and in real-time has become a more critical research direction. However, in most application scenarios, the problem of small sample is often hidden in performance evaluation tasks of lithium-ion batteries. A model-based transfer learning framework to solve this problem is presented in this paper. Firstly, a CNN-LSTM fusion model is proposed by combining the solid spatial feature extraction capability of convolutional neural network (CNN) and the solid temporal dimensional feature extraction capability of long short-term memory network (LSTM); further, a model-based transfer learning approach is introduced to accomplish the performance evaluation task by pre-training and re-training. The experiments are conducted on NASA’s public dataset of lithium-ion batteries, and multiple sets of comparison experiments are set up. The results show that the method can better solve the small sample problem encountered in the lithium-ion batteries performance evaluation task.

Due to the intermittency and instability of power output of solar power stations (SPS), the safety and stationarity of the electric grid are facing considerable challenges. So, it is essential to predict the power output of SPS accurately. To date, as the most important meteorological factor determining the power output of SPS, the prediction of direct normal irradiation (DNI) has always been a hotspot, however at the same time a challenging problem. In recent years, with the improvement of hardware performance, deep learning methods have witnessed rapid development in the field of forecasting of renewable energies. In this paper, a hybrid method combining convolutional neural network (CNN) and longshort term memory (LSTM) neural network is proposed, the former can be effectively used for extraction of spatial feature, while the latter is used for extraction of temporal feature. As a case study, the proposed method is used for prediction of DNI of four typical days, i.e. spring equinox, summer solstice, autumn equinox, and winter solstice, based on the meteorological conditions of Zhangbei. The results show that deep learning methods can be effectively used for prediction of DNI, however, the proposed method in this paper achieves higher prediction accuracy than that of the compared methods.

Due to the intermittency and instability of solar power plant output, the key components are often in danger of being scrapped. Therefore, it is necessary to accurately predict the output of solar power plants. At present, the solar radiation intensity is considered to be one of the most important factors affecting the output of solar power plants. In essentially, the solar radiation intensity is a general concept, which is composed of several parameters. Among these parameters, direct normal Irradiance (DNI) prediction has become a hot and difficult research topic. In recent years, with the continuous improvement of hardware performance, a deep learning model has become one of the best methods to solve most time series prediction problems. In this paper, an ensemble deep learning model is proposed. This model integrates the convolutional neural network (CNN) and long short-term memory (LSTM) neural network. The former is responsible for extracting spatial features from data, while the latter is responsible for extracting temporal features. As a case study, the proposed method will predict the DNI of four typical days (spring equinox, summer solstice, autumn equinox and winter solstice) and its seven days before and after which is based on the meteorological data of Zhangbei. The results show that the deep learning model can be effectively applied to DNI prediction. However, the method proposed in this paper has a higher prediction accuracy compared with other models.

Due to the non-specific staining of existing fluorescent markers, which mask many positive signal acquisition, the nanoscale imaging of a small bioactive molecule such as peroxynitrite (ONOO–), however, is currently unavailable. Herein, we propose a “landmine warfare strategy”, probe L-1 evenly “buries” in the cellular matrix as a “landmine” (no fluorescence), when ONOO– “stepped on” the probe L-l, causing the “landmine explosion” to release fluorophore, thus capturing ONOO– particles, under structured illumination microscopy (SIM). We found that probe L-1 shows high sensitivity and selectivity for ONOO– in vivo, with a detection limit as low as 85.7 nM in vitro. Using this “landmine warfare strategy”, the ONOO– formation, up to a resolution of 100 nm, bounding to the mitochondrial cristae was revealed for the first time. Under lipopolysaccharide induction, the state of ONOO– labeled by L-1 changes from a single particle to an aggregated state. Thus, this system represents an attractive strategy for the imaging the structure and tracking of functional bioactive small molecules by resolving the issue of non-specific staining in living cells under SIM.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by overproduction of numerous autoantibodies. Many studies have sought to identify such biomarkers to distinguish patients with active lupus nephritis from SLE patients without renal involvement. Because antibodies to complement C1q appear to be prevalent in patients with active lupus nephritis, we analyzed the frequency of antigenic epitopes of C1q and their clinical significance in a large multicenter study of Chinese patients. The lupus cohort consisted of 210 patients with active lupus nephritis as a discovery cohort, 130 active patients as a validation cohort along with 130 SLE patients without clinical renal involvement, and 100 healthy controls. Serum antibodies to intact C1q, the collagen-like region, the globular head region, and the new linear A08 epitope to C1q were screened by specific ELISA. The frequency of antibodies to intact C1q, the C1q-collagen-like region, and the A08 antibodies in the discovery cohort were significantly higher than that in patients without renal involvement or healthy controls. Antibodies to the globular head region were not prevalent enough for further study. The results were confirmed in the validation cohort. The area under the curve for anti-A08 antibodies was significantly greater than those for both the intact and collagen-like region antibodies to discriminate between active lupus nephritis and active SLE without clinical renal involvement. The A08 antibodies were all negative at remission. The serum A08 antibody level correlated better with disease relapse than that of antibodies to either the intact or the collagen-like region, significantly predicting renal prognosis. Thus, serum levels of A08 C1q antibodies are closely associated with disease activity and prognosis in lupus nephritis.

For a more insightful investigation into the specificity of bacterial heparinase I, a series of structurally well-defined heparin oligosaccharides was synthesized using a highly efficient chemoenzymatic strategy. Apart from the primary cleavage site, five glycosidic linkages of oligosaccharides with varying modifications to obtain secondary cleavage sites were degraded by a high concentration of heparinase I. The reactivity of linkages toward heparinase I was not entirely dependent on the 2-O-sulfated iduronic acid being cleaved or the neighboring 6-O-sulfated glucosamine residues, but it was dependent on higher degrees of sulfation of oligosaccharides and indispensable N-substituted glucosamine adjacent to the cleavable linkage. Moreover, the enzyme demonstrated less preferential cleavage toward glycosidic linkages containing glucuronic acid than those containing iduronic acid of the counterpart oligosaccharides. Biolayer interferometry revealed differences in reactivity that are not completely consistent with different affinities of substrates to enzyme. Our study presented accurate information on the cleavage promiscuity of heparinase I that is crucial for heparin depolymerization.

Background/Aims: Ginsenoside Rb1 (GS-Rb1) is one of the most important active pharmacological extracts of the Traditional Chinese Medicine ginseng, with extensive evidence of its cardioprotective properties. Mir-208 has been shown to act as a biomarker of acute myocardial infarction in vivo studies including man. However the impact of miR-208 on the protective effect of GS-Rb1 in hypoxia/ischemia injured cardiomyocytes remains unclear. The current study aims to investigate the target gene of miR-208 and the impact on the protective effect of GS-Rb1 in hypoxia/ischemia (H/I) injuried cardiomyocytes. Materials and Methods: Primary cultures of neonatal rat cardiomyocytes (NRCMs) was subjected to the H/I conditions with or without GS-Rb1. Cell viability was calculated by MTT assay and confirmed by flow cytometry analysis. Mir-208 was then detected by qRT-PCR. Luciferase reporter assay was carried out to detect the target gene of Mir-208. Then the NRCMs were transfected with miR-208 mimics and inhibitors to evaluate the impact on cardioprotective properties of Rb1. Results: The miR-208 expression level was clearly upregulated in the H/I treated NRCMs accompanied by the percentage of the apoptotic cells which could be reversed by GS-Rb1 pretreatment. The nemo-like kinase (NLK) mRNA and protein expression levels were decreased in H/I group measured by RT-PCR and western blotting. Luciferase activity assay was then carried out to identify that NLK may be a direct target of mir-208. MTT assay showed that miR-208 inhibitor slightly decreased the protective effect of Rb1 on the H/I impaired NRCMs. However, results showed no statistical difference. Conclusions: These findings proved that NLK was a direct target of mir-208 and miR-208 act indirectly during Rb1 protecting H/I impaired NRCMs and further researches were needed to explore the relationship that microRNAs and other signal pathways in the protective effect of GS-Rb1 on the hypoxia/ischemia injuries in cardiomyocytes.

Concentrating solar power systems are proliferating around the world. However, the non-schedulable characteristic of thermal output presents considerable challenges to safe utilization of solar heat. So, seasonable forecasting of thermal output is going to be essential to both power grid and plant. In this paper, a hybrid forecasting method based on mechanism modeling and deep learning method is proposed. By mechanism modeling, the major meteorological factors used for forecasting are identified accurately, avoiding the subjectivity of chosen of model input features. By convolutional neural network and long short-term memory network, the input features are reconstructed, and the spatial-temporal coupling characteristics between meteorological factors are fully explored. Finally, the thermal power is output by fully connected layers. As a case study, the thermal power of a Solar Two-like concentrating solar power plant based on meteorological conditions of Zhangbei is forecasted, and the mean values of root mean square error and mean absolute error are 5.061 MWt and 2.871 MWt on the whole year, respectively. The results show that the methods proposed in paper can be effectively used for thermal power forecasting of concentrating solar power system.

Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytesin vitroand the mitochondrial apoptotic pathway mediated mechanism.Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were kept in DMEM without glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from 2.5 to 40 µM was given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. Cell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic translocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined by Western blot. Caspase-3 and caspase-9 activities were determined by the assay kit.Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst. Moreover, GS-Rb1 markedly decreased the translocation of cytochrome c from the mitochondria to the cytosol, increased the Bcl-2/ Bax ratio, and preserved mitochondrial transmembrane potential (ΔΨm). Its administration also inhibited activities of caspase-9 and caspase-3.Conclusion. Administration of GS-Rb1 during H/Iin vitrois involved in cardioprotection by inhibiting apoptosis, which may be due to inhibition of the mitochondrial apoptotic pathway.

Ginsenoside (GS-Rb1) is one of the most important active compounds of ginseng, with extensive evidence of its cardioprotective properties. However, the miRNA mediated mechanism of GS-Rb1 on cardiomyocytes remains unclear. Here, the roles of miRNAs in cardioprotective activity of GS-Rb1 were investigated in hypoxic- and ischemic-damaged cardiomyocytes. Neonatal rat cardiomyocytes (NRCMs) were first isolated, cultured, and then incubated with or without GS-Rb1 (2.5–40μM)in vitrounder conditions of hypoxia and ischemia. Cell growth, proliferation, and apoptosis were detected by MTT and flow cytometry. Expressions of various microRNAs were analyzed by real-time PCR. Compared with that of the control group, GS-Rb1 significantly decreased cell death in a dose-dependent manner and expressions of mir-1, mir-29a, and mir-208 obviously increased in the experimental model groups. In contrast, expressions of mir-21 and mir-320 were significantly downregulated and GS-Rb1 could reverse the differences in a certain extent. The miRNAs might be involved in the protective effect of GS-Rb1 on the hypoxia/ischemia injuries in cardiomyocytes. The effect might be based on the upregulation of mir-1, mir-29a, and mir-208 and downregulation of mir-21 and mir-320. This might provide us a new target to explore the novel strategy for ischemic cardioprotection.

Lupus nephritis always elicits immune inflammatory tissue damages in kidney. Pentraxin 3 (PTX3), mainly produced at inflammatory sites, is known to be involved in the regulation of the innate immunity system. The aim of this study was to investigate the serum and urine levels of PTX3, and the expression of PTX3 in renal tissues in lupus nephritis patients from a large Chinese cohort.The study used cross-sectional survey and 288 active lupus nephritis patients, including discovery cohort and validation cohort, 115 systemic lupus erythematosus (SLE) patients without clinical renal involvement and 46 healthy controls were enrolled. Serum and urine PTX3 were screened by enzyme-linked immunosorbent assay (ELISA). The renal deposition of PTX3 was detected by immunohistochemistry and immunofluorescence.The average level of serum PTX3 in the discovery cohort of lupus nephritis was significantly higher than that in nonrenal involvement SLE group and normal controls (P < 0.001, P < 0.001, respectively), which was confirmed by the validation cohort. Serum PTX3 levels of 15 lupus nephritis patients in remission decreased significantly compared with that in active phase. Serum PTX3 levels were significantly higher in patients with hematuria (P = 0.014), leucocyturia (P = 0.002), acute renal failure (P = 0.001), and nephrotic syndrome (P = 0.036). There were significant correlations between serum PTX3 levels and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scores, serum creatinine value, renal pathological activity indices, and serum complement 3 (C3) in active lupus nephritis patients. The urinary PTX3 levels were significantly higher in active lupus nephritis patients compared with patients in remission and normal controls (P = 0.011, P = 0.008, respectively). There were significant associations between urinary PTX3 levels and multiple indices of tubulointerstitial lesions, including urinary KIM-1 (r = 0.368, P = 0.016), neutrophil gelatinase-associated lipocalin (NGAL) (r = 0.320, P = 0.039), microalbumin (r = 0.621, P = 0.003), transferring (r = 0.451, P = 0.040) levels and renal pathological indices scores, especially interstitial inflammation (r = 0.349, P = 0.025) in active lupus nephritis patients. A significant correlation was found between serum and urine PTX3 levels (r = 0.431, P = 0.006). PTX3 staining was mainly observed in tubulointerstitial areas of patients with lupus nephritis, and immunofluorescence study showed that PTX3 could colocalize with fibroblast in interstitium.Circulating and local PTX3 levels were significantly increased in patients with active lupus nephritis and might be a biomarker for the disease progression, especially of tubulointerstitial injury.