Mechanical strain regulates osteogenesis via Antxr1/LncRNA H19/Wnt/ß-catenin axis.

Alleviating bone loss is an essential way to prevent osteoporotic fractures. Proper exercise improves bone density without the side effects of long-term medications, but the mechanism is unclear. Our study explored the role of Antxr1/LncRNA H19/Wnt/ß-catenin axis in the process of exercise-mediated alleviation of bone loss. Here we discovered that moderate-intensity treadmill exercise alleviates bone loss caused by ovariectomy and ameliorates bone strength accompanied by an increased lncRNA H19 expression. Concomitantly, Antxr1, a mechanosensitive protein was found downregulated by exercise but upregulated by ovariectomy. Interestingly, knockdown expression of Antxr1 increased lncRNA H19 expression and Wnt/ß-catenin signaling pathway in bone marrow mesenchymal stem cells, whereas overexpression of Antxr1 decreased lncRNA H19 expression and Wnt/ß-catenin signaling pathway. Hence, our study demonstrates the regulation of Antxr1/LncRNA H19/Wnt/ß-catenin axis in the process of mechanical strain-induced osteogenic differentiation, which provides further mechanistic insight into the role of mechanical regulation in bone metabolism.

Prediction of the effects of small molecules on the gut microbiome using machine learning method integrating with optimal molecular features.

BACKGROUND: The human gut microbiome (HGM), consisting of trillions of microorganisms, is crucial to human health. Adverse drug use is one of the most important causes of HGM disorder. Thus, it is necessary to identify drugs or compounds with anti-commensal effects on HGM in the early drug discovery stage. This study proposes a novel anti-commensal effects classification using a machine learning method and optimal molecular features. To improve the prediction performance, we explored combinations of six fingerprints and three descriptors to filter the best characterization as molecular features. RESULTS: The final consensus model based on optimal features yielded the F1-score of 0.725 ± 0.014, ACC of 82.9 ± 0.7%, and AUC of 0.791 ± 0.009 for five-fold cross-validation. In addition, this novel model outperformed the prior studies by using the same algorithm. Furthermore, the important chemical descriptors and misclassified anti-commensal compounds are analyzed to better understand and interpret the model. Finally, seven structural alerts responsible for the chemical anti-commensal effect are identified, implying valuable information for drug design. CONCLUSION: Our study would be a promising tool for screening anti-commensal compounds in the early stage of drug discovery and assessing the potential risks of these drugs in vivo.

Application and Molecular Mechanisms of Extracellular Vesicles Derived from Mesenchymal Stem Cells in Osteoporosis.

Osteoporosis (OP) is a chronic bone disease characterized by decreased bone mass, destroyed bone microstructure, and increased bone fragility. Accumulative evidence shows that extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) (MSC-EVs), especially exosomes (Exos), exhibit great potential in the treatment of OP. However, the research on MSC-EVs in the treatment of OP is still in the initial stage. The potential mechanism has not been fully clarified. Therefore, by reviewing the relevant literature of MSC-EVs and OP in recent years, we summarized the latest application of bone targeted MSC-EVs in the treatment of OP and further elaborated the potential mechanism of MSC-EVs in regulating bone formation, bone resorption, bone angiogenesis, and immune regulation through internal bioactive molecules to alleviate OP, providing a theoretical basis for the related research of MSC-EVs in the treatment of OP.

An automated, rapid fluorescent immunoassay to quantify serum soluble programmed death-1 (PD-1) protein using testing-on-a-probe biosensors.

OBJECTIVES: Soluble programmed death-1 (sPD-1) plays an essential role in the pathogenesis and progression of various diseases, including chronic hepatitis B (CHB) and hepatocellular carcinoma (HCC). Currently, there is no Food and Drug Administration-approved sPD-1 immunoassay available for routine clinical testing. Most sPD-1 detections employed enzyme-linked immunosorbent assay (ELISA) method for research purpose, which is complicated by intensive manual operation and cannot achieve automatic detection. Therefore, we aimed to develop an automated, rapid immunoassay for sPD-1 measurement based on testing-on-a-probe (TOP) biosensors and evaluate its performance in patients with hepatic diseases. METHODS: We developed an automatic fluorescent immunoassay using TOP biosensors using a pair of mouse anti-PD-1 monoclonal antibodies (mAbs), which were evaluated by biolayer interferometry. The sensitivity, linearity, and repeatability of the novel immunoassay were analyzed, and its compatibility with an established ELISA kit was evaluated. Further, we quantified sPD-1 level in healthy individuals as well as patients with CHB, hepatic cirrhosis, and HCC. RESULTS: The TOP assay to quantify sPD-1 was developed and performed on an automatic fluorescent analyzer within 20 min, which showed good precision with coefficients of variation less than 10% and good linearity ranging from 2 to 3,000 pg/mL. The results tested by our TOP assay correlated well with the established ELISA assay (r=0.92, p<0.0001). Using our TOP assay, sPD-1 was significantly elevated in patients with chronic hepatitis, hepatic cirrhosis and hepatocarcinoma if compared to healthy control, respectively (p<0.0001). CONCLUSIONS: An automated, rapid fluorescent immunoassay to quantify serological sPD-1 protein using TOP biosensors was developed and showed acceptable analytical performance including precision, linearity, and good correlation with the established ELISA assay, with the great potential in clinical practice.

The Role of Long Non-coding RNA, Nuclear Enriched Abundant Transcript 1 (NEAT1) in Cancer and Other Pathologies.

Nuclear enriched abundant transcript 1 (NEAT1), consisting of two kinds of lncRNAs of 3.7 kB NEAT1-1 and 23 kB NEAT1-2, can be highly expressed in organs and tissues such as the ovary, prostate, colon, and pancreas, and is involved in paraspeckle formation and mRNA editing and gene expression. Therefore, NEAT1 is a potential biomarker for the treatment of a variety of diseases, which may be caused by two factors (isoforms of NEAT1 and NEAT1 sponging miRNA as ceRNA). However, there is still much confusion about the mechanism and downstream effector between the abnormal expression of NEAT1 and various diseases. This review summarizes recent research progress on NEAT1 in cancer and other pathologies and provides a more reliable theoretical basis for the treatment of related diseases.

The effects of biophysical stimulation on osteogenic differentiation and the mechanisms from ncRNAs.

Ample proof showed that non-coding RNAs (ncRNAs) play a crucial role in proliferation and differentiation of osteoblasts and bone marrow stromal cells (BMSCs). Varied forms of biophysical stimuli like mechanical strain, fluid shear stress (FSS), microgravity and vibration are verified to regulate ncRNAs expression in osteogenic differentiation and influence the expression of target genes associated with osteogenic differentiation and ultimately regulate bone formation. The consequences of biophysical stimulation on osteogenic differentiation validate the prospect of exercise for the prevention and treatment of osteoporosis. In this review, we tend to summarize the studies on regulation of osteogenic differentiation by ncRNAs beneath biophysical stimulation and facilitate to reveal the regulatory mechanism of biophysical stimulation on ncRNAs, and provide an update for the prevention of bone metabolism diseases by exercise.

Circular RNAs in childhood-related diseases and cancers: A review.

Research into the diagnosis, treatment and prevention of childhood-related diseases is the key to reducing their morbidity and mortality. Circular RNAs (circRNAs) play critical roles, both in physiology and pathology, and there is ample evidence to show that they play varying roles in tissue development and gene regulation. Studies on circRNAs in different childhood-related diseases have confirmed their great potential for disease prevention and treatment. These breakthroughs highlight the pathological role of circRNAs in cancers, as well as cardiovascular and hereditary childhood illnesses. In this review, we summarize the role of circRNAs in childhood-related diseases and cancer, and provide an update of the possible diagnostic and therapeutic application of circRNAs.

Molecular structure, expression, and functional role of Clec11a in skeletal biology and cancers.

C-type lectin domain family 11 member A (Clec11a), also known as stem cell growth factor (SCGF), C-type lectin superfamily member 3 (CLECSF3), or osteolectin was initially identified as a growth factor for hematopoietic progenitor cells. The human Clec11a gene encodes a polypeptide of 323 amino acids with characteristics of a secreted glycoprotein encompassing two integrin-binding motifs, RGD (Arg-Gly-Asp) and LDT (Leu-Asp-Thr), a putative leucine zipper domain, and a functional C-type lectin domain. It regulates hematopoietic differentiation and homeostasis and exhibits a protective effect against severe malarial anemia and lipotoxicity. Furthermore, Clec11a promotes the differentiation of mesenchymal progenitors into mature osteoblasts in vitro and plays an important role in the maintenance of adult skeleton age-related bone loss and fracture repair. Receptor ligand binding results in activation of downstream signaling cascades including glycogen synthase kinase 3 (GSK3), ß-catenin, and Wnt, resulting in the expression of osteoblast-related gene transcripts including Alp, Runx2, Lef1, and Axin2. In addition, Clec11a is also associated with the development of several cancers, including leukemia, multiple myeloma, and gastrointestinal tract tumors. To date, however, the mechanisms governing transcription regulation of the Clec11a gene are not known and remain to be uncovered. Understanding the function and mechanism of action of Clec11a will pave the way for the development of Clec11a as a novel therapeutic target for conditions such as cancer, anemia, and skeletal diseases.

Inhibition of circular RNA CDR1as increases chemosensitivity of 5-FU-resistant BC cells through up-regulating miR-7.

This study aims to explore the mechanism of Circular RNA CDR1as implicating in regulating 5-fluorouracil (5-FU) chemosensitivity in breast cancer (BC) by competitively inhibiting miR-7 to regulate CCNE1. Expressions of CDR1as and miR-7 in 5-FU-resistant BC cells were determined by RT-PCR. CCK-8, colony formation assay and flow cytometry were applied to measure half maximal inhibitory concentration (IC50), 5-Fu chemosensitivity and cell apoptosis. Western blot was used to detect the expressions of apoptosis-related factors. CDR1as was elevated while miR-7 was inhibited in 5-FU-resistant BC cells. Cells transfected with si-CDR1as or miR-7 mimic had decreased IC50 and colony formation rate, increased expressions of Bax/Bcl2 and cleaved-Caspase-3/Caspase-3, indicating inhibition of CDR1as and overexpression of miR-7 enhances the chemosensitity of 5-FU-resistant BC cells. Targetscan software indicates a binding site of CDR1as and miR-7 and that CCNE1 is a target gene of miR-7. miR-7 can gather CDR1as in BC cells and can inhibit CCNE1. In comparison to si-CDR1as group, CCNE1 was increased and chemosensitivity to 5-Fu was suppressed in si-CDR1as + miR-7 inhibitor group. When compared with miR-7 mimic group, CDR1as + miR-7 mimic group had increased CCNE1 and decreased chemosensitivity to 5-Fu. Nude mouse model of BC demonstrated that the growth of xenotransplanted tumour in si-CDR1as + miR-7 inhibitor group was faster than that in si-CDR1as group. The tumour growth in CDR1as + miR-7 mimic group was faster than that in miR-7 mimic group. CDR1as may regulate chemosensitivity of 5-FU-resistant BC cells by inhibiting miR-7 to regulate CCNE1.

Silencing CDR1as enhances the sensitivity of breast cancer cells to drug resistance by acting as a miR-7 sponge to down-regulate REGγ.

In our study, we aimed to investigate the role of CDR1as during competitive inhibition of miR-7 in the regulation of cisplatin chemosensitivity in breast cancer via regulating REGγ. RT-qPCR was applied to detect the expression of CDR1as and miR-7 in breast cancer tissues, breast cancer cell lines and corresponding drug-resistant cell lines. The correlation between CDR1as and miR-7 and between miR-7 and REGγ was evaluated. MCF-7-R and MDA-MB-231-R cells were selected followed by transfection of a series of mimics, inhibitors or siRNA. The effect of CDR1as on the half maximal inhibitor concentration (IC50), cisplatin sensitivity and cell apoptosis was also analysed. Furthermore, a subcutaneous xenograft nude mouse model was established to further confirm the effect of CDR1as on the chemosensitivity of breast cancer to cisplatin in vivo. Immunohistochemical staining was conducted to test the Ki-67 expression in nude mice. A positive correlation was found between the drug resistance and CDR1as expression in breast cancer. CDR1as could increase the resistance of breast cancer cells to cisplatin. miR-7 expression was low, while REGγ was highly expressed in MCF-7-R and MDA-MB-231-R cells. CDR1as competitively inhibited miR-7 and up-regulated REGγ. Overexpression of miR-7 could reverse the enhanced sensitivity of silenced CDR1as to drug-resistant breast cancer cells. Additionally, in vivo experiments demonstrated that CDR1as mediated breast cancer occurrence and its sensitivity to cisplatin. Silencing CDR1as decreased Ki-67 expression. Silencing CDR1as may inhibit the expression of REGγ by removing the competitive inhibitory effect on miR-7 and thus enhancing the sensitivity of drug-resistant breast cancer cells.

Comparison of Outcomes of Frontline Immunosuppressive Therapy and Frontline Haploidentical Hematopoietic Stem Cell Transplantation for Children with Severe Aplastic Anemia Who Lack an HLA-Matched Sibling Donor.

We compared the outcomes of immunosuppressive therapy (IST) with those of T cell-replete haploidentical donor hematopoietic stem cell transplantation (haplo-HSCT) in children and adolescents with severe aplastic anemia (SAA). The medical records of 49 patients with SAA who received frontline IST (n = 29) or frontline haplo-HSCT (n = 20) between 2012 and 2016 were analyzed retrospectively. Fourteen patients responded after the first IST, and 1 patient responded after the second IST in the frontline IST group; 12 patients underwent salvage HSCT after IST failure. Sixteen of the 20 patients who underwent frontline haplo-HSCT survived without treatment failure. The 3-year overall survival of the frontline IST group was comparable to that of the frontline haplo-HSCT group (79.3 ± 7.5% versus 85.0 ± 8.0%; χ2 = 0.110; P = .740). The 3-year failure-free survival was lower in the frontline IST group compared with the frontline haplo-HSCT group (35.9 ± 10.9% versus 80.0 ± 8.9%; χ2 = 4.089; P = .043). Five patients of the IST group who underwent salvage HSCT achieved long survival without event. The event-free survival was lower in the salvage HSCT group compared with the haplo-HSCT group (41.7 ± 14.2% versus 80.0 ± 8.9%; χ2 = 3.992; P = .046), and the incidences of acute GVHD, grade II-IV acute GVHD, chronic GVHD, and severe infection were comparable between the 2 groups. Our results suggest that frontline haplo-HSCT may be a better treatment than IST for children and adolescents with SAA who lack an HLA age-matched familial donor.

MiR-214 Attenuates the Osteogenic Effects of Mechanical Loading on Osteoblasts.

Exercise is an effective way to prevent osteoporosis, but its mechanism remains unclear. MicroRNAs (miRNAs) play an essential role in bone metabolism. Recently, mechanical loading was reported to induce changes in miRNA expression in osteoblasts. However, the role of miRNAs in bone under exercise and its underlining mechanisms of action still remain unknown. MiR-214 was reported to regulate the process of osteogenesis and is considered a biomarker of osteoporosis. In this study, we aimed to investigate whether exercise could induce changes in miRNA expression in bone and to study the effects of miR-214 on mechanical loading-induced osteogenesis in osteoblasts. The results showed that miR-214 was down-regulated in both tibia from C57BL/6 mice after exercise in vivo and in osteoblasts after mechanical strain in vitro. Mechanical strain could enhance the ALP activity, promote matrix mineralization, up-regulate the expression of osteogenic factors such as ATF4, Osterix, ALP and ß-catenin, and down-regulate RANKL and RANK expression. Over-expression of miR-214 not only inhibited the expression of these osteogenic factors but also attenuated mechanical strain-enhanced osteogenesis in osteoblasts. Collectively, our results indicated that miR-214 could attenuate the osteogenic effects of mechanical loading on osteoblasts, suggesting that inhibition of miR-214 may be one of the ways in which exercise prevents osteoporosis.

Polyphyllin I inhibits gastric cancer cell proliferation by downregulating the expression of fibroblast activation protein alpha (FAP) and hepatocyte growth factor (HGF) in cancer-associated fibroblasts.

The aim of this study was to identify the anti-cancer mechanism of Polyphyllin I (PPI) on gastric cancer cells via its activity on cancer-associated fibroblasts (CAFs). We cultured purified gastric CAFs obtained from fresh human gastric cancer tissue and examined the effect of Polyphyllin I on CAF proliferation using a colorimetric viability assay. In addition, we established a nude mouse xenograft model to examine the effect of Polyphyllin I administration on tumorigenesis. Using Western analysis, we quantified protein expression of the CAF-derived cytokines fibroblast activation protein alpha (FAP), secreted protein acidic and cysteine rich (SPARC), stromal cell-derived factor 1 (SDF-1), hepatocyte growth factor tenascin-C (TNC), and hepatocyte growth factor (HGF) in both in vitro and in vivo models. We found that Polyphyllin I inhibits the proliferation of CAFs in a concentration-dependent manner. Following treatment with 2 µg/ml PPI for 24 h in vitro, the expression of FAP, SDF-1 and HGF protein in CAFs was significantly lower than that in the control group, but there was no significant difference in SPARC and TNC protein expression between the two groups. In the nude mouse xenograft model, the tumor inhibition rate was 45.5% when PPI was administered early and 29.4% with administration in the third week. The expression of FAP and HGF in the xenografts was significantly decreased, while the expression of SPARC, SDF-1, and TNC was largely unaltered. Altogether, these data suggest that Polyphyllin I can inhibit the proliferation of gastric cancer cells by downregulating the expression of FAP and HGF in CAFs in vivo.

[Research progress on the effect of long non-coding RNA H19 on osteogenic differentiation and bone diseases].

A growing number of studies have shown that long non-coding RNAs (lncRNAs) widely participate in the process of osteogenic differentiation of stem cells, regulate the proliferation and apoptosis of a variety of stem cells and osteoblasts, and play an important role in maintaining the balance of bone metabolism. LncRNA H19 regulates the expression of microRNAs (miRNAs) as upstream gene or through direct adsorption, changes the expressions of osteogenic differentiation related genes (RUNX2, OCN, etc.) via Wnt/ß-catenin, transforming growth factor ß (TGF-ß) and Notch signal transduction pathways, and consequently adjusts the process of bone formation. This paper reviews some research progress on the effect of lncRNA H19 on bone diseases, which may help to understand the function and mechanism of lncRNA H19 in regulating the occurrence and development of bone diseases and provide more reliable theoretical basis for the prevention and treatment of bone metabolism related diseases.

[Analysis of meteorological conditions affecting the upper respiratory outpatients in Ningbo City].

OBJECTIVE: To actively and effectively prevent upper respiratory diseases and providing basic research for medical meteorological forecast. METHODS: Using daily upper respiratory outpatients from a third-grade class-A hospital, a children's hospital and meteorological data of 2014 in Ningbo City, to analyze the relationship between upper respiratory outpatients and meteorological factors including emperature, pressure, humidity, sunshine, haze and others by the curve fitting method and principal component analysis method. RESULTS: The upper respiratory outpatient in Ningbo City had a season distribution feature which was significantly more during autumn to early spring. The most was in Dec and Jan, and the secondly in Mar and Nov for children. Temperature was the most obvious impact of upper respiratory outpatients. Children would be ill the next day of temperature changed significantly, and adult would postpone one-two days. In addition, continuous high pressure, low temperature, low humidity and less sunshine obviously influenced on upper respiratory diseases than single day. The longer the time, the greater the impact. Correlation coefficient between minimum temperature of five consecutive days and cough was 0. 555. In winter, outpatients were stable when average temperature was above 8 ℃, or maximum temperature was above 15 ℃, or minimum temperature was above 4 ℃ during five consecutive days. Outpatients were increased significantly to more than 1 times the usual when average temperature was below 5 ℃, or maxinum temperature was below 10 ℃, or minimum temperature was below 0 ℃ during five consecutive days. Outpatients were stability when f_1 was from-2. 5 to 3. 0, which was the first eigenvector of principal component, and outpatients were decreased obviously when f_1 was from-5. 5 to-2. 5, and outpatients were hopping increases to about 2 times the usual when f_1 was below-5. 0. CONCLUSION: Meteorological factors are one of the main causes of upper respiratory diseases, and there will be obvious relationship in continuous haze day.

The effects of different intensities of exercise and active vitamin D on mouse bone mass and bone strength.

Physical exercise is beneficial to bone health. However, little is known how different intensities of exercise affect bone mass and strength. In the present study, we used young mice to study the effects of different intensities of exercise on bone mass and bone strength in comparison to pharmacological doses of active vitamin D (calcitriol). We found that only the medium level of exercise tested showed a positive effect on bone mineral density, trabecular bone volume, and bone strength, which are attributable to a decrease in bone resorption and an increase in bone formation, with the latter being accompanied by an increase in the number of osteogenic mesenchymal stem cells in the bone marrow. Calcitriol increases bone volume and bone strength, yet the combination of calcitriol and medium-intensity exercise did not further improve bone mass or strength. Moreover, calcitriol also showed some protective effect on the bone in mice with high levels of exercise. These results indicate that exercise at medium intensity increases bone mass and strength via affecting both bone formation and resorption and that its beneficial effects on bone mass cannot be further improved by calcitriol.

A new N-methoxyl-carbonyl benzylisoquinoline from Litsea cubeba.

A new benzylisoquinoline alkaloid (•)-N-methoxycarbonyl-norjuziphine (1) was isolated from Litsea cubeba. Its structure was identified by extensively spectroscopic techniques and confirmed by the single-crystal X-ray diffraction analysis. Compound 1 showed cytotoxicity against HL-60 and MCF-7 cells, with IC50 values of 18.1 and 15.0 µM, respectively, comparable to 3.1 and 17.5 µM of the cisplatin (positive control).

Surgical treatment of huge hepatocarcinoma with invasion or severe adhesion of diaphragm using the technique of orthotopic liver resection.

BACKGROUND/AIMS: To explore the clinical application and significance of the technique of orthotopic liver resection. METHODOLOGY: From January 2004 to December 2011, five patients with huge hepatocellular carcinoma with invasion or severe adhesion of diaphragm were undergone right semi-liver resection using the technique of orthotopic liver resection. The right hemi-liver was isolated from the first liver portal, second liver portal and third liver portal, then isolated from the normal liver, finally the tumor and the invaded diaphragm were resected or removed from the severe adhesion. The approach to hepatic resection involved routine use of Peng's multifunctional operative dissector, selective control of in and out-flow of liver, control of inferior vena cava (IVC) and liver hanging maneuver, anterior approach, etc. RESULTS: The operations were successfully performed in 5 patients. Operative time was 120, 180, 150, 150 and 160 min, respectively. The amount of blood loss were 350, 350, 400, 450, 600 ml, respectively. Postoperative complications were pleural effusion in 3 cases, and other 2 cases recovered without complications. CONCLUSIONS: Although the technique of orthotopic liver resection has a high technical requirement for surgeons, it provides a surgical method and operative opportunity for the patients whose tumor has invaded diaphragm or has been severe adhesion with diaphragm and conventional liver resection cannot be performed.

[Experimental study and mechanism research of 701 diedazhentonggao on acute and chronic soft tissue injury in rabbit].

OBJECTIVE: To study the effect and mechanism of 701 Diedazhentonggao on acute and chronic soft tissue injury in rabbit. METHODS: The rabbit model of acute and chronic soft tissue injury were established by heavy hammer blow method. The tissue damage scored, pain threshold value and blood rheology were detected, and histopathological and inflammatory cytokines in damaged tissue and gene chip were observed. RESULTS: 701 Diedazhentonggao significantly improved the acute soft tissue injury symptoms, increased the pain threshold, reduced the score values of local damage, improved subcutaneous ecchymosis symptoms, reduced the content of inflammatory cytokines in damaged tissue, repaired the injuried tissue, and reduced blood viscosity and the content of IL-1 and 5-HT. But the contents of IL-6 and PGE2 in acute soft tissue injury were not reduced. The gene chip study expressed the drug interfered the pathway of IL-1R and white blood cell cling. 701 Diedazhentonggao also improved the chronic soft tissue injury symptoms and the main performance on anti-inflammatory effect, and reduced the contents of IL-6, IL-1 and 5-HT, but it had little effet on reducing the contents of PGE2, Fbg, blood and histopathological examination. CONCLUSION: 701 Diedazhentonggao has ameliorative effect on acute and chronic soft tissue injury, but the effect on acute soft tissue injuries is better than on chronic soft tissue injuries, and its mechanism may be related to reducing the contents of IL-1, IL-6, 5-HT and other related inflammatory mediators.

Soluble Programmed Cell Death 1 Protein Is a Promising Biomarker to Predict Severe Liver Inflammation in Chronic Hepatitis B Patients.

Background and Aims: Liver inflammation is important in guiding the initiation of antiviral treatment and affects the progression of chronic hepatitis B(CHB). The soluble programmed cell death 1 protein (sPD-1) was upregulated in inflammatory and infectious diseases and correlated with disease severity. We aimed to investigate the correlation between serum sPD-1 levels and liver inflammation in CHB patients and their role in indicating liver inflammation. Methods: 241 CHB patients who underwent liver biopsy were enrolled. The correlation between sPD-1 levels and the degree of liver inflammation was analyzed. Univariate and multivariate logistic regression analyses were performed to analyze independent variables of severe liver inflammation. Binary logistic regression analysis was conducted to construct a predictive model for severe liver inflammation, and the receiver operating characteristic curve (ROC) was used to evaluate the diagnostic accuracy of the predictive model. Results: sPD-1 was highest in CHB patients with severe liver inflammation, which was higher than that in CHB patients with mild or moderate liver inflammation (P < 0.001). Besides, sPD-1 was weakly correlated with AST (r = 0.278, P < 0.001). Multivariable analysis showed that sPD-1 was an independent predictor of severe liver inflammation. The predictive model containing sPD-1 had areas under the ROC (AUROCs) of 0.917 and 0.921 in predicting severe liver inflammation in CHB patients and CHB patients with ALT ≤ 1× upper limit of normal (ULN), respectively. Conclusions: Serum sPD-1 level is associated with liver inflammation in CHB patients, and high levels of sPD-1 reflect severe liver inflammation. Serum sPD-1 is an independent predictor of severe liver inflammation and shows improved diagnostic accuracy when combined with other clinical indicators.