Research on hypoglycemic activity of Osmanthus fragrans var. thunbergii extract / 药学学报

This study aimed to assess the hypoglycemic activity, and in vitro inhibition of α-glucosidase, inhibition of the advanced glycation end products (AGEs), and total antioxidant capacity were used to clarify its bioactivity. Furthermore, the potential hypoglycemic active chemical constituents in the aqueous extract of Osmanthus fragrans var. thunbergii flower were characterized using high performance liquid chromatography-electrospray ionization-quadruple time-of-flight mass spectrometry (HPLC-ESI-QTOF-MS) method. The result showed that in vitro inhibition of α-glucosidase of the extract (IC50 = 2.11 ± 0.26 mg·mL-1) were similar to acarbose (IC50 = 2.88 ± 0.32 mg·mL-1), and it inhibited the AGEs formation and the total antioxidant capacity in a certain extent. Based on the MS fragmentation pathway analysis of reference chemical acteoside contained in this extract, and related references, 73 constituents were tentatively identified from the aqueous extract of Osmanthus fragrans var. thunbergii flower, including 58 phenylethanoids, 8 caffeoylquinic acids, 1 flavonoid vicenin-2, and 6 common organic chemicals in plant. Furthermore, 8 unknown alkaloids were characterized in this work. Among of these chemicals, 61 phenylethanoids were supposed to be detected for the first time. In conclusion, this work disclosed the potential hypoglycemic active constituents of Osmanthus fragrans var. thunbergii flower.

Establishment and evaluation of in vitro galectin-3 inhibitor screening model / 药学学报

Galectin-3 (Gal-3) belongs to the galectin family and is specific in binding β-galactoside. Through its C-terminal domain, Gal-3 binds to the galactoside group of the glycosylated insulin receptor (IR) and inhibits IR signaling pathway, which leads to the insulin resistance. Thus, Gal-3 is a potential therapeutic target for the treatment of insulin resistance and type 2 diabetes. Here we report a simple Gal-3 screening model based on the property that Gal-3 binds to the galactoside. We expressed and purified human Gal-3 in Escherichia coli (E.coli), and labeled it with fluorescein isothiocyanate (FITC) in vitro. After incubating FITC labeled Gal-3 (Gal-3-FITC) with PANC-1 cells, which express glycosylated membrane protein, PANC-1 cells started to show green fluorescent signal due to the Gal-3-FITC binding to the glycosylated membrane protein. Gal-3 inhibitor disrupts the binding of Gal-3-FITC and PANC1 cells, subsequently leads to the decrease of the fluorescent signal in PANC-1 cells. We can evaluate the inhibitory efficiency of Gal-3 inhibitors through measurement of the fluorescent signal. Further studies show this model is simple, stable, and repeatable with a Z' factor between 0.7 and 0.85. In sum, we have successfully established an in vitro high-throughput screening model for Gal-3 inhibitors.

Advances in the diagnosis and treatment of phosphomannomutase 2 deficiency / 中国当代儿科杂志

Phosphomannomutase 2 deficiency is the most common form of N-glycosylation disorders and is also known as phosphomannomutase 2-congenital disorder of glycosylation (PMM2-CDG). It is an autosomal recessive disease with multi-system involvements and is caused by mutations in the PMM2 gene (OMIM: 601785), with varying severities in individuals. At present, there is still no specific therapy for PMM2-CDG, and early identification, early diagnosis, and early treatment can effectively prolong the life span of pediatric patients. This article reviews the advances in the diagnosis and treatment of PMM2-CDG.

Dystroglycanopathies: Genetic Bases of Muscular Dystrophies Due to Alteration in the O-Glycosylation of α-Dystroglycan

Abstract Congenital muscular dystrophies (CMDs) are inherited, progressive and heterogeneous muscle disorders. A group of CMDs are dystroglycanopathies, also called α-dystroglycanopathies, where there is an abnormal glycosylation of protein α-dystroglycan. Hypoglycosylation of α-DG results in different severities of congenital muscular dystrophies and they present with progressive muscle weakness and loss of motor functions. This article first focuses on the CMDs, their classification according to the observed symptoms or the protein involved in the resulting phenotype. We then focus on dystroglycanopathies, the importance of its correct O-glycosylation of the α-dystroglycan given its important structural function, considering the enzymes involved in said glycosylation and the phenotypes that can result, to finally address current therapeutics for these diseases with the aim of increasing current knowledge.

Characterization of the SRD5A3-CDG Clinical Spectrum

Abstract We aimed to characterize the clinical spectrum of patients diagnosed with SRD5A3-CDG, a subtype of congenital disorders of glycosylation (CDG) due to variants in the steroid 5a-reductase type 3 (SRD5A3) gene. It presents with multi-systemic involvement including neurological disability, dermatologic abnormalities, and ophthalmological defects. We conducted a cross-sectional study of children (n=6, ages 4-16 years) with a confirmed diagnosis of SRD5A3-CDG (c.57G>A, p.W19X). Families completed a detailed medical history questionnaire, two quality of life measures, and an adaptive behavior scale. Prevalent clinical features in our cohort included visual impairment (6/6), developmental delay (6/6), nystagmus (5/6), retinal dystrophy (4/6), and hypotonia (3/6). The Vineland Adaptive Behavior Scales demonstrated deficits across all functional domains (Composite Mean 36.17 ± 26.88), although one child did not show significant deficits. The QI-Disability Form demonstrated a mean total score of 64.8 (±12.7), and the PedsQL-Family Impact Module demonstrated a mean total score of 56.5 (±31.5). Vineland composite scores did not correlate with levels of disability captured by the QI-Disability Form (Pearson Correlation range -0.63 to +0.69, p>0.05 on all subscales). Ultimately, despite genotypic homogeneity, there is notable variability in adaptive functioning and quality of life among affected children that does not correlate with age.

Optimization of glycosylation type of recombinant human growth hormone-Fc fusion protein expressed in CHO cells / 中国生物制品学杂志

@#Objective To optimize the expression of recombinant human growth hormone-Fc(rhGH-Fc)fusion protein in CHO cells in order to obtain better glycosylation ratio and lower content of highmannose.Methods CHO cells expressing rhGH-Fc were cultured in a 7 L bioreactor.The glycosylation modifications of rhGH-Fc were adjusted by improving the composition of feeding media(using three commercial media:Gly-1:EX-CELL Glycosylation Adjust,Gly-2:SHEFF-CHO PLUS PG ACF and Gly-3:EfficientFeed C + AGT Supplement & GlycanTune C + Total Feed),and the glycosylation type and proportion of the target proteins were analyzed by mass spectrometry.Results The G0F(main glycosylation types:G0,G1 and G2;F:fucose)of Gly-1,Gly-2 and Gly-3 were 32.89%,58.66% and 33.28%,the G1F were 31.39%,18.03%and 34.90%,and the G2F were 31.39%,18.03% and 34.90%,respectively.Gly-1 and Gly-3 made the target protein contain less G0F while more G2F;Gly-3 feeding scheme-showed less high mannose modification than the other two schemes.Conclusion Gly-1 medium changed the glycosylation modification from G0F to G1F and G2F,while Gly-2 medium changed that from G2F and G1F to G0F.However,Gly-3 medium changed the glycosylation modification from G0F to G1F and G2F,and the contentof high mannose was less than 5%,which may have a better effect on modifying glycosylation type and proportion of the target protein.

Recent progress of protein glycosylation characterization utilizing native conformer-resolved mass spectrometry / 中国药科大学学报

@#Glycosylation of proteins, one of the most prevalent and complex post-translational modifications occurring in nature, plays a crucial role in regulating protein net charge, conformation, binding properties and, ultimately, biological function.Traditional structural techniques are not amenable for glycoproteins due to the inherent heterogeneity of oligosaccharides.With the advances in analytical technique, mass spectrometry displays an increasingly crucial role in elucidating the structure of glycoproteins.Mass spectrometry-based proteomic technique can dissect the chemical composition and site information of low-abundance glycosylation at the peptide level.Instead, native mass spectrometry (nMS) can analyze intact glycoproteins while maintaining the information for glycan heterogeneity, and the insights into the regulatory effects of glycosylation on protein higher order structures and interactions with other proteins or ligands.As a representative structural mass spectrometry tool, ion mobility-based nMS strategy is powered by its conformer-resolving capability and by the feasibility of conformer manipulation through collision-induced unfolding.Consequently, native IM-MS analysis can provide rich information of dynamic protein conformations, allowing for the rapid identification and differentiation of protein isoforms in an unprecedented manner.In this review, we briefly introduced two emerging native IM-MS analytical modes, dynamic conformer-resolving mode and glycoform-resolving mode.Besides, we also discussed the recent progress of conformational and topological characterization of intact glycoproteins with three typical model systems based on two above-mentioned emerging modes of native IM-MS.

Progresses of mass spectrometry-based analysis of N-glycoproteins / 中国药科大学学报

@#N-linked glycosylation is a common post-translational modification on proteins, which exhibits the same macro-heterogeneity of modification site as other small molecule modifications (such as methylation, acetylation, phosphorylation), i.e., the amino acid sequence of a protein has multiple putative modification sites. However, compared to small molecule modifications with single structures, N-glycosylation modification have tens of thousands of structures from multiple structural dimensions such as different monosaccharide compositions, sequence structures, linking structures, isomerism, and three-dimensional conformation.This results in additional micro-heterogeneity of modification site of N-glycosylation, i.e., the same N-glycosylation site can be modified with different glycans with a certain stoichiometric ratio.N-glycosylation modification regulates the structure and function of N-glycoproteins in a site- and structure-specific manner, and differential expression of N-glycosylation under disease conditions needs to be characterized through site- and structure-specific quantitative analysis.This article mainly introduces the latest development of mass spectrometry-based site- and structure-specific quantitative N-glycoproteomics and its applications in biomedical fields.

Congenital glycosylation disorder type Ⅱm caused by SLC35A2 mutations: a report of 3 cases and literature review / 中华神经科杂志

Objective:To summarize the clinical manifestations, gene variations, diagnosis and treatment of 3 cases with SLC35A2 variations characterized by congenital glycosylation disorder Ⅱm (CDG Ⅱm). Methods:A total of 3 patients admitted to the Department of Pediatrics of Xiangya Hospital of Central South University in China from 2018 to 2020 were examined in detail. The studies till January 2022 were searched with key words of "congenital disorders of glycosylation Ⅱm", " SLC35A2" and "CDG Ⅱm" in both English and Chinese in the databases of China National Knowledge Infrast Ructure (CNKI), Wanfang, Online Mendelian Inheritance in Man and PubMed, and the clinical manifestations, genetic variation, treatments and prognosis of patients with SLC35A2 mutation were summarized. Results:The patients all presented with intractable infantile spasm and global developmental delay, onset in infancy. A variety of antiepileptic treatments had temporary and partial efficacy. Otherwise, proband 2 and 3 presented with abnormal glutamic-pyruvic transaminase and increased platelets. Funduscopy showed dysplasia of the retinal pigment epithelium in both eyes, and they both received D-galactose treatment. A total of 22 relevant case reports, including 99 patients, were collected. The 99 patients all were heterozygous mutations, and a total of 75 different variation sites were reported. The clinical manifestations were characterized by global developmental delay or mental retardation ( n=89), epileptic seizure ( n=75), hypotonia ( n=57), facial deformity ( n=57), skeletal abnormality ( n=50), visual impairment ( n=42), elevated glutamic-pyruvic transaminase ( n=31), gastrointestinal symptoms ( n=28), skin deformity ( n=26), microcephaly ( n=23) and congenital heart disease ( n=12). Craniocerebral magnetic resonance imaging may be normal in the early stage. With age, magnetic resonance imaging may show abnormal white matter signals, brain atrophy, dysplasia of corpus callosum, delayed myelination, enlargement of lateral ventricle, brain stem atrophy and so on. Studies have shown that galactose treatment may be effective. Conclusions:SLC35A2 variants lead to CDG Ⅱm, whose clinical manifestations mainly include epileptic encephalopathy and global developmental delay. Multiple antiepileptic therapies can temporarily or partially control seizures, while oral galactose may improve the clinical symptoms, showing its prospect as a dietary therapy.

Overview of protein posttranslational modifications in Arthropoda venoms

Accidents with venomous animals are a public health issue worldwide. Among the species involved in these accidents are scorpions, spiders, bees, wasps, and other members of the phylum Arthropoda. The knowledge of the function of proteins present in these venoms is important to guide diagnosis, therapeutics, besides being a source of a large variety of biotechnological active molecules. Although our understanding about the characteristics and function of arthropod venoms has been evolving in the last decades, a major aspect crucial for the function of these proteins remains poorly studied, the posttranslational modifications (PTMs). Comprehension of such modifications can contribute to better understanding the basis of envenomation, leading to improvements in the specificities of potential therapeutic toxins. Therefore, in this review, we bring to light protein/toxin PTMs in arthropod venoms by accessing the information present in the UniProtKB/Swiss-Prot database, including experimental and putative inferences. Then, we concentrate our discussion on the current knowledge on protein phosphorylation and glycosylation, highlighting the potential functionality of these modifications in arthropod venom. We also briefly describe general approaches to study "PTM-functional-venomics", herein referred to the integration of PTM-venomics with a functional investigation of PTM impact on venom biology. Furthermore, we discuss the bottlenecks in toxinology studies covering PTM investigation. In conclusion, through the mining of PTMs in arthropod venoms, we observed a large gap in this field that limits our understanding on the biology of these venoms, affecting the diagnosis and therapeutics development. Hence, we encourage community efforts to draw attention to a better understanding of PTM in arthropod venom toxins.(AU)

Correlation between serum IgG N-glycan and Lauren classification of gastric cancer / 中华检验医学杂志

Objective:Analyze the correlation between serum immunoglobulin G (IgG) N-glycan and Lauren classification of gastric cancer.Methods:A retrospective study was performed on 17 patients with diffuse type gastric cancer and 21 patients with intestinal type who received treatment in Zhongshan Hospital from 2017 to 2018, and the general medical history data and disease characteristics were summarized. The serum IgG glycome profiles were analyzed by ultraperformance liquid chromatography, and the difference between intestinal type and diffuse type gastric cance was compared.Logistic regression was used to evaluate the correlation between serum IgG N-glycan and Lauren classification.Results:IgG N-glycome analysis included 27 directly detected glycans and 4 derived traits. H=Hexose, N=N-acetylglucosamine, F=Fucose, S=Sialic acid.There was no significant difference in IgG N-glycan among different chemotherapy protocol. Compared with intestinal type, H3N3F1 ( t=3.785, P=0.001), H3N4( t=3.919, P=0.002), H3N4F1( t=2.770, P=0.005), H3N5F1( t=2.888, P=0.010) were decreased in diffuse type; H4N4F1(6)( t=?3.488, P<0.001), H5N4F1( t=?3.401, P=0.003), H5N5F1( t=?2.303, P=0.023), H5N4F1S1 ( t=?3.068, P=0.008) were increased.H3N3F1( OR:1.20, P=0.008), H3N4( OR:1.32, P=0.005), H3N4F1 ( OR:1.13, P=0.017), H3N5F1 ( OR:1.78, P=0.015), H4N4F1(6)( OR:0.43, P=0.008), H5N4F1(6)( OR:0.74, P=0.008), H5N5F1 ( OR:0.32, P=0.036), H5N4F1S1( OR:0.48, P=0.009) were significantly correlated with Lauren classification. Sialylated ( t=?2.717, P=0.012) and galactosylated ( t=?3.400, P=0.001) IgG N-glycan were reduced in patients with intestinal type gastric cancer.Galactosylated ( OR:0.87, P=0.007) and sialylated ( OR:0.62, P=0.015) IgG N-glycan were significantly correlated with Lauren classification. Conclusion:Some IgG N-glycan are significantly correlated with Lauren classification, which can be used as potential biomarkers.

Establishment of lectin-ELISA for sialylated fetuin-A and its diagnostic value in primary hepatocellular carcinoma / 中华检验医学杂志

Objective:To establish a lectin enzyme-linked immunosorbent assay (lectin-ELISA) for the dection of sialylated fetuin-A and to explore the clinical diagnostic value of sialylated fetuin-A in hepatocellular carcinoma (HCC).Methods:From January 2017 to December 2020, 300 HCC patients and 160 disease controls, including 36 liver cirrhosis subgroups and 124 chronic hepatitis B subgroups, were collected from Shanghai Eastern Hepatobiliary Surgery Hospital. At the same time, 100 healthy subjects were collected as healthy controls. Lectin-ELISA method for detecting sialylated fetuin A was established based on the principle that Sambucus nigra lectin (SNA) can recognize the structure of α-2, 6-linked sialic acid residues. Differences between groups were compared using t-test or analysis of variance. Logistic regression method was used to establish the multi-index joint detection model, and receiver operating characteristic curve (ROC) was used to evaluate the efficacy of single index and joint detection model in the diagnosis of HCC.Results:A lectin-ELISA method for the detection of serum Sia-fetuin A was established. The linear regression coefficient of the system was 0.978 5, and the precision evaluation and interference experiments were in line with the clinical detection requirements. Using this method to detect serum Sia-fetuin A levels in each group, the levels of HCC group, disease control group and healthy control group were 1.362±0.310, 1.199±0.370, 1.086±0.420, respectively, and the three groups decreased in turn. The areas under the curve of Sia-fetuin A, α-fetoprotein, and their combined detection models for differential diagnosis of HCC were 0.790, 0.809, and 0.860, respectively. The diagnostic model had a sensitivity of 79.3% (238/300) and a specificity of 95.0% (247/260). Among the 300 patients in the HCC group, 138 (46%) patients were negative for serum AFP (<20 μg/L), and their serum Sia-fetuin A level was 1.364±0.305. Combining the disease control group and the healthy control group into the non-Cancer group, the serum Sia-fetuin A level was 1.146±0.381. The serum level of Sia-fetuin A in AFP-negative HCC patients was higher than that in non-HCC group ( t=6.134, P<0.001). The areas under the curve of Sia-fetuin A and the combined diagnostic model for the diagnosis of AFP-negative HCC were 0.776 and 0.919, respectively. The combined diagnostic model had a sensitivity of 93.4% (129/138) and a specificity of 77.3% (201/260). Conclusion:Serum Sia-fetuin A and combined determination model can provide a new auxiliary diagnostic index for AFP-negative HCC.

Application of IgG sialylation in the diagnosis and therapy of autoimmune diseases / 中华检验医学杂志

Glycosylation is a part of the structure and function of immunoglobulin G (IgG). Sialic acid is located at the end of IgG N-glycan and regulates IgG anti-inflammatory and pro-inflammatory activities by changing the binding of IgG with fragment crystallizable gamma receptors (FcγRs) and complements. Low IgG sialylation is closely related to the occurrence, development and prognosis of autoimmune diseases and shows great potential in the field of diagnosis, monitoring and treatment, and may function as a new biomarker and therapeutic target for autoimmune diseases.

A potential therapeutic target: platelet glycosylation / 中华检验医学杂志

Platelet surface is rich in glycocalyx. It has been found that platelet glycosylation plays an important role in the physiological hemostasis mechanism, regulating the interaction between platelets and receptor proteins, and dynamically reshaping the surface glycosylation through its own glucose metabolism system. Platelet glycosylation also participates in platelet aging and clearance, and regulates platelet counts. Meanwhile, abnormal platelet glycosylation is closely related to primary immune thrombocytopenia, coronary heart disease and other related diseases, being a potential therapeutic target.

Glycosylation: new era for diseases biomarkers / 中华检验医学杂志

Glycosylation is one of the most important posttranslational modification (PTM) for proteins. Glycans of glycoproteins play pivotal effects in cell recognition, signal transduction, differentiation, proliferation and immigration. The sialylation, fucosylation and degree of branching are intimately related to the development and progression of various malignancies and autoimmune diseases. Both glycans as well as glycoprotein have become the hot targets for disease biomarker exploration and therapeutic interventions.

Progress in biological function and application of bacterial protein glycosylation / 中华微生物学和免疫学杂志

Bacteria play an important role in human health and disease. Their biological functions are often related to the glycans attached to the protein surface. In recent years, the glycosylation modification of bacterial proteins has attracted increasingly widespread attention. With the continuous development of synthetic biology and the in-depth research on glycosylation modification systems, some modification systems have been applied in engineered bacteria to play the role of protein modification independently, making it possible to "customized glycoproteins" . This paper reviewed the current status of research on the basic components, types and pathways of bacterial protein glycosylation modification as well as the biological function and application.

Congenital disorder of glycosylation caused by de novo variant of SLC35A2 gene: a case report / 中华神经科杂志

Congenital disorder of glycosylation (CDG) is a group of genetic metabolic diseases involving multiple organs. A case of CDG caused by SLC35A2 gene mutation was diagnosed. The clinical characteristics included spasms, developmental retardation and multiple malformations. Video-electroencephalogram showed dysrhythmia. A de novo heterozygous missense mutation of SLC35A2 gene was detected by whole exome sequencing: c.844G>A (p.Gly282Arg). It was predicted to be likely pathogenic according to American College of Medical Genetics and Genomics guidelines which had not been reported in China.

A multicenter study of the correlation between advanced glycation end products in the lens and type 2 diabetes / 中华健康管理学杂志

Objective:To investigate the relationship between advanced glycation end products (AGEs) in the lens and type 2 diabetes mellitus.Methods:226 subjects were recruited between August 14 to September 14, 2018 from the Endocrinology Department of Central South University Xiangya Hospital, the Third Hospital of Changsha City, and the Fourth Hospital of Changsha City. The OGTT test, combined with clinical indicators, were used as the gold standard. Subjects were screened for type 2 diabetes using both the lens AGE fluorescence assay and the gold standard. Drawing the receiver operating characteristic (ROC) curve, we calculated the area under the curve (AUC) and its 95% CI and calculated the AGE for the diagnosis of type 2 diabetes. Sensitivity, specificity, Youden index, Kappa value, and its 95% CI, and the optimal cut-off value were determined according to the Youden index. Taking diabetes as the outcome indicator and AGE as the binary indicator, three logistic regression models were constructed. Stratified by age and sub-center, the differences between fasting blood glucose and 2 h postprandial blood glucose were compared between the AGE-negative and AGE-positive groups to determine the relationship between AGE and diabetes. Results:The area under the ROC curve was 0.86(95% CI: 0.81-0.91). According to the Youden index, the optimal cut-off point for AGE was 0.24. At this time, the sensitivity was 82.86(95% CI: 77.81-87.91), the specificity was 77.06(95% CI: 71.43-82.7), the Youden index was 59.92(95% CI: 53.36-66.49), the Kappa value was 79.62(95% CI: 74.22-85.02). Except for the 20-39-year-old group, the fasting blood glucose and 2 h postprandial blood glucose of the AGE-positive group in different age groups, different sub-centers, and the general population were higher than those of the AGE-negative group (all P<0.05). After adjusting for the confounding effects of age, gender, and sub-center (model 3), the relative risk of diabetes in the AGE-positive group was 11.75 times higher than the AGE-negative group (95% CI: 5.61-24.60), all with P<0.001. Conclusion:There was a high correlation between AGE in the lens and the risk of type 2 diabetes. When the cut-off point of AGE is 0.24, it had high sensitivity and specificity and could be used as a practical tool for early screening of type 2 diabetes.

CAR T cells redirected against tumor-specific antigen glycoforms: can low-sugar antigens guarantee a sweet success? / 医学前沿

Immune-based therapies have experienced a pronounced breakthrough in the past decades as they acquired multiple US Food and Drug Administration (FDA) approvals for various indications. To date, six chimeric antigen receptor T cell (CAR-T) therapies have been permitted for the treatment of certain patients with relapsed/refractory hematologic malignancies. However, several clinical trials of solid tumor CAR-T therapies were prematurely terminated, or they reported life-threatening treatment-related damages to healthy tissues. The simultaneous expression of target antigens by healthy organs and tumor cells is partly responsible for such toxicities. Alongside targeting tumor-specific antigens, targeting the aberrantly glycosylated glycoforms of tumor-associated antigens can also minimize the off-tumor effects of CAR-T therapies. Tn, T, and sialyl-Tn antigens have been reported to be involved in tumor progression and metastasis, and their expression results from the dysregulation of a series of glycosyltransferases and the endoplasmic reticulum protein chaperone, Cosmc. Moreover, these glycoforms have been associated with various types of cancers, including prostate, breast, colon, gastric, and lung cancers. Here, we discuss how underglycosylated antigens emerge and then detail the latest advances in the development of CAR-T-based immunotherapies that target some of such antigens.

Correlation between proteoglycan and alveolar bone resorption in a mouse periodontitis model / 口腔疾病防治

Objective@#To analyze changes in proteoglycan and its correlation with alveolar bone resorption in periodontitis. @*Methods @#Twelve eight-week-old C57BL/6J male mice were selected, and the periodontitis model was established by ligating the right maxillary second molar with 6-0 silk thread. The nonligated part of the left maxilla was used as the control. The mice were killed 14 days after the operation. Micro-CT was used to assess alveolar bone resorption. HE staining was used to observe the alveolar bone profile, and TRAP staining was conducted to examine the positive rate of osteoclasts. The expression of proteoglycan-related genes, such as aggrecan (ACAN), biglycan (BGN), versican (VCAN), decorin (DCN), osteoclast-related genes, such as cathepsin K (CTSK), matrix metalloprotein-9 (MMP-9), and receptor activator of nuclear factor kappa-B ligand (RANKL), and inflammation-related genes, such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), was detected by real-time quantitative PCR. Additionally, the correlation of the expression of proteoglycans with osteoclast-related genes and inflammation-related genes was evaluated by Pearson correlation analysis.@* Results@#The resorption of alveolar bone on the periodontitis side increased. TRAP staining showed that the number of osteoclasts was substantially increased in the maxilla with periodontitis. Real-time quantitative PCR demonstrated that compared with the control side, the expression of proteoglycan-related genes, such as ACAN, BGN, and DCN, was decreased, whereas the expression of the VCAN gene was significantly increased in the periodontitis side. Meanwhile, the expression of osteoclast-related genes, such as CTSK, MMP-9, and RANKL, and inflammation-related genes, such as IL-1β, IL-6, and TNF-α, was markedly increased in the periodontitis side (P<0.05). Pearson correlation analysis indicated a negative correlation between the expression of proteoglycans and the mRNA levels of osteoclast-related genes and inflammation-related genes (P<0.05). @*Conclusion @#The expression of proteoglycan was closely related to alveolar bone resorption in a periodontitis model.