Sjogren's syndrome (SS) is a common autoimmune disorder that primarily targets exocrine glands, leading to hallmark manifestations of xerostomia and xerophthalmia, with potential progression to multisystem involvement. The rapid advances in omics technologies-including metabolomics, proteomics, and transcriptomics-have yielded substantial insights into SS pathophysiology. This review consolidates current evidence on omics-derived biomarkers in SS. Studies consistently implicate aberrant glucose metabolism, neutrophil-derived enzyme activity, mitochondrial bioenergetic impairment, ferroptosis, and apoptotic pathways as central to SS development. These findings refine our understanding of disease mechanisms and the heterogeneity of therapeutic responses. Hydroxyproline has emerged as a candidate marker for distinguishing SS from IgG4-related disease, whereas distinct cytokine and chemokine signatures may enable earlier diagnosis. Genomic analyses demonstrate a robust association between expression of the rs11797 locus and SS-related lymphomagenesis, and several genes controlling DNA methylation represent promising therapeutic targets. Collectively, these findings lay the groundwork for personalized risk stratification and intervention in SS. The review concludes by summarizing existing progress and outlining priorities for future omics-based investigations.
Humans ; Sjogren's Syndrome/diagnosis* ; Biomarkers/analysis* ; Metabolomics/methods* ; Proteomics/methods* ; Genomics ; Multiomics

Objective:To explore the effect and possible mechanism of Semen euryales mixture(QSHJ)on renal injury in lu-pus nephritis.Methods:The 14-week-old C57BL/6 mice were the control group of 8.The 14-week-old MRL/lpr mice were randomly di-vided into model group,QSHJ low,medium and high doses groups(7.48,14.95,29.90 g/kg),and prednisone group(5 mg/kg)of 8 mice each.The control group and the model group were given the same volume of normal saline by gavage once a day for 4 weeks.Urine was collected to detect urinary protein content.HE and PASM staining were used to observe renal tissue injury.The serum levels of Anti-dsDNA,IL-6 and TNF-α were detected by ELISA.The protein expressions of phosphatidylinositol 3-kinase(PI3K),phosphor-ylated PI3K(p-PI3K),protein kinase B(AKT),phosphorylated AKT(p-AKT),nuclear factor kappa B p65(NF-κB p65)and phos-phorylated NF-κB p65(p-NF-κB p65)were detected by Western blot.The protein expressions of PI3K,p-PI3K,AKT and p-AKT were detected by immunohistochemistry.The positive expression of NF-κB p65 was observed by immunofluorescence.Results:Com-pared with the control group,the urinary protein content in the model group increased significantly(P<0.05),the renal tissue was in-filtrated with inflammatory cells,and the tissue structure was destroyed obviously,the contents of Anti-dsDNA,IL-6 and TNF-α in se-rum were significantly increased(P<0.05),the expressions of p-PI3K/PI3K,p-AKT/AKT and p-NF-κB p65/NF-κB p65 were signifi-cantly increased(P<0.05),the protein expressions of p-PI3K and p-AKT were increased significantly(P<0.05),the positive expres-sion of NF-κB p65 was increased significantly.Compared with the model group,the urinary protein content of QSHJ low,medium and high doses groups and prednisone group decreased significantly(P<0.05),the infiltration of inflammatory cells in renal tissue was re-lieved,and the damage of tissue structure was alleviated.the contents of Anti-dsDNA,IL-6 and TNF-α in serum were significantly de-creased(P<0.05),the expressions of p-PI3K/PI3K,p-AKT/AKT and p-NF-κB p65/NF-κB p65 were significantly decreased(P<0.05),the protein expressions of p-PI3K and p-AKT were significantly decreased(P<0.05),the positive expression of NF-κB p65 flu-orescence was decreased.Conclusion:QSHJ can improve the pathological manifestations of renal tissue in MRL/lpr mice and alleviate the disease process.The mechanism may be related to the inhibition of PI3K-AKT/NF-κB signaling pathway in renal tissue and the re-duction of inflammatory response by QSHJ.

Sj?gren's syndrome(SS)is one of the common rheumatic diseases in clinical practice.Modern medicine commonly uses drugs such as artificial tears,saliva,glucocorticoids,immunosuppressants,and biologics to control the condition.Clinical practice has shown that in addition to modern medical basic treatment,the use of traditional Chinese medicine(TCM)can help improve the clinical efficacy of SS.According to the symptoms and signs of Sj?gren's syndrome in TCM,it is classified as"dryness and obstruction",and the core pathogenesis of the disease is spleen deficiency and deficiency of body fluids.Subsequently,toxic and pathogenic factors gather,leading to the decline of internal organs.The initial causes are spleen damage,unstable barrier,and invasion of pathogenic factors.The core link is spleen dysfunction,insufficient body fluid,and dryness arising from it.Spleen deficiency generates evil,obstruction of qi,and lack of body fluids are the root causes of illness.The main treatment method is the"spleen strengthening method",which treats spleen deficiency,dampness and stagnation,and the body fluid is not distributed.The treatment focuses on strengthening the spleen and qi,supplementing the lungs and generating fluids.Spleen deficiency leads to loss of vitality,blood stasis obstructs blood vessels,and the treatment is to strengthen the spleen,soothe the liver,remove blood stasis,and unblock the orifices.The spleen yang is not vigorous,and qi transformation is impaired.The treatment is to invigorate the spleen and warm the stomach,promote yang circulation,and promote diuresis.

Sj?gren's syndrome(SS)is one of the common rheumatic diseases in clinical practice.Modern medicine commonly uses drugs such as artificial tears,saliva,glucocorticoids,immunosuppressants,and biologics to control the condition.Clinical practice has shown that in addition to modern medical basic treatment,the use of traditional Chinese medicine(TCM)can help improve the clinical efficacy of SS.According to the symptoms and signs of Sj?gren's syndrome in TCM,it is classified as"dryness and obstruction",and the core pathogenesis of the disease is spleen deficiency and deficiency of body fluids.Subsequently,toxic and pathogenic factors gather,leading to the decline of internal organs.The initial causes are spleen damage,unstable barrier,and invasion of pathogenic factors.The core link is spleen dysfunction,insufficient body fluid,and dryness arising from it.Spleen deficiency generates evil,obstruction of qi,and lack of body fluids are the root causes of illness.The main treatment method is the"spleen strengthening method",which treats spleen deficiency,dampness and stagnation,and the body fluid is not distributed.The treatment focuses on strengthening the spleen and qi,supplementing the lungs and generating fluids.Spleen deficiency leads to loss of vitality,blood stasis obstructs blood vessels,and the treatment is to strengthen the spleen,soothe the liver,remove blood stasis,and unblock the orifices.The spleen yang is not vigorous,and qi transformation is impaired.The treatment is to invigorate the spleen and warm the stomach,promote yang circulation,and promote diuresis.

Objective:To explore the effect and possible mechanism of Semen euryales mixture(QSHJ)on renal injury in lu-pus nephritis.Methods:The 14-week-old C57BL/6 mice were the control group of 8.The 14-week-old MRL/lpr mice were randomly di-vided into model group,QSHJ low,medium and high doses groups(7.48,14.95,29.90 g/kg),and prednisone group(5 mg/kg)of 8 mice each.The control group and the model group were given the same volume of normal saline by gavage once a day for 4 weeks.Urine was collected to detect urinary protein content.HE and PASM staining were used to observe renal tissue injury.The serum levels of Anti-dsDNA,IL-6 and TNF-α were detected by ELISA.The protein expressions of phosphatidylinositol 3-kinase(PI3K),phosphor-ylated PI3K(p-PI3K),protein kinase B(AKT),phosphorylated AKT(p-AKT),nuclear factor kappa B p65(NF-κB p65)and phos-phorylated NF-κB p65(p-NF-κB p65)were detected by Western blot.The protein expressions of PI3K,p-PI3K,AKT and p-AKT were detected by immunohistochemistry.The positive expression of NF-κB p65 was observed by immunofluorescence.Results:Com-pared with the control group,the urinary protein content in the model group increased significantly(P<0.05),the renal tissue was in-filtrated with inflammatory cells,and the tissue structure was destroyed obviously,the contents of Anti-dsDNA,IL-6 and TNF-α in se-rum were significantly increased(P<0.05),the expressions of p-PI3K/PI3K,p-AKT/AKT and p-NF-κB p65/NF-κB p65 were signifi-cantly increased(P<0.05),the protein expressions of p-PI3K and p-AKT were increased significantly(P<0.05),the positive expres-sion of NF-κB p65 was increased significantly.Compared with the model group,the urinary protein content of QSHJ low,medium and high doses groups and prednisone group decreased significantly(P<0.05),the infiltration of inflammatory cells in renal tissue was re-lieved,and the damage of tissue structure was alleviated.the contents of Anti-dsDNA,IL-6 and TNF-α in serum were significantly de-creased(P<0.05),the expressions of p-PI3K/PI3K,p-AKT/AKT and p-NF-κB p65/NF-κB p65 were significantly decreased(P<0.05),the protein expressions of p-PI3K and p-AKT were significantly decreased(P<0.05),the positive expression of NF-κB p65 flu-orescence was decreased.Conclusion:QSHJ can improve the pathological manifestations of renal tissue in MRL/lpr mice and alleviate the disease process.The mechanism may be related to the inhibition of PI3K-AKT/NF-κB signaling pathway in renal tissue and the re-duction of inflammatory response by QSHJ.

Objective To explore the effect and possible pharmacological mechanism of Bufei Tongbi Decoction in the treatment of systemic lupus erythematosus interstitial lung disease (SLE-ILD).Methods The effective components and related targets of Bufei Tongbi Decoction were obtained using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and Uniprot database. Key genes for SLE-ILD were screened based on DrugBank,DisGeNET,GeneCards,PharmGKB,OMIM,and GEO databases. Using Cytoscape software,a drug active ingredient-target-disease relationship network diagram was constructed to obtain the effective active ingredients and possible mechanisms of action of Bufei Tongbi Decoction in the treatment of SLE-ILD. Gene ontology (GO) function enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were used to reveal related target genes and pathway functions. Taking C57BL/6 mice as normal group,MRL/lpr mice were injected with bleomycin 5mg/kg in the nasal cavity. According to the random number table method,the mice were divided into model group,Bufei Tongbi Decoction low-dose group (10.4 g/(kg·d)),Bufei Tongbi Decoction medium-dose group (20.8 g/(kg·d)),Bufei Tongbi Decoction high-dose group (41.6 g/(kg·d)) and prednisone group (3 mg/(kg·d)). The intervention lasted for 28 days. Hematein eosin and Masson staining were used to observe the pathological changes of mouse lung tissue,the expressions of transforming growth factor-β1 (TGF-β1) and collagen type Ⅲ (Col-Ⅲ) in lung tissue were detected by immunohistochemistry,and the expressions of interleukin-1β(IL-1β),interleukin-10 (IL-10) and interleukin-17 (IL-17) in serum were detected by ELISA. The mRNA expressions of matrix metallopeptidase 1(MMP-1),hypoxia inducible factor-1α(HIF-1α),retinoid-related orphan receptor γt (RORγt ) and forkhead box P3 (FOXP3) in lung tissue were analyzed by RT-PCR,the protein expressions of HIF-1α and MMP-1 in lung tissue were detected by Western blotting,and the expressions of T helper 17 cells (Th17) and regulatory T cells (Treg cells) in blood were detected by cytometry.Results A total of 163 effective ingredients,259 targets,1729 SLE-ILD disease targets,958 SLE-ILD differential genes and 40 drug-disease interaction targets were obtained by screening. GO functional enrichment and KEGG pathway enrichment showed that IL-17 signaling pathway activated by IL-1β and MMP-1,and Th17 cell differentiation activated by IL-1β and HIF-1α were the main pathways. Animal experiments showed that Bufei Tongbi Decoction could effectively improve the degree of lung interstitial lesion and reduce the expressions of TGF-β1 and Col-Ⅲ in SLE-ILD mice (P<0.01). The expressions of IL-1β,HIF-1α and IL-17 were decreased (P<0.01). Medium and high doses of Bufei Tongbi Decoction decreased the expressions of MMP-1 and RORγt mRNA (P<0.01),and increased the expressions of IL-10 and FOXP3 mRNA (P<0.01). Bufei Tongbi Decoction could reduce the proportion of Th17 cells,increase the proportion of Treg cells,downregulate the balance of Th17/Treg (P<0.05),and improve the immune disorder. Conclusion Bufei Tongbi Decoction has the characteristics of multi-target and multi-pathway in treating SLE-ILD,and its mechanism may be related to the regulation of Th17/Treg cell balance.

Blocking the programmed death-ligand 1 (PD-L1) on tumor cells with monoclonal antibody therapy has emerged as powerful weapon in cancer immunotherapy. However, only a minority of patients presented immune responses in clinical trials. To develop an alternative treatment method based on immune checkpoint blockade, we designed a novel and efficient CRISPR-Cas9 genome editing system delivered by cationic copolymer aPBAE to downregulate PD-L1 expression on tumor cells specifically knocking out Cyclin-dependent kinase 5 () gene . The expression of PD-L1 on tumor cells was significantly attenuated by knocking out , leading to effective tumor growth inhibition in murine melanoma and lung metastasis suppression in triple-negative breast cancer. Importantly, we demonstrated that aPBAE/Cas9-Cdk5 treatment elicited strong T cell-mediated immune responses in tumor microenvironment that the population of CD8 T cells was significantly increased while regulatory T cells (Tregs) was decreased. It may be the first case to exhibit direct PD-L1 downregulation CRISPR-Cas9 genome editing technology for cancer therapy. It will provide promising strategy for preclinical antitumor treatment through the combination of nanotechnology and genome engineering.

[Objective]To investigate the efficacy of total hip arthroplasty(THA)on the treatment of traumatic arthritis that caused by internal fixation failures of intertrochanteric fractures.[Methods]During January 2009 and March 2016,35 cases of trau?matic arthritis(male:18 cases;female17 cases;49 ~ 86 years old,with an average age of 68.5 years)caused by internal fixation failures or malunion of intertrochanteric fractures,were undergo THA. Among 35 cases,13 cases were performed with the proximal femoral fixation stems,10 cases were with distal fixation stems,and 12 cases were with extended stems.[Results]With 3~65 months follow-up,the hip joint HSS score was elevated from 44.1(31 ~ 65)preoperative to 82.5(58 ~ 94)postoperative without obvious loosening. No postoperative deep infectionwas found. The femoral stems in 2 cases were found to sink 5 mm and 10 mm,respectively. No obvious prosthesis loosening was found. Taken together ,the satisfaction rate of THA on the joint function of traumatic arthritis was 91.4%.[Conclusion]Total hip arthroplasty is recommended as an effective approach for treating traumatic arthritis caused by internal fixation failures of intertrochanteric fractures. Distal fixed prosthesis was recommended due to bone sclerosis or defects of proximal femur. Coupled with emphasis on reconstruction of the greater trochanter ,good therapeutic effects could be achieved.