SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Qiao Lichun) "

Sökning: WFRF:(Qiao Lichun)

  • Resultat 1-5 av 5
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Deng, Huan, et al. (författare)
  • Altered Expression of the Hedgehog Pathway Proteins BMP2, BMP4, SHH, and IHH Involved in Knee Cartilage Damage of Patients With Osteoarthritis and Kashin-Beck Disease
  • 2022
  • Ingår i: Cartilage. - : Sage Publications. - 1947-6035 .- 1947-6043. ; 13:1
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate the expression of Hedgehog (HH) signaling pathway proteins in knee articular cartilage from Kashin-Beck disease (KBD) and osteoarthritis (OA) patients.METHODS: Knee articular cartilage samples were collected from normal (N), OA, and KBD adults (aged 38-60 years) and divided into 3 groups with 6 subjects in each group. The localization of the HH pathway proteins bone morphogenetic protein 2 (BMP2), bone morphogenetic protein 4 (BMP4), Sonic hedgehog (SHH), and Indian hedgehog (IHH) was observed with the microscope after immunohistochemical (IHC) staining. Positive staining cell rates of each proteins were compared.RESULTS: The strongest stainings of all proteins were observed in the middle zones of all 3 groups. The positive staining rates of BMP4 and IHH were significantly lower in the OA and KBD groups than those in the N group in all 3 zones. The positive staining rates of BMP2 and SHH tend to be lower in the OA and KBD groups than those in the N group in the deep zone, while higher in the OA and KBD groups than those in the N group in superficial and middle zones.CONCLUSIONS: Altered expression of the HH pathway proteins BMP2, BMP4, SHH, and IHH was found in OA and KBD articular cartilage. There seemed to be a compensatory effect between SHH and IHH in cartilage damage. Further studies on the pathogenesis of OA and KBD may be carried out from these aspects in the future.
  •  
2.
  • Han, Jing, et al. (författare)
  • Identification of N-glycoproteins of knee cartilage from adult osteoarthritis and Kashin-Beck disease based on quantitative glycoproteomics, compared with normal control cartilage
  • 2022
  • Ingår i: Cells. - : MDPI. - 2073-4409. ; 11:16, s. 2513-2513
  • Tidskriftsartikel (refereegranskat)abstract
    • Glycoproteins are involved in the development of many diseases, while the type and content of N-glycoproteins in the cartilage of osteoarthritis (OA) and Kashin-Beck disease (KBD) are still unclear. This research aims to identify N-glycoproteins in knee cartilage patients with OA and KBD compared with normal control (N) adults. The cartilage samples were collected from gender- and age-matched OA (n = 9), KBD (n = 9) patients, and N (n = 9) adults. Glycoproteomics and label-free liquid chromatography-tandem mass spectrometry (LC-MS/MS) obtained N-glycoproteins of KBD and OA. A total of 594 N-glycoproteins and 1146 N-glycosylation peptides were identified. The identified data were further compared and analyzed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Protein-Protein Interactions (PPI). Pairwise comparison of the glycoproteins detected in the three groups showed that integrin beta-1 (ITGB1), collagen alpha-1 (II) chain (COL2A1), collagen alpha-1 (VII) chain (COL7A1), carbohydrate sulfotransferase 3 (CHST-3), carbohydrate sulfotransferase 4 (CHST-4), thrombospondin 2 (THBS2), bone morphogenetic protein 8A (BMP8A), tenascin-C (TNC), lysosome-associated membrane protein (LAMP2), and beta-glucuronidase (GUSB) were significantly differentially expressed. GO results suggested N-glycoproteins mainly belonged to protein metabolic process, single-multicellular and multicellular organism process, cell adhesion, biological adhesion, and multicellular organism development. KEGG and PPI results revealed that key N-glycoproteins were closely related to pathways for OA and KBD, such as phagosome, ECM-receptor interaction, lysosome, focal adhesion, protein digestion, and absorption. These results reflected glycoprotein expression for OA and KBD in the process of ECM degradation, material transport, cell-cell or cell-ECM interaction, and information transduction. These key significantly differentially expressed N-glycoproteins and pathways lead to the degeneration and degradation of the cartilage of OA and KBD mainly by disrupting the synthesis and catabolism of basic components of ECM and chondrocytes and interfering with the transfer of material or information. The key N-glycoproteins or pathways in this research are potential targets for pathological mechanisms and therapies of OA and KBD.
  •  
3.
  • Han, Jing, et al. (författare)
  • Nano-elemental selenium particle developed via supramolecularself-assembly of chondroitin sulfate A and Na2SeO3 to repaircartilage lesions
  • 2023
  • Ingår i: Carbohydrate Polymers. - : Elsevier. - 0144-8617 .- 1879-1344. ; 316
  • Tidskriftsartikel (refereegranskat)abstract
    • Cartilage repair is a significant clinical issue due to its restricted ability to regenerate and self-heal after cartilage lesions or degenerative disease. Herein, a nano-elemental selenium particle (chondroitin sulfate A‑selenium nanoparticle, CSA-SeNP) is developed by the supramolecular self-assembly of Na2SeO3 and negatively charged chondroitin sulfate A (CSA) via electrostatic interactions or hydrogen bonds followed by in-situ reducing of l-ascorbic acid for cartilage lesions repair. The constructed micelle exhibits a hydrodynamic particle size of 171.50 ± 2.40 nm and an exceptionally high selenium loading capacity (9.05 ± 0.03 %) and can promote chondrocyte proliferation, increase cartilage thickness, and improve the ultrastructure of chondrocytes and organelles. It mainly enhances the sulfation modification of chondroitin sulfate by up-regulating the expression of chondroitin sulfate 4-O sulfotransferase-1, −2, −3, which in turn promotes the expression of aggrecan to repair articular and epiphyseal-plate cartilage lesions. The micelles combine the bio-activity of CSA with selenium nanoparticles (SeNPs), which are less toxic than Na2SeO3, and low doses of CSA-SeNP are even superior to inorganic selenium in repairing cartilage lesions in rats. Thus, the developed CSA-SeNP is anticipated to be a promising selenium supplementation preparation in clinical application to address the difficulty of healing cartilage lesions with outstanding repair effects.
  •  
4.
  • Lyu, Yizhen, et al. (författare)
  • Identification of proteins and N-glycosylation sites of knee cartilage in Kashin-Beck Disease compared with osteoarthritis
  • 2022
  • Ingår i: International Journal of Biological Macromolecules. - : Elsevier. - 0141-8130 .- 1879-0003. ; 210, s. 128-138
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to identify crucial proteins and N-glycosylated sites in the pathological mechanism of Kashin-Beck Disease (KBD) compared with osteoarthritis (OA). Nine KBD knee subjects and nine OA knee subjects were selected for the study. Quantitative proteomics and N-glycoproteomics data of KBD and OA were obtained by protein and N-glycoprotein enrichment and LC-MS/MS analysis. Differentially expressed proteins or N-glycosylation sites were examined with a comparative analysis between KBD and OA. Total 2205 proteins were identified in proteomic analysis, of which 375 were significantly different. Among these, 121 proteins were up-regulated and 254 were down-regulated. In N-glycoproteomic analysis, 278 different N-glycosylated sites that were related to 187 N-glycoproteins were identified. Proteins and their N-glycosylated sites are associated with KBD pathological process including ITGB1, LRP1, ANO6, COL1A1, MXRA5, DPP4, and CSPG4. CRLF1 and GLG1 are proposed to associate with both KBD and OA pathological processes. Key pathways in KBD vs. OA proteomic and N-glycoproteomic analysis contained extracellular matrix receptor interaction, focal adhesion, phagosome, protein digestion, and absorption. N-glycosylation may influence the pathological process by affecting the integrity of chondrocytes or cartilage. It regulated the intercellular signal transduction pathway, which contributes to cartilage destruction in KBD.
  •  
5.
  • Xiao, Xiang, et al. (författare)
  • Chondroitin Sulfate and Hyaluronic Acid Perfusion for Interstitial Cystitis/Bladder Pain Syndrome : A Systematic Review and Meta-Analysis
  • 2021
  • Ingår i: Science Insights. - : Insights Publisher. - 2372-8191 .- 2329-5856. ; 39:4, s. 361-373
  • Forskningsöversikt (refereegranskat)abstract
    • Currently, no suitable delivery methods are available for the drugs to interstitial cystitis/ bladder pain syndrome (IC/BPS). Herein we systematically evaluated the therapeutic effects of intravesical infusion of hyaluronic acid (HA) and chondroitin sulfate (CS) in patients with IC/BPS. This study includes randomized controlled trials (RCT) and self-controlled studies of IC/BPS patients treated with HA, CS, or both. English databases like PubMed, Cochrane Library, Embase, and Medline were searched until up to January 31, 2021. Information was extracted based on the inclusion and exclusion criteria, and then meta-analysis was performed. Sixteen studies including 491 patients were included and analyzed. The responsive rate of treatment was 91.24%. In 3 RCTs, the analogue scale (VAS) for pain on fix-effect model was [mean difference, MD -0.57 (95%CI, -1.55, -0.41)]. A significant improvement on random-effect model was [MD -2.78 (95%CI, -3.48, -2.07)] in 13 self-controlled studies. Outcomes on O’Leary-Sant Interstitial Cystitis Symptom Index, Problem Index, frequency, urgency, and bladder capacity were also significantly improved. Subgroup analysis showed significant difference between HA, CS, and the combination, and the perfusion of HA was more effective (Z = 29.97, P < 0.01). Also, different follow-up times after last treatment showed significant difference (Z = 7.69, P < 0.01). It can be beneficial for IC/BPS patients who have not responded to conventional treatments.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-5 av 5

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy