Abstract
Background/aim We aimed to explore the roles of glycoprotein glycosylation in the pathogenesis of Kashin–Beck disease (KBD), and evaluated the effectiveness of sodium hyaluronate treatment. Materials and methods Blood and saliva were collected from KBD patients before and after the injection of sodium hyaluronate. Normal healthy subjects were included as controls. Saliva and serum lectin microarrays and saliva and serum microarray verifications were used to screen and confirm the differences in lectin levels among the three groups. Results In saliva lectin microarray, bindings to Sophora japonica agglutinin (SJA), Griffonia (Bandeiraea) simplicifolia lectin I (GSL-I), Euonymus europaeus lectin (EEL), Maackia amurensis lectin II (MAL-II), Sambucus nigra lectin (SNA), Hippeastrum hybrid lectin (HHL), and Aleuria aurantia lectin (AAL) were higher in the untreated KBD patients than in the control group. Increased levels of HHL, MAL-II, and GSL-I in the untreated KBD patients discriminated them in particular from the treated ones. Jacalin was lower in the untreated KBD patients compared to the treated KBD and control groups. In serum lectin microarray, HHL and peanut agglutinin (PNA) were increased in the untreated KBD group in comparison to the control one. AAL, Phaseolus vulgaris agglutinin (E+L) (PHA-E+L), and Psophocarpus tetragonolobus lectin I (PTL-I) were lower in the untreated KBD patients compared to the treated KBD and control groups. Hyaluronate treatment appeared to normalize SNA, AAL, and MAL-II levels in saliva, and HHL, PNA, AAL, PTL-I, and PHA-E+L levels in serum. Saliva reversed microarray verification confirmed significant differences between the groups in SNA and Jacalin, in particular for GSL-I levels, while serum reversed microarray verification indicated that HHL, PNA, and AAL levels returned to normal levels after the hyaluronate treatment. Lectin blot confirmed significant differences in HHL, AAL, and Jacalin in saliva, and HHL, PNA, PHA-E+L, and AAL in serum. Conclusion HHL in saliva and serum may be a valuable diagnostic biomarker of KBD, and it may be used as follow-up for the hyaluronate treatment.
Highlights
Kashin–Beck disease (KBD) is an endemic osteoarthritis, which is characterized by chondrocyte necrosis and apoptosis, cartilage degeneration, and extracellular matrix degradation
Jacalin was lower in the untreated KBD patients compared to the treated KBD and control groups
aurantia lectin (AAL), Phaseolus vulgaris agglutinin (E+L) (PHAE+L), and Psophocarpus tetragonolobus lectin I (PTL-I) were lower in the untreated KBD patients compared to the treated KBD and control groups
Summary
Kashin–Beck disease (KBD) is an endemic osteoarthritis, which is characterized by chondrocyte necrosis and apoptosis, cartilage degeneration, and extracellular matrix degradation. It is endemic in a crescent-shaped area extending from southeastern Siberia to northeastern and southwestern China. The capacity for hyaluronate synthesis is decreased in chondrocytes from patients with KBD. Exogenous hyaluronate increases its synthesis in chondrocytes, which provides the foundation for the theory that the KBD patient should be treated with an intraarticular injection of hyaluronate. Compared with the normal control group, IL1β and TNF-α levels were higher in the KBD group, while their expression levels decreased after administration of hyaluronate [2].
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