The urinary levels of CTX-II, C2C, PYD, and Helix-II increased among adults with KBD: a cross-sectional study.

BACKGROUND: Kashin-Beck disease (KBD) is an endemic osteoarthropathy, and its pathogenesis is still not entirely clear. Pathologically, many KBD changes are similar to those of osteoarthritis (OA). Therefore, this study aimed to identify changes in the levels of potential urinary biomarkers for OA, including C-telopeptide of type II collagen (uCTX-II), type II collagen cleavage neoepitope (uC2C), pyridinoline (uPYD), and uHelix-II, among adults with KBD. METHODS: Urinary samples of 83 external control (EC) subjects, 91 KBD patients, and 86 internal control (IC) subjects were tested by ELISA after the subjects completed a questionnaire and X-ray examination. RESULTS: The medians of the four markers in the KBD group were higher than those in the EC group and those in the IC group. The medians in the grade II KBD group were higher than those in the grade I group but were not statistically significant (P = 0.301, P = 0.408, P = 0.204, and P = 0.898 for uCTX-II, uC2C, uPYD, and uHelix-II, respectively). The area under the curve (AUC) of uCTX-II (0.775) was higher than that of the others (0.672, 0.639, and 0.628 for uC2C, uPYD, and uHelix-II, respectively). CONCLUSION: The levels of uCTX-II, uC2C, uPYD, and uHelix-II were elevated in adults with KBD and showed an increasing trend as the severity of KBD increased. The prediction accuracy of uCTX-II was more useful than that of the others for assisting in the diagnosis of KBD.

ClC-7/Ostm1 contribute to the ability of tea polyphenols to maintain bone homeostasis in C57BL/6 mice, protecting against fluorosis.

Epidemiological investigations indicate that certain ingredients in tea bricks can antagonize the adverse effects of fluoride. Tea polyphenols (TPs), the most bioactive ingredient in tea bricks, have been demonstrated to be potent bone-supporting agents. ClC­7 is known to be crucial for osteoclast (OC) bone resorption. Thus, in this study, we investigated the potential protective effects of TPs against fluorosis using a mouse model and explored the underlying mechanisms with particular focus on ClC­7. A total of 40, healthy, 3­week­old male C57BL/6 mice were randomly divided into 4 groups (n=10/group) by weight as follows: distilled water (control group), 100 mg/l fluoridated water (F group), water containing 10 g/l TPs (TP group) and water containing 100 mg/l fluoride and 10 g/l TPs (F + TP group). After 15 weeks, and after the mice were sacrificed, the long bones were removed and bone marrow-derived macrophages were cultured ex vivo in order to perform several experiments. OCs were identified and counted by tartrate­resistant acid phosphatase (TRAP) staining. The consumption of fluoride resulted in severe fluorosis and in an impaired OC function [impaired bone resorption, and a low mRNA expression of nuclear factor of activated T-cells 1 (NFATc1), ATPase H+ transporting V0 subunit D2 (ATP6v0d2) and osteopetrosis­associated transmembrane protein 1 (Ostm1)]. In the F + TP group, fluorosis was attenuated and OC function was restored, but not the high bone fluoride content. Compared with the F group, mature OCs in the F + TP group expressed higher mRNA levels of ClC­7 and Ostm1; the transportation and retaining of Cl­ was improved, as shown by the fluorescence intensity experiment. On the whole, our findings indicate that TPs mitigate fluorosis in C57BL/6 mice by regulating OC bone resorption. Fluoride inhibits OC resorption by inhibiting ClC­7 and Ostm1, whereas TPs attenuate this inhibitory effect of fluoride.

[Inhibitory effect of antisense oligonucleotide of integrin-linked kinase on cell proliferation of human epithelial ovarian cancer].

OBJECTIVE: To explore the inhibitory effect of integrin-linked kinase antisense oligonucleotide (ILK-ASODN) on cell proliferation in human ovarian cancer cell line (HO8910). METHODS: We transfected ILK-ASODN into HO8910 to block ILK gene expression, measured the expression levels of integrin-linked kinase (ILK) mRNA by RT-PCR and ILK protein by western-blotting; the inhibiting effects of the transfection on HO8910 proliferation, the cell cycles, and cell apoptosis were assessed by water soluble tetrazolium-1 (WST-1) and flow cytometry (FCM). RESULTS: After transfection of ILK-ASODN, the expression levels of ILK mRNA decreased significantly in groups D, E, F being 0.307 +/- 0.011, 0.198 +/- 0.008, 0, respectively, when compared with those of the two control groups of A and B (P < 0.05). The expression levels of ILK protein of the groups D, E and F decreased significantly also, being 26.3 +/- 0.8, 20.6 +/- 0.4 and 0, respectively. HO8910 cell proliferation was inhibited significantly, and the rates of apoptosis of the groups D, E and F increased significantly, being 7.31%, 8.84% and 11.27% respectively. The cell population increased in G0/G1 phase of the groups D, E and F, being 49.25%, 56.28% and 67.61% respectively, significantly different in comparison with those of groups of A and B (P < 0.01). CONCLUSIONS: Transfection of ILK-ASODN into human ovarian cancer line inhibited cancer cell proliferation significantly.