Objective To investigate the effect of different types of jumps on the expressions of interleukin 6 (IL-6), osteoprotegerin(OPG), ligand of receptor activator of NF-?B(RANKL) genes related to bone metabolism in rat tibia, and explore the molecular mechanism underlying bone destruction associated with over-loading jumping. Methods Twenty-four male SD rats were randomly assigned to control group (C), jump group (J) and loading jump group (JL), 8 rats in each group. J group participated in incremental load training. The rats in JL group carried loads that were 5% of their body mass. Same training plan was used in J and JL groups, while control group was not treated. The experiment was completed after 6 weeks. The serum samples were collected and assayed for the contents of alkaline phosphatase (ALP) and tartrate resistant acid phosphatase (TRACP). One-side tibia was used for paraffin section and HE staining, and the other side was used for real time quantitative PCR(qRT-PCR) to detect the expressions of IL-6, OPG and RANKL mRNA. Results Compared with control group and J group, the collagen fibers in periost was more disordered in JL group. We further observed a more serious damage of the cortical bone and increased cavities in JL group. The serum ALP levels in JL group were significantly higher than those in control and J groups (P<0.05). The serum TRACP levels in JL and J groups were significantly higher compared to control group (P<0.05). Furthermore, there was a significantly higher expression level of IL-6 in both jump groups (P<0.01), while the JL group had a higher IL-6 expression compared with J group (P<0.01). There was a higher expression of OPG mRNA in JL and J groups (P<0.05). The highest expression level of OPG was observed in J group. The expression level of RANKL was significantly higher in JL group compared with control and J groups (P<0.01). Conclusion After loading jump for 6 weeks, the expressions of IL-6 and RANKL were markedly elevated in rat tibia, suggesting that IL-6 and RANKL might be involved in the process of bone destruction due to increased bone turnover.
Ultrasound molecular imaging has the potential to detect activated platelets, thus identifying atherosclerotic plaque instability before onset of serious clinical events. However, it has not been well defined in inflammatory arterial thrombosis. We hypothesized that microbubbles (MBs) target glycoprotein IIb/IIIa (GP IIb/IIIa) could achieve a noninvasive in vivo detection of inflammatory thrombosis in large arteries through contrast-enhanced ultrasound (CEU) imaging.
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