The nature of muscle‐bone crosstalk has been historically considered to be only mechanical, where the muscle is the load applier while bone provides the attachment sites. However, this dogma has been challenged with the emerging notion that bone and muscle act as secretory endocrine organs affect the function of each other. Biochemical crosstalk occurs through myokines such as myostatin, irisin, interleukin (IL)‐6, IL‐7, IL‐15, insulin‐like growth factor‐1, fibroblast growth factor (FGF)‐2, and β‐aminoisobutyric acid and through bone‐derived factors including FGF23, prostaglandin E2, transforming growth factor β, osteocalcin, and sclerostin. Aside from the biochemical and mechanical interaction, additional factors including aging, circadian rhythm, nervous system network, nutrition intake, and exosomes also have effects on bone‐muscle crosstalk. Here, we summarize the current research progress in the area, which may be conductive to identify potential novel therapies for the osteoporosis and sarcopenia, especially when they develop in parallel.

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It is widely held that endothelial dysfunction plays a crucial role in various pathological inflammatory conditions. Although triptolide, an active ingredient of Traditional Chinese Medicine Tripterygium wilfordii Hook.F., has been shown to possess anti‐inflammatory effects in vivo, little information is available that describes the effects of triptolide on inflammatory responses in endothelial cells (ECs). In this study, we determined whether triptolide suppresses inflammatory responses of ECs via inhibition of NF‐κB signaling. In human umbilical vein endothelial cells (HUVECs), treatment with lipopolysaccharide (LPS) enhanced cytokine and chemokine production, adhesion molecule expression, and monocyte adhesion. These effects were associated with increased activation of NF‐κB pathway. Furthermore, we found that pretreatment with triptolide dose‐dependently attenuated LPS‐induced actions. Our results indicate that triptolide suppresses the inflammatory responses of ECs via the inhibition of NF‐κB signaling. [This work was supported by the National Natural Science Foundation of China (No. 81673734) and Henan Provincial Science and Technique Foundation for International Cooperation Program (No. 162102410048)].Support or Funding InformationThis work was supported by the National Natural Science Foundation of China (No. 81673734) and Henan Provincial Science and Technique Foundation for International Cooperation Program (No. 162102410048)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The objective of this study was to investigate the effect of Ropivacaine lactate glycolic acid copolymer nanoparticles on the apoptosis of vascular endothelial cells after cerebral vasospasm (CVS) in rabbits. Thirty New Zealand rabbits were randomly divided into five groups: Sham Operation, control, blank nanoparticles, nanoparticles drug-loaded, and Ropivacaine. A model of subarachnoid hemorrhage (SAH) was established by injecting blood into the rabbits' cisterna magna twice. The mean velocity (VM) and peak systolic velocity (VP) of basilar artery were compared at one, three, and seven days, after which the shape was observed under a light microscope. The diameter of the lumen was measured at seven days after injection. The TUNEL method was used to detect the apoptosis of endothelial cells in the basilar artery. There was no obvious edema or blood clot and the basilar artery was clear in the Sham Operation group. In the control and blank nanoparticles groups, there was obvious swelling of brain tissue, and obvious blood clots were found at the bottom of brain, mostly around the basilar artery and Willis ring. The pool of brain bottom was dark red. Compared with the control and blank nanoparticles group, the swelling of brain tissue in the nanoparticles and Ropivacaine groups was reduced. Administration of Ropivacaine lactate glycolic acid copolymer nanoparticles into the epidural space of the upper thoracic segment in rabbits can reduce the apoptosis of CVS vascular endothelial cells after SAH.