A steroid‑induced osteonecrosis model established using an organ‑on‑a‑chip platform
- Authors:
- Published online on: July 28, 2021 https://doi.org/10.3892/etm.2021.10504
- Article Number: 1070
-
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
Bone microvascular endothelial cells (BMECs) constitute the central part of the femoral head's intramural microenvironment network and have an essential role in the development of steroid‑induced osteonecrosis of the femoral head. Recently, the rapid development of microfluidic technology has led to innovations in the fields of chemistry, medicine and life sciences. It is now possible to use microfluidics organ‑on‑a‑chip techniques to assess osteonecrosis. In the present study, BMECs were cultured on a microfluidic organ‑on‑a‑chip platform to explore the pathogenesis of femoral‑head necrosis. The aim of the present study was to explore the effects of different interventions on BMECs and study the pathogenesis of steroid‑induced osteonecrosis through a microfluidic organ‑on‑a‑chip platform. Methods including SU‑8 lithography were used to produce a microfluidic organ‑on‑a‑chip and human umbilical vein endothelial cells (HUVECs) were used to test whether it was possible to culture cells on the chip. Subsequently, a set of methods were applied for the isolation, purification, culture and identification of BMECs. Hydroxyapatite (HA) was used for co‑culture, dexamethasone was used at different concentrations as an intervention in the cells and icariin was used for protection. BMECs were isolated and cultured from the femoral head obtained following total hip arthroplasty and were then inoculated into the microfluidic organ‑on‑a‑chip for further treatment. In part I of the experiment, HUVECs and BMECs both successfully survived on the chip and a comparison of the growth and morphology was performed. HA and BMECs were then co‑cultured for comparison with the control group. The cell growth was observed by confocal microscopy after 24 h. In part II, the effects of different concentrations of glucocorticoid (0.4 or 0.6 mg/ml dexamethasone) and the protection of icariin were evaluated. The morphology of BMECs and the cleaved caspase‑3/7 content were observed by immunofluorescence staining and confocal microscopy after 24 h. In the microfluidic organ‑on‑a‑chip, the response of the cells was able to be accurately observed. In part I, at the same concentration of injected cells, BMECs exhibited improved viability compared with HUVECs (P<0.05). In addition, it was indicated that HA was not only able to promote the germination and growth of BMECs but also improve the survival of the cells (P<0.05). In part II, it was identified that dexamethasone was able to induce BMECs to produce cleaved caspase 3/7; the caspase 3/7 content was significantly higher than that in the blank control group (P<0.05) and a dose correlation was observed. Icariin was able to inhibit this process and protect the microvascular structure of BMECs. The content of cleaved caspase 3/7 in the icariin‑protected group was significantly lower than that in the group without icariin (P<0.05). It was concluded that BMECs are more likely to survive than HUVECs and HA promoted the growth of BMECs on the microfluidic organ‑on‑a‑chip platform. Glucocorticoid caused damage to BMECs through the production of cleaved caspase 3/7, which was observed through the microfluidic organ‑on‑a‑chip platform, and icariin protected BMECs from damage.
