Dried root of Rehmannia glutinosa extracts prevents steroid-induced avascular necrosis of femoral head by activating the wingless-type (Wnt)/ß-catenin signal pathway.

Steroid-induced avascular necrosis of femoral head (SANFH) is one of the most common complications caused by long-term or excessive clinical use of glucocorticoids. This study aimed to investigate the effects of dried root of Rehmannia glutinosa extracts (DRGE) in SANFH. First, SANFH rat model was established by dexamethasone (Dex). Tissue change and proportion of empty lacunae were detected by hematoxylin and eosin staining. Protein levels were detected by western bloting analysis. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was performed to assess apoptosis of femoral head tissue. Cell viability and apoptosis of MC3T3-E1 cells were assessed by Cell Counting Kit-8 assay and flow cytometry. ALP activity and cell mineralization were detected by ALP staining assay and Alizarin red staining. The findings showed that DRGE improved tissue damage, inhibited apoptosis, and promoted osteogenesis in SANFH rats. In vitro, DRGE increased cell viability, inhibited cell apoptosis, promoted osteoblast differentiation, reduced the levels of p-GSK-3ß/GSK-3ß, but increased the levels of ß-catenin in cells treated with Dex. Furthermore, DKK-1, an inhibitor of the wingless-type (Wnt)/ß-catenin signaling pathway, reversed the effect of DRGE on cell apoptosis and ALP activity in cells treated with Dex. In conclusion, DRGE prevents SANFH by activating the Wnt/ß-catenin signaling pathway, indicating that DRGE may be a hopeful choice drug to prevent and treat patients with SANFH.

Knockdown of lncRNA JPX suppresses IL-1ß-stimulated injury in chondrocytes through modulating an miR-25-3p/PPID axis.

The aim of this study was to investigate the potential mechanisms of long noncoding (lnc) RNA Just proximal to X-inactive specific transcript (JPX) in interleukin (IL)-1ß-stimulated chondrocytes. Human C28/I2 chondrocytes were treated with IL-1ß to simulate osteoarthritic (OA) injury. The expression levels of JPX, microRNA (miRNA/miR)-25-3p, and peptidylprolyl isomerase D (PPID) were measured using reverse transcription-quantitative PCR or western blotting. The IL-1ß-stimulated injury was assessed using a Cell Counting Kit-8 assay, flow cytometry, and western blot analysis. The targeted relationship between miR-25-3p, JPX, and PPID was verified using a dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The results showed that JPX expression was upregulated in OA patients and IL-1ß-stimulated chondrocytes. JPX knockdown enhanced cell viability and suppressed apoptosis of IL-1ß-stimulated chondrocytes. miR-25-3p inhibition rescued the inhibitory effect of JPX knockdown on IL-1ß-stimulated injury. PPID overexpression eliminated the effects of JPX knockdown on IL-1ß-stimulated chondrocytes. In conclusion, JPX knockdown increased cell viability and reduced apoptosis in IL-1ß-stimulated chondrocytes, and this involved modulation of a miR-25-3p/PPID axis.