Dexamethasone (Dex) and other glucocorticoids are widely used to treat serious infections and immunological diseases, however they may cause steroid-induced avascular necrosis of the femoral head (SANFH). Salidroside (Sal) has demonstrated an anti-apoptotic effect on neurocytes by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. In the present study, primary osteoblasts were used in vitro and in rats in vivo to determine the anti-apoptotic effect of Sal on SANFH. The result of the present study demonstrated that pretreatment with Sal increased the cell survival rate while decreasing the cell apoptosis and lactate dehydrogenase release rate. Additionally, Sal also caused the reduction of TUNEL positive cells in TUNEL staining assay. Sal decreased the expression of cleaved caspase-3, cleaved caspase-9, apoptosis regulator BAX and cytochrome C, while it increased the expression of B cell lymphoma-2 and phosphorylated-Akt in Dex-induced osteoblasts. In vivo Sal protected against SANFH in rats by decreasing the percentage of empty lacunae. The present study demonstrated that Sal alleviated Dex-induced osteoblast apoptosis by activating the PI3K/Akt signaling pathway and downregulating caspase-3 expression in osteoblasts. Sal also protected against SANFH in a rat model of SANFH by decreasing the percentage of empty lacunae. The inhibition of the mitochondrial apoptosis pathway was also involved. Further research is required to determine the full underlying mechanisms by which Sal has an effect.

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Gastric cancer (GC) is the fourth most common type of cancer, worldwide. The major molecular factors associated with the pathogenesis of GC remain unclear. Previous studies found that zinc finger proteins are highly abundant in human eukaryotes and tissues, and play an important role in maintaining normal cellular functions and have an association with tumor initiation. In the current study, interference technology was used to silence the ZNF139 protein, a zinc finger protein that was previously found to be closely associated with GC. The results showed that cell viability and proliferation were inhibited in the Znf139-knockdown of GC cells. Additional study found that the expression levels of B cell lymphoma-2 (Bcl-2) and survivin messenger RNAs and proteins were downregulated in Znf139-silenced cells, indicating that cells expression Znf139 are able to induce the growth of tumor cells by mediating the apoptosis pathway. Further in vivo experiments showed that Znf139 knockdown downregulated the expression levels of Bcl-2 and survivin in mice. Overall, the in vitro and in vivo findings of the present study indicate that ZNF139 may be actively involved in the progression of GC.