Malignant gliomas are a common type of primary tumor of the central nervous system. In spite of current intensive therapy, the prognosis of patients with malignant glioma remains poor, hence the development of novel therapeutic modalities is necessary. Cell apoptosis is a frequent target in the development of anti‑cancer drugs. Fatsioside A, a novel baccharane‑type triterpenoid glycoside, is extracted from the fruits of Fatsia japonica. Previous studies have shown that Fatsioside A induces growth inhibition, cell cycle arrest and apoptosis in C6 rat glioma cells and U251 human glioma cells. However, to the best of our knowledge, no detailed studies have reported its effect on U87MG glioma cells and its exact mechanisms remain unknown. In the current study, the growth inhibitory effect of Fatsioside A on U87MG cells was evaluated and the underlying molecular mechanisms were explored. Through the use of flow cytometry and a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, it was determined that Fatsioside A markedly inhibits the growth of U87MG cells. Mechanistic studies demonstrated that Fatsioside A induces growth inhibition of U87MG cells via the induction of endoplasmic reticulum (ER) stress, which was supported by the upregulation of ER stress markers, including elevated levels of phosphorylation of PERK and eIF2α, the increased expression levels of CHOP and the accelerated cleavage of caspase‑4. The downregulation of CHOP via CHOP‑specific siRNA reduced the growth‑inhibitive effect of Fatsioside A on U87MG cells, further confirming the role of the ER stress response in mediating Fatsioside A‑induced growth inhibition. In conclusion, Fatsioside A inhibits glioma cell growth via the induction of ER stress‑mediated apoptosis. This may provide a molecular basis for the development of Fatsioside A into a drug candidate for the treatment of malignant glioma.

Predictive value of serum complement Clq tumor necrosis factor-related protein 9 (CTRP9) and serum stromal interaction molecule 1 (STIM1) was investigated for restenosis after cerebrovascular stent implantation, as well as its relationship with vasoactive substances and inflammatory cytokines. In this prospective study, 128 patients with cerebral infarction treated with cerebrovascular stent implantation in Yantaishan Hospital were recruited. A total of 66 cases with restenosis after cerebrovascular stent implantation were included in group A, and 62 cases without stenosis were included in group B. Serum CTRP9 and STIM1 levels were measured by enzyme-linked immunosorbent assay (ELISA). ROC curves of serum CTRP9 and STIM1 levels in patients with postoperative restenosis were drawn. The vasoactive substances nitric oxide (NO), tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) were analyzed by ELISA. The correlation of serum CTRP9, STIM1 levels and NO, TNF-α, IL-6 were analyzed by Pearson correlation coefficient. Serum CTRP9 and NO levels in group A were significantly lower than those in group B. The levels of serum STIM1, TNF-α and IL-6 in group A were significantly higher than those in group B (P<0.001). The sensitivity and specificity of serum CTRP9 level in the diagnosis of restenosis after cerebrovascular stent implantation were, respectively, 59.68 and 75.76%. Those of serum STIM1 were, respectively, 87.10 and 46.97% and those of the combination of serum CTRP9 and STIM1 were 90.32 and 48.48%. Serum CTRP9 level was positively correlated with NO, and negatively correlated with TNF-α and IL-6. STIM1 was positively correlated with TNF-α and IL-6, and negatively correlated with NO (P<0.001). Serum CTRP9 level was significantly decreased in patients with restenosis after cerebrovascular stent implantation, while STIM1 level was significantly up-regulated. Both were correlated with the change of NO, IL-6 and TNF-α levels, therefore they could be used as biological indicators for prediction of restenosis after cerebrovascular stent implantation.