Breast cancer tissues and adjacent tissues were collected from 32 patients who were treated in The Third Hospital of Chengde City. Reverse transcription‑quantitative polymerase chain reaction results demonstrated that, compared with the adjacent tissues, interleukin (IL)‑23/IL‑23 receptor (R) gene expression levels were notably higher in breast cancer tissues. Furthermore, IL‑23 and IL‑23R expression levels were positively correlated with patients' tumor size, TNM stage and metastasis. Recombinant human (rh) IL‑23 (10 ng/ml) was used for the stimulation of the MCF‑7 cell line. Effects of rh IL‑23 (10 ng/ml) on cell proliferation was detected after MCF‑7 cells were incubated with rh IL‑23 for 48 h. Whether pre‑treatment with polyclonal antibody (PAb) IL‑23p19, a neutralizing antibody specific for IL‑23, may influence the effects of IL‑23 on cell behavior was also investigated. Cell proliferation assay and cell apoptosis assay were evaluated using MTT assay and flow cytometry assay, respectively. Results suggested that PAb IL‑23p19 reduced IL-23-induced cell proliferation whereas induced IL‑23 inhibited cell apoptosis. Western blot analysis was performed for the detection of molecules that may be responsible for the aforementioned changes. Results indicated that PAb IL‑23p19 treatment reduced IL‑23‑induced upregulation of B‑cell lymphoma‑2 protein expression and activation of the janus kinase 2/signal transducer and activator of transcription 3 signaling pathway. The present results suggested that IL‑23 may be a potential prognosis marker and target for the treatment of breast cancer patients.
Most breast cancer survivors receiving chemotherapy have severe cognitive impairment, often referred to as “chemobrain.” Polydatin (PLD) is known to have many biological activities. Thus, this study aimed to determine whether symptoms of chemobrain can be prevented or relieved by PLD. The chemobrain models were established by intraperitoneal injection of doxorubicin (DOX, 2 mg/kg) in rats once a week for 4 weeks (DOX group and DOX+PLD group). In the PLD group and DOX+PLD group, PLD (50 mg/kg) was administered orally to rats every day. We found that PLD treatment significantly protected against DOX-induced learning and memory impairment, restored hippocampal histopathological architecture. Furthermore, PLD suppressed DOX-induced oxidative stress through up-regulating Nrf2, inhibited inflammatory response by activating the NF-κB pathway, and reduced hippocampal apoptosis. Therefore, the present study indicated that PLD offered neuroprotection against DOX-induced chemobrain. PLD may assist in preventing chemobrain after chemotherapy in patients with cancers.
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