Hyperbaric oxygen on rehabilitation of brain tumors after surgery and effects on TNF-α and IL-6 levels.

Hyperbaric oxygenation (HBO) on postoperative rehabilitation of brain tumors and effects on tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were explored. A retrospective analysis of 132 patients with brain tumors treated in the People's Hospital of Rizhao from October 2014 to October 2017 was performed. There were 62 patients in the observation group and 70 patients in the control group. Patients in the control group were treated with conventional drugs, and patients in the observation group were treated with HBO on the basis of conventional drug therapy. Levels of serum TNF-α and IL-6 were measured by ELISA before and after treatment. Cerebral arterial flow velocity and spasticity were measured by cranial color Doppler ultrasonography. Neurological function deficit (NFD) and activities of daily living (ADL) were used to evaluate the clinical recovery of the patients. Clinical efficacy was compared and analyzed. There were no significant differences between the two groups before treatment (P>0.05). After treatment, serum TNF-α and IL-6 levels were significantly lower than pretreatment levels (P<0.05), and serum TNF-α and IL-6 levels in the observation group were lower than those in the control group (P<0.05). Cerebral arterial flow velocity in observation group after treatment was significantly lower than that in the control group. The number of patients with cerebral arterial spasm after treatment in the observation group was significantly smaller than that in the control group. NFD scores in the observation group were lower than those in the control group after treatment. After treatment, ADL scores in the observation group were significantly higher than those in the control group (P<0.05). The comprehensive treatment effect of HBO is significant. It can inhibit the expression of inflammatory factors in serum and reduce cerebral arterial flow velocity and effectively reduce the number of patients with cerebral arterial spasm. It can reduce NFD and improve the quality of life of patients. Therefore, it is worthy of clinical popularization.

MicroRNA-155 increases colon cancer chemoresistance to cisplatin by targeting forkhead box O3.

To investigate the effect of microRNA (miR)-155 on colon cancer chemoresistance to cisplatine and its mechanism. Reverse transcription quantitative polymerase chain reaction was used to measure the levels of miR-155 and forkhead box O3 (FOXO3) in colon cancer specimens and cell lines. Overexpression of miR-155 and miR-155 inhibitor were transfected into colon cancer cell lines to investigate its role of chemoresistance to cisplatin in colon cancer. MTS assays were used to analyse cell viability in vitro. In vivo tumor formation assays were performed in C57BL/6 wild type and miR-155 knockout mice (miR-155-/-). A luciferase reporter assay was used to measure the translation of FOXO3. Additionally, the expression of FOXO3 was detected by western blot analysis. It was identified that miR-155 was markedly upregulated in colon cancer tissue and cell lines. Overexpression of miR-155 enhanced colon cancer cell chemoresistance to cisplatin in vitro and tumorigenesis in vivo. In addition, overexpression of miR-155 was associated with decreased levels of FOXO3, primarily through inhibiting the expression of FOXO3 to increase colon cancer resistanec to cisplatin. The present study demonstrated that miR-155 increased colon cancer drug resistance and decreased FOXO3 expression in vivo and in vitro. This may provide a novel method for the treatment of drug-resistant colon cancer.