Objective To explore the enhanced effect of miR-199a-3p on radiotherapy sensitivity of glioma U251 by the targeting p21 protein activated kinase 4 (PAK4).Methods Human malignant glioma U251 was chosen for study.Following culture and radiation of the harvested cells,RT-PCR was used to detect the expression level of miR-199a-3p in the glioma tissues and cells of U251,CCK-8,cloning formation assay and flow cytometry were used to detect the effects of miR-199a-3p/PAK4 on the proliferation,cloning formation and apoptosis of glioma U251 cells when treated with irradiation.Results As compared with the U251 cells without radiation,the expression level of miR-199a-3p in the irradiated glioma tissues was lower(P ＜ 0.05).The overexpression of miR-199a-3p could reduce the growth and clonal formation of U251 cells,and promoted cell apoptosis,when treated with 4 Gy-irradiation.Statistical significance could be noted,when comparisons were made between them(P ＜ 0.05 or P ＜ 0.01) MiR-199a-3p could inhibit the expression of PAK4 by direct binding to the 3'UTR of PAK4.Moreover,the overexpression of PAK4 could significantly weaken the roles of miR-199a-3p in the inhibition of U251 cell activity.Conclusion This study has demonstrated that miR-199a-3p could enhance the radiosensitivity of glioma by inhibiting the expression of PAK4.

Objective To explore the effects of hyperbaric oxygen (HBO) on the symptoms of stroke through regulation of nuclear transcription factor-kB (NF-kB) signal pathway in rats and the mechanism involved.Methods Forty SD rats were used in the study and were randomly divided into the sham group,the model group,the model + HBO group and the model + HBO + NF-κBover-expression group.Middle cerebral artery occlusion (MCAO) method was used to develop ischemic stroke rat model.The effects of HBO/NF-κB on cerebral infarction,nerve function,oxidative stress,inflammatory response and brain cell apoptosis were evaluated in the study.Results HBO could significantly reduce the size of brain infarction induced by MCAO (P ＜ 0.05),improve the scores of nerve function (P ＜ 0.05) and enhance the levels of inflammatory response and oxidative stress (P＜0.05 or P ＜0.01) and in the meantime inhibit brain cell apoptosis.However,the over-expression of NF-κB could obviously weaken the therapeutic effects of HBO,and statistical significance could be noticed when comparisons were made between the groups (P ＜ 0.05).Conclusion HBO could alleviate symptoms of cerebral stroke through inhibition of NF-κB activation and improve nerve function,which might be associated with the inhibition of oxidative stress,inflammatory response and brain cell apoptosis.

Objective To explore the enhanced effect of miR-199a-3p on radiotherapy sensitivity of glioma U251 by the targeting p21 protein activated kinase 4 (PAK4).Methods Human malignant glioma U251 was chosen for study.Following culture and radiation of the harvested cells,RT-PCR was used to detect the expression level of miR-199a-3p in the glioma tissues and cells of U251,CCK-8,cloning formation assay and flow cytometry were used to detect the effects of miR-199a-3p/PAK4 on the proliferation,cloning formation and apoptosis of glioma U251 cells when treated with irradiation.Results As compared with the U251 cells without radiation,the expression level of miR-199a-3p in the irradiated glioma tissues was lower(P ＜ 0.05).The overexpression of miR-199a-3p could reduce the growth and clonal formation of U251 cells,and promoted cell apoptosis,when treated with 4 Gy-irradiation.Statistical significance could be noted,when comparisons were made between them(P ＜ 0.05 or P ＜ 0.01) MiR-199a-3p could inhibit the expression of PAK4 by direct binding to the 3'UTR of PAK4.Moreover,the overexpression of PAK4 could significantly weaken the roles of miR-199a-3p in the inhibition of U251 cell activity.Conclusion This study has demonstrated that miR-199a-3p could enhance the radiosensitivity of glioma by inhibiting the expression of PAK4.

Objective To explore the effects of hyperbaric oxygen (HBO) on the symptoms of stroke through regulation of nuclear transcription factor-kB (NF-kB) signal pathway in rats and the mechanism involved.Methods Forty SD rats were used in the study and were randomly divided into the sham group,the model group,the model + HBO group and the model + HBO + NF-κBover-expression group.Middle cerebral artery occlusion (MCAO) method was used to develop ischemic stroke rat model.The effects of HBO/NF-κB on cerebral infarction,nerve function,oxidative stress,inflammatory response and brain cell apoptosis were evaluated in the study.Results HBO could significantly reduce the size of brain infarction induced by MCAO (P ＜ 0.05),improve the scores of nerve function (P ＜ 0.05) and enhance the levels of inflammatory response and oxidative stress (P＜0.05 or P ＜0.01) and in the meantime inhibit brain cell apoptosis.However,the over-expression of NF-κB could obviously weaken the therapeutic effects of HBO,and statistical significance could be noticed when comparisons were made between the groups (P ＜ 0.05).Conclusion HBO could alleviate symptoms of cerebral stroke through inhibition of NF-κB activation and improve nerve function,which might be associated with the inhibition of oxidative stress,inflammatory response and brain cell apoptosis.