Objective To investigate the inhibitory effects of RNA interference targeting GFI?1 on growth and proliferation of atypical chronic myelogenous leukemia ( aCML) NT1 cells. Methods NT1 cells were transfected with PBS and liposome complex ( vehicle group) , scrambled siRNA and liposome complex ( negative control, NC group ) , and GFI?1 siRNA and liposome complex ( GFI?1 siRNA group ) , respectively. Real?time quantitative RT?PCR ( qRT?PCR) and Western blot were performed to examine the expression levels of GFI?1 mRNA and protein, respectively. The proliferation abilities of NT1 cells of the three groups were evaluated by MTT assay. The cell cycle in cells of the three groups was analyzed by flow cytometry. Moreover, nude mouse xenograft model was used to detect the tumor formation ability in the three group cells. Results Quantitative real?time PCR data showed that the expression level of GFI?1 mRNA in GFI?1 siRNA group was significantly lower than those of NC group and vehicle group [(0.367±0.017) vs. (0.918±0.006) and (1.010±0.005), respectively, (P<0.05)]. Western blot results showed that the GFI?1 protein expression level in the GFI?1 siRNA group was also significantly reduced, compared with those of the NC group and vehicle group ( P<0.05 for both) . From MTT assay data, the absorbance value of NT1 cells in the GFI?1 siRNA group (0.667±0.059) was significantly lower than those of the NC group (1.096±0.049) and vehicle group (1.193±0.064, P=0.023). Flow cytometry data showed that sub?G1 and G0/G1 phase proportions of the GFI?1 siRNA group were significantly higher than those of the NC and vehicle groups [ sub?G1: (8.2±2.5)% vs. (1.9±1.3)% and (2.0±3.6)%, respectively, (P<0.05);G0/G1:(66.7±3.8)% vs. (53.3±4.5)% and (48.6±3.2)%, respectively, (P<0.05)]. Furthermore, the tumor weight in the GFI?1 siRNA group [(0.37±0.02) g] was significantly lower than those in the NC group [(0.83±0.06) g] and vehicle group [(0.92±0.04) g] (P<0.05). Conclusions RNA interference targeting GFI?1 inhibits the growth and proliferation of NT1 cells, which may provide a new therapeutic target for atypical chronic myelogenous leukemia.

Objective To investigate the inhibitory effects of RNA interference targeting GFI?1 on growth and proliferation of atypical chronic myelogenous leukemia ( aCML) NT1 cells. Methods NT1 cells were transfected with PBS and liposome complex ( vehicle group) , scrambled siRNA and liposome complex ( negative control, NC group ) , and GFI?1 siRNA and liposome complex ( GFI?1 siRNA group ) , respectively. Real?time quantitative RT?PCR ( qRT?PCR) and Western blot were performed to examine the expression levels of GFI?1 mRNA and protein, respectively. The proliferation abilities of NT1 cells of the three groups were evaluated by MTT assay. The cell cycle in cells of the three groups was analyzed by flow cytometry. Moreover, nude mouse xenograft model was used to detect the tumor formation ability in the three group cells. Results Quantitative real?time PCR data showed that the expression level of GFI?1 mRNA in GFI?1 siRNA group was significantly lower than those of NC group and vehicle group [(0.367±0.017) vs. (0.918±0.006) and (1.010±0.005), respectively, (P<0.05)]. Western blot results showed that the GFI?1 protein expression level in the GFI?1 siRNA group was also significantly reduced, compared with those of the NC group and vehicle group ( P<0.05 for both) . From MTT assay data, the absorbance value of NT1 cells in the GFI?1 siRNA group (0.667±0.059) was significantly lower than those of the NC group (1.096±0.049) and vehicle group (1.193±0.064, P=0.023). Flow cytometry data showed that sub?G1 and G0/G1 phase proportions of the GFI?1 siRNA group were significantly higher than those of the NC and vehicle groups [ sub?G1: (8.2±2.5)% vs. (1.9±1.3)% and (2.0±3.6)%, respectively, (P<0.05);G0/G1:(66.7±3.8)% vs. (53.3±4.5)% and (48.6±3.2)%, respectively, (P<0.05)]. Furthermore, the tumor weight in the GFI?1 siRNA group [(0.37±0.02) g] was significantly lower than those in the NC group [(0.83±0.06) g] and vehicle group [(0.92±0.04) g] (P<0.05). Conclusions RNA interference targeting GFI?1 inhibits the growth and proliferation of NT1 cells, which may provide a new therapeutic target for atypical chronic myelogenous leukemia.

Objective To explore the effects of astaxanthin on pressure injury wounds.Methods In vitro experiment:Fibroblasts were treated with different concentrations of astaxanthin and their proliferation activity was detected by CCK-8 assay.Subsequently,fibroblasts were induced by hypoxia/reoxygenation,and the optimal concentration of astaxanthin was administered.Then the intracellular reactive oxygen species(ROS)level was detected by DHE fluorescent probes and the mRNA expression level of TNF-α,IL-1β,IL-6,IL-10,TGF-β was evaluated by RT qPCR.In vivo experiment:to construct a pressure injury model,two circular magnets were symmetrically adsorbed on both sides of the mouse skin for 5 hours everyday.Subsequently,equal amounts of physiological saline,low-dose astaxanthin(10 mg/kg),and high-dose astaxanthin(20 mg/kg)were administered by gavage in groups.Wound images were taken regularly.After 7-day treatment,wound healing rates were counted and wound tissues were collected for histopathological staining.Results In vitro,the fluorescence intensity of DHE in the astaxanthin groups were reduced dramatically.The relative mRNA expression level of TNF-α,IL-1β,IL-6 in the astaxanthin group declined,and the level of TGF-β and IL-10 mRNA increased significantly(P<0.05).In vivo,the wound healing rate and the level of TGF-β,IL-10 in high-dose astaxanthin group increased significantly.The ROS content and the level of TNF-α,IL-1β and IL-6 dropped markedly in astaxanthin groups(P<0.05).Conclusions Astaxanthin can significanlty alleviate oxidative stress,mitigate inflammation,thus exerting a protective effect on pressure injury wounds.