[Retracted] Serum­free­medium­type mesenchymal stem cell culture supernatant exerts a protective effect on A549 lung epithelial cells in acute lung injury induced by H2O2.

The authors wish to retract their research article entitled 'Serum­free­medium­type mesenchymal stem cell culture supernatant exerts a protective effect on A549 lung epithelial cells in acute lung injury induced by H2O2', published in Oncology Reports 40, 3033­3039, 2018. After the publication of this article, the authors have become concerned that there were flaws in their study design that have called into question the reported results. On repeating certain of the experiments, the authors found that the Nrf2­Keap1­ARE signaling pathway only has a role in the lung epithelial cell injury model, whereas it does not serve a role in the A549 model. Further studies are required to validate the role of the Nrf2­Keap1­ARE signaling pathway and the apoptosis­associated proteins. In particular, the results presented in Fig. 5, showing the difference between Bax and Bcl­2, appear to be incorrect. For these reasons, the authors have decided to retract the article from the publication. All the named authors on the paper agree to this retraction. The authors sincerely apologize for any inconvenience that might result from the retraction of this article. [the original article was published in the Oncology Reports 40: 3033­3039, 2018; DOI: 10.3892/or.2018.6656].

The Protective Effects and the Involved Mechanisms of Tanshinone IIA on Sepsis-Induced Brain Damage in Mice.

To evaluate the protective effect of tanshinone IIA on sepsis using a mouse model as well as to preliminarily explore the mechanism behind its application. The mouse model of sepsis was established using the cecal ligation and puncture (CLP) method. Eighty mice were randomly divided into four groups: Sham operation group (Sham group), model group (CLP group), tanshinone IIA group (DS group), and dexamethasone group (DEX group). ELISA method was used to detect the levels of TNF-α and IL-6 in the hippocampal tissue of mouse. Western blot method was used to detect the expression levels of PSD-95, SYP, and Iba-1 in the hippocampus tissue. Immunohistochemistry was used to detect the expression level and distribution of astrocytes (GFAP antibody). Morris water maze test was used to determine the ability of learning and memory in mice. Tanshinone IIA could improve the postoperative survival and 7-day survival rate in the septic mice after operation, which shortens the escape latency and increases the number of crossing platform in the septic mice. It also reduces the expression of TNF-α, IL-6, and Iba-1 in the peripheral blood/hippocampus and the number of astrocytes in hippocampal CA3 area after 7 days of sepsis in mice. However, tanshinone IIA increases the expression levels of SYP and PSD-95 in the hippocampus of septic mice on the seventh day after operation. Tanshinone IIA has a protective effect on the nerve of septic mice, and its mechanism may be related to the anti-inflammatory effects of the peripheral and hippocampal parts as well as inhibiting the over-activation of astrocytes and microglia.

Correlation between tripartite motif-containing protein 44 protein expression and the prognosis of postoperative patients exhibiting skin squamous cell carcinoma.

Tripartite motif-containing protein 44 (TRIM44) plays an important role in the development and progression of some human cancers; however, its role in skin squamous cell carcinoma (SCC) remains unknown. The aim of the present study was to investigate TRIM44 expression and clinicopathological significance of TRIM44 in SCC.Immunohistochemistry (IHC) technique, reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot were performed to evaluate differences in TRIM44 protein expression in SCC and normal skin tissues.IHC showed that the positive rate of TRIM44 staining in SCC tissues 26.00% (9/30), while the positive rate of normal control group was 83.33% (25/30). The positive rate of TRIM44 staining in SCC tissues is significantly lower than normal skin tissue (P <.01). RT-PCR showed that the positive rates of TRIM44 mRNA expression in SCC tissues were 16.67% (5/30), but the positive rate of normal control group was 86.67% (26/30). TRIM44 mRNA expression in SCC group was significantly lower than that in the normal group (P <.01). Kaplan-Meier survival analysis showed that low expression was associated with poor overall survival in SCC patients (P =.004). Multi-factor survival analysis indicated that both low TRIM44 expression and tumor stage were independent factors affecting the overall survival of patients with SCC (P =.038 and P =.001, respectively). Low expression of TRIM44 in SCC was associated with staging (P =.009 and P =.008, respectively) and metastasis (P =.003 and P =.004, respectively).The levels of TRIM44 protein and TRIM44 mRNA in SCC are both lowly expressed which is strongly associated with tumor staging, metastasis, and poor survival. And it also is an independent factor affecting the overall survival of patients with SCC.

Serum­free­medium­type mesenchymal stem cell culture supernatant exerts a protective effect on A549 lung epithelial cells in acute lung injury induced by H2O2.

The aim of the present study was to investigate the mechanisms and protective effect of serum­free­medium­type fetal placental mesenchymal stem cell (fPMSC) culture supernatant on A549 lung epithelial cells following treatment with hydrogen peroxide (H2O2). A549 lung epithelial cells were stimulated with different concentrations of H2O2, and the survival rate of the cells was examined by Cell Counting Kit­8 (CCK­8) assay. It was concluded that the H2O2 concentration when the cell survival rate was at 50% was the optimum condition to create an oxidative damage model. Hoechst 33258 staining and western blot analysis was used to validate the A549 lung epithelial cell model. Serum­free medium was used to culture fPMSCs, and A549 lung epithelial cells treated with H2O2 were cultured with passage 3 MSC supernatant for 24 h. This was termed the supernatant group. Simultaneously, a damage group that was stimulated with H2O2 only, and a vitamin C (VC) group that was treated with H2O2 followed by 100 µmol/l VC in culture medium was also established. The apoptosis of the three groups was detected by flow cytometry, and western blotting was used to detect apoptosis­associated and nuclear factor erythroid 2­like 2 (Nrf2)­kelch­like ECH­associated protein 1 (Keap1)­antioxidant response element/oxidative stress­associated protein expression. Following the CCK­8 test, 600 µmol/l H2O2 was selected to stimulate the A549 lung epithelial cells for 24 h, which resulted in a A549 cell survival rate of 56.41±3.31%. Hoechst 33258 staining and western blotting also confirmed the reliability of the model. Flow cytometry demonstrated that the apoptotic rate of the cells in the VC and supernatant groups was reduced compared with that in the injury group. The difference between the supernatant group and the injury group was statistically significant. The detection of apoptosis­associated proteins by western blotting revealed that the expression of apoptosis regulator BAX and Caspase­3 in the VC and supernatant groups was decreased. Furthermore, the expression of B­cell lymphoma­2 was increased compared with that in the injury group, and the difference was statistically significant (P<0.05). Compared with that in the injury group, the expression of Nrf2 increased in the VC and supernatant groups, whereas the expression of Keap1 was decreased, and the difference was statistically significant (P<0.05). In conclusion, fPMSC supernatant exhibited an antioxidant capacity in A549 lung epithelial cells treated with H2O2 as a model of acute lung injury. The supernatant was found to reduce oxidative damage and inhibit apoptosis.

Blocking beta 2-adrenergic receptor inhibits dendrite ramification in a mouse model of Alzheimer's disease.

Dendrite ramification affects synaptic strength and plays a crucial role in memory. Previous studies revealed a correlation between beta 2-adrenergic receptor dysfunction and Alzheimer's disease (AD), although the mechanism involved is still poorly understood. The current study investigated the potential effect of the selective ß2-adrenergic receptor antagonist, ICI 118551 (ICI), on Aß deposits and AD-related cognitive impairment. Morris water maze test results demonstrated that the performance of AD-transgenic (TG) mice treated with ICI (AD-TG/ICI) was significantly poorer compared with NaCl-treated AD-TG mice (AD-TG/NaCl), suggesting that ß2-adrenergic receptor blockage by ICI might reduce the learning and memory abilities of mice. Golgi staining and immunohistochemical staining revealed that blockage of the ß2-adrenergic receptor by ICI treatment decreased the number of dendritic branches, and ICI treatment in AD-TG mice decreased the expression of hippocampal synaptophysin and synapsin 1. Western blot assay results showed that the blockage of ß2-adrenergic receptor increased amyloid-ß accumulation by downregulating hippocampal α-secretase activity and increasing the phosphorylation of amyloid precursor protein. These findings suggest that blocking the ß2-adrenergic receptor inhibits dendrite ramification of hippocampal neurons in a mouse model of AD.