miR­155 mediates inflammatory injury of hippocampal neuronal cells via the activation of microglia.

MicroRNA (miR)­155 has a crucial role in various cellular functions, including differentiation of hematopoietic cells, immunization, inflammation and cardiovascular diseases. The present study aimed to investigate the roles and mechanisms of miR­155 in treatment­resistant depression (TRD). A Cell Counting Kit­8 assay and flow cytometry were performed to assess the cell viability and apoptosis of microglial cells, respectively. Western blotting and reverse transcription­quantitative polymerase chain reaction assays were used to evaluate the associated protein and mRNA expression, respectively. The results revealed that miR­155 reduced the cell viability of BV­2 microglial cells, and miR­155 enhanced the expression levels of pro­inflammatory cytokines in BV­2 microglial cells. Furthermore, conditioned medium from miR­155­treated microglia decreased the cell viability of HT22 hippocampal cells. miR­155­treated microglia increased the apoptosis of neuronal hippocampal cells by modulating the expression levels of apoptosis regulator Bax, apoptosis regulator Bcl­2, pro­caspase­3 and cleaved­caspase­3. The cell cycle distribution was disrupted by miR­155­treated microglia through induction of S phase arrest. Furthermore, the overexpression of suppressor of cytokine signaling 1 reversed the pro­apoptotic effect of activated microglia on hippocampal neuronal cells. In conclusion, the present results suggested that miR­155 mediated the inflammatory injury in hippocampal neuronal cells by activating the microglial cells. The potential effects of miR­155 on the activation of microglial cells suggest that miR­155 may be an effective target for TRD therapies.

[The investigation of DNA double-strand breaks of lymphocytes in workers exposed to lead and DNA double-strand breaks of human lymphocytes induced by lead in vitro].

OBJECTIVE: To study DNA double-strand breaks of human peripheral lymphocytes exposed to lead with flow cytometry (FCM). METHODS: The lymphocytes were obtained from 36 workers occupationally exposed to lead and 70 residents without occupational exposure to lead. DNA double-strand breaks were detected by flow cytometer assay. The lymphocytes from health people were incubated with lead at different doses and time, FCM assay was used to detect DNA double-strand breaks. RESULTS: DNA double-strand breaks and fluorescence intensity of high exposed group and low exposed group were 41.76% ± 28.57%, 9.90 ± 3.35 and 33.18% ± 30.64%, 9.39 ± 4.83, respectively, which were significantly higher than those (0.28% ± 0.28% and 6.95 ± 2.93) of control group (P<0.05). The results of in vitro experiment indicated that DNA double-strand breaks of lymphocytes exposed to Pb at the dose of 125.0, 250.0, 500.0 µmol/L for 1 and 2 h were significantly different from those of the negative control group and positive control group (P<0.01). DNA double-strand breaks increased at beginning and then decreased with lead doses. CONCLUSION: Lead can induce DNA double-strand breaks, γH2AX detected using flow cytometer assay can be used to measure the DSBs of DNA in large samples.

[The effects of 1,2-dichloroethane on the cellular proliferation, cellular cycle and apoptosis of SW620 cells in vitro].

OBJECTIVE: To explore the effects of 1,2-dichloroethane (1,2-DCE) on the cellular proliferation, cellular cycle and apoptosis of SW620 cells in vitro. METHODS: SW620 cells were exposed to 1,2-DCE at different concentrations for 0.5 and 1 h. MTT assay was used to detect the relative number and relative viability, the low cytometry (FCM) assay was utilized to measure the cell cycle and apoptosis. RESULTS: The results of MTT assay showed that the cellular relative viability decreased with the 1,2-DCE's dose and exposure time. Compared with the DMSO group, the relative cellular viability of cells exposed to 1,2-DCE at the doses of 75, 100, 125, 150, 175, 200 µmol/L for 1 h decreased (P<0.05 or P<0.01). Compared with the groups exposed to 1,2-DCE for 0.5 h, the relative cellular viability of cells exposed to 175 µmol/L 1,2-DCE for 1 h decreased significantly (P<0.01). IC(50) of cellular proliferation in cells exposed to 1,2-DCE for 0.5 h was 89.41 µmol/L, and 95% confidence interval was 85.23 to 93.79 µmol/L. IC(50) of cellular proliferation in cells exposed to 1,2-DCE for 1 h was 87.68 µmol/L, and 95% confidence interval was 83.71 to 91.82 µmol/L. The results of FCM indicated that compared with the control group, the G(0)/G(1) phase in groups exposed to 1,2-DCE at the doses of 25, 50, 100, 150 and 200 µmol/L for 1 h decreased significantly (P<0.05 or P<0.01), the S phase in groups exposed to 1,2-DCE at the doses of 25, 50 and 100 µmol/L for 1 h reduced significantly (P<0.05 or P < 0.01), the G(2)/M phase in groups exposed to 1,2-DCE at the doses of 25, 50, 100, 150 and 200 µmol/L for 1 h increased significantly (P<0.05 or P<0.01). However, 1,2-DCE could not induce apoptosis of SW620 cells. CONCLUSION: 1,2-DCE could inhibit the proliferation of SW620 cells, and arrest SW620 cells at G(2)/M phase, but could not induce the apoptosis of SW620 cells in vitro.