Influence of object material and inter-trial interval on novel object recognition test in mice / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the efficacy of novel object recognition (NOR) test in assessment of learning and memory ability in ICR mice in different experimental conditions.</p><p><b>METHODS</b>One hundred and thirty male ICR mice were randomly divided into 10 groups: 4 groups for different inter-trial intervals (ITI: 10 min, 90 min, 4 h, 24 h), 4 groups for different object materials (wood-wood, plastic-plastic, plastic-wood, wood-plastic) and 2 groups for repeated test (measured once a day or every 3 days, totally three times in each group). The locomotor tracks in the open field were recorded. The amount of time spent exploring the novel and familiar objects, the discrimination ratio (DR) and the discrimination index (DI) were analyzed.</p><p><b>RESULTS</b>Compared with familiar object, DR and DI of novel object were both increased at ITI of 10 min and 90 min (P<0.01). Exploring time, DR and DI were greatly influenced by different object materials. DR and DI remained stable by using identical object material. NOR test could be done repeatedly in the same batch of mice.</p><p><b>CONCLUSION</b>NOR test can be used to assess the learning and memory ability in mice at shorter ITI and with identical material. It can be done repeatedly.</p>

Glucagon-like peptide-1 protects INS-1 cells from interleukin-1β-induced damage by inhibiting the nuclear factor-κB pathway / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effect of glucagon-like peptide-1 (GLP-1) on interleukin-1β (IL-1β)-induced damage in INS-1 cells and explore its possible mechanisms.</p><p><b>METHODS</b>INS-1 cells were divided into normal control group, IL-1β group, and GLP-1+IL-1β group with corresponding treatments. The cell viability was determined by MTT assay, the expression of IKKβ mRNA was detected by real-time PCR, and that of the protein p65 was detected by Western blotting.</p><p><b>RESULTS</b>In comparison with the normal control group, the cells in the IL-1β group showed a significantly decreased viability by 29% (P < 0.01); compared with those in IL-1β group, the cells in GLP-1+IL-1β group exhibited an significant increase in the cell viability by 30% (P < 0.01). In comparison with the normal control group, the cells in IL-1β group showed an significantly increased expression of IKKβ mRNA (1.967 ± 0.091 vs 1 ± 0, P < 0.05); GLP-1 significantly reduced IL-1β-induced increment of IKKβ mRNA expression to 1.287 ± 0.084 (P < 0.05). IL-1β treatment significantly increased NF-κB protein expression as compared to the control level (0.814 ± 0.111 vs 0.396 ± 0.026, P < 0.01), and GLP-1 significantly inhibited such effect (0.622 ± 0.059, P < 0.05).</p><p><b>CONCLUSIONS</b>GLP-1 inhibits IL-1β-induced β-cell damage probably by inhibiting the NF-κB pathway.</p>

High glucose induces INS-1 cell apoptosis by activating nuclear factor-κB / 南方医科大学学报

<p><b>OBJECTIVE</b>To study of the role of nuclear transcription factor-κB (NF-κB) in high glucose-induced apoptosis in INS-1 cells.</p><p><b>METHODS</b>Rat insulinoma (INS-1) cells cultured in RPMI 1640 medium were treated with 11.1 mmol/L glucose, 33.3 mmol/L glucose, or 33.3 mmol/L glucose plus 5 µmol/L NF-κB inhibitors for 48 h. The expression of NF-κB subunit P65 protein in the cell nuclei was detected by Western blotting, IKK belta mRNA level by quantitative RT-PCR, and cell apoptosis by Annexin V-PI double staining.</p><p><b>RESULTS</b>Compared with the control levels, IKK belta mRNA levels of the cells significantly increased in response to 33.3 mmol/L glucose exposure (P<0.01), which also resulted in significantly increased P65 protein expression in the cell nuclei (P<0.01) and cell apoptosis rate (P<0.05). Compared with those in the high glucose group, the expression of IKK belta mRNA and P65 protein and cell apoptosis rate decreased significantly after treatment with 33.3 mmol/L glucose plus 5 µmol/L NF-κB inhibitors (P<0.05).</p><p><b>CONCLUSION</b>High glucose induces NF-κB activation in INS-1 cells, and inhibition of NF-κB activation may protect INS-1 cells from high glucose-induced cell apoptosis.</p>