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目的观察FoxO3a基因缺失致小鼠脾脏进行性慢性炎性反应。方法分别于16周、24周和12个月称取FoxO3a基因敲除小鼠和对照小鼠体重;于16、24和38周处死各组小鼠,取脾脏,肉眼观察脾脏变化,并制备脾细胞悬液,进行细胞计数,同时取各组小鼠卵巢、肺及皮下等组织,观察其炎性变化。流式细胞术检测24周的FoxO3a基因敲除小鼠和对照小鼠脾细胞中T、B淋巴细胞和Mac-1+细胞数量及百分率;Real-time PCR检测脾细胞中炎性细胞因子S100A8和S100A9基因mRNA的表达水平。结果与对照小鼠相比,FoxO3a基因敲除小鼠脾脏明显肥大,且随年龄增加更加显著,卵巢、肺及皮下等组织内可见大量炎性细胞浸润,脾细胞数明显升高;基因敲除组老年小鼠的体重明显低于对照小鼠;FoxO3a基因敲除小鼠的脾细胞中T、B淋巴细胞数增加明显,但所占脾细胞的百分率无明显增加,Mac-1+细胞数和百分率均明显增加;S100A8和S100A9基因mRNA的表达水平明显高于对照小鼠。结论 FoxO3a基因缺失致小鼠脾脏进行性慢性炎性反应。
Objective To observe the chronic inflammatory reaction of mouse spleen induced by deletion of FoxO3a gene. Methods The body weight of FoxO3a knockout mice and control mice were weighed at 16 weeks, 24 weeks and 12 months respectively. Mice were sacrificed at weeks 16, 24 and 38, and their spleens were harvested. Cell suspension, cell count, while taking the mouse ovaries, lungs and subcutaneous tissue, observe the inflammatory changes. The number and percentages of T, B lymphocytes and Mac-1 + cells in splenocytes of FoxO3a knockout mice and control mice at 24 weeks were determined by flow cytometry. The levels of inflammatory cytokines S100A8 and S100A9 gene mRNA expression level. Results Compared with the control mice, FoxO3a knockout mice spleen significantly hypertrophy, and with more significant increase in age, ovarian, lung and subcutaneous tissue showed a large number of inflammatory cell infiltration, the number of splenocytes was significantly increased; knockout The body weight of the aged mice was significantly lower than that of the control mice. The numbers of T and B lymphocytes in the FoxO3a knockout mice increased significantly, but the percentage of the splenocytes did not increase significantly. The number of Mac-1 + The percentages of S100A8 and S100A9 mRNA expression were significantly higher than that of control mice. Conclusion FoxO3a gene deletion causes chronic inflammatory reaction in mice spleen.