| 何宁宁,高志旭,杨蒙蒙,陆欣然,樊赛军,王芹.褪黑素在辐射诱导的小鼠放射性肠损伤作用中的全基因体表达图谱分析[J].中华放射医学与防护杂志,2023,43(5):335-342 |
| 褪黑素在辐射诱导的小鼠放射性肠损伤作用中的全基因体表达图谱分析 |
| Analysis of whole genome expression profile for the effect of melatonin on radiation-induced intestinal injury in mice |
| 投稿时间：2023-02-20 |
| DOI：10.3760/cma.j.cn112271-20230220-00043 |
| 中文关键词: 褪黑素 放射性肠损伤 辐射防护 DNA微阵列分析 |
| 英文关键词:Melatonin Radiation-induced intestinal injury Radiation protection DNA microarray analysis |
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| 中文摘要: |
| 目的 探讨褪黑素在小鼠放射性肠损伤作用中的全基因体表达图谱变化。方法 对C57BL/6J雄性小鼠按10 mg/kg体重进行腹腔注射褪黑素,1次/d,连续5 d,然后,对小鼠腹部进行14 Gy γ射线照射。照射后3 d收集小鼠小肠组织,进行DNA微阵列检测,对小肠组织差异基因进行基因本体论(GO)注释及京都基因与基因组百科全书(KEGG)通路分析。结果 与对照组相比,照射前给药组小鼠差异基因中上调基因584个,下调基因538个。照射组和照射前给药组小鼠取交集的差异基因中,照射前给药组特有的上调基因324个,下调基因246个。这些差异基因的GO注释分析显示,照射前给药组排名前15的显著富集的生物过程主要包括自噬体组装(GO:0000045)、自噬体组织(GO:1905037)和急性炎症反应调节(GO:0002673)。其中,ATG12、ATG16L2和AMBRA1基因参与自噬体组装和自噬体组织,C3、CPN1、CD55、CFP、CNR1、C1QA、C2和CREB3L3基因参与急性炎症反应调节。这些差异基因参与的KEGG通路分析显示,照射前给药组排名前15的显著富集的通路主要包括O-聚糖生物合成(hsa00512)、鞘糖脂生物合成(hsa00603)、细胞外基质-受体互作(hsa04512)和不饱和脂肪酸生物合成(hsa01040)。qRT-PCR验证显示,照射前给药组参与自噬生物过程中的ATG12和ATG16L2基因的表达量较照射组显著增加(t=2.40、4.35,P<0.05)。结论 与自噬和急性炎症反应相关生物过程中的差异基因,以及参与不饱和脂肪酸生物合成的通路,可能参与褪黑素在辐射诱导的放射性肠损伤中的作用。 |
| 英文摘要: |
| Objective To elucidate the change of whole genome expression profile for the effect of melatonin on radiation-induced intestinal injury in mice. Methods C57BL/6J male mice were administrated with melatonin at 10 mg/kg body weight by intraperitoneal injection once a day for five consecutive days before abdominal irradiation with 14 Gy of γ-rays. Small intestines were harvested 3 d after radiation. GO annotation and KEGG pathway of the differential genes involved in small intestine were explored by DNA microarray analysis. Results Compared with the control group, 584 differential genes were up-regulated and 538 differential genes were down-regulated for administration group pre-irradiation. The overlapping differential genes were selected from the irradiated mice and the administrated mice pre-irradiation. There were 324 up-regulated genes and 246 down-regulated genes unique to the administrated mice pre-irradiation. GO annotation analysis of the differential genes indicated that the top 15 significantly enriched biological processes for the administrated mice pre-irradiation mainly included autophagosome assembly (GO: 0000045), autophagosome organization (GO: 1905037) and regulation of acute inflammatory response (GO: 0002673). The genes ATG12, ATG16L2 and AMBRA1 were involved in autophagosome assembly and autophagosome organization. The genes C3, CPN1, CD55, CFP, CNR1, C1QA, C2 and CREB3L3 were involved in the regulation of acute inflammation response. KEGG pathway analysis of the differential genes involved indicated that the top 15 significantly enriched pathways for the administrated mice pre-irradiation mainly included O-glycan biosynthesis (hsa00512), glycosphingolipid biosynthesis (hsa00603), ECM-receptor interaction (hsa04512) and biosynthesis of unsaturated fatty acids (hsa01040). qRT-PCR verification showed that the expressions of ATG12 and ATG16L2 genes involved in autophagy for the administrated mice pre-irradiation increased significantly compared with the irradiated mice (t=2.40,4.35, P<0.05). Conclusions The differential genes related with the biological process of autophagy, acute inflammatory response and the pathway of unsaturated fatty acid biosynthesis might be involved in the effect of melatonin on radiation-induced intestinal injury. |
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