亚低温促进大鼠颅脑创伤后海马新生 神经元长期存活及成熟

目的 探讨亚低温（MHT）对大鼠颅脑创伤（TBI）后海马齿状回区（DG）新生神经元长期存活及成熟的影 响。方法 59只健康成年SD大鼠随机分为假手术（sham）组、TBI组及TBI+MHT组，sham组15只，其余两组各22只。 TBI大鼠模型借助液压冲击脑损伤仪建立，打击压力设置为2.0 atm（1 atm=101.325 kPa）。TBI+MHT组大鼠在损伤后 立即接受MHT，降温后直肠目标温度为33.5 ℃，维持4 h，并于1.5 h内缓慢复温至37 ℃。在不同时间点应用Morris水 迷宫试验，mNSS评分比较大鼠神经功能恢复情况，免疫荧光染色等方法检测各组海马新生神经元长期存活及成熟 情况。结果 与TBI组比较，TBI+MHT组大鼠伤后4周的逃避潜伏期明显缩短，平台穿越次数及目标象限停留时间 均显著增加（P＜0.05）。损伤后1、2、4周TBI+MHT组大鼠较TBI组mNSS评分均降低（P＜0.01）。与sham组比较，损 伤后1、4、8周TBI组和TBI+MHT组大鼠损伤侧海马DG区BrdU阳性细胞数及BrdU/NeuN双阳性细胞数均增加（P＜ 0.05），且TBI+MHT组较TBI组增加更明显（P＜0.05）。此外，与损伤后1周相比，损伤后4周及8周TBI组BrdU/NeuN 双阳性细胞数减少，而TBI+MHT组进一步增加（P＜0.05）。结论 MHT可促进TBI后新生神经元的长期存活及成 熟，促进TBI后神经功能恢复。

The expression of lncRNA UCA1 and its role on the proliferation and invasion in hepatic cancer and HepG2 cells

Objective To investigate the effects of long non-coding RNA urothelial carcinoma-associated 1 (lncRNA UCA1) silencing on cell proliferation and invasion of human hepatic cancer HepG2 cells, and its mechanism thereof. Methods The expression of lncRNA UCA1 was analyzed by real-time PCR in 20 tumor tissue and 20 adjacent non-tumor tissue samples of hepatic cancer. HepG2 cells was cultured in vitro, and lncRNA UCA1 specific short hairpin RNA (shRNA1 and shRNA2) was transfected. CCK-8 assay, Transwell assay and Wound-healing assay were used to detect the effect of lncRNA UCA1 silencing on cell proliferation, invasion and migration of HepG2 cells. The effect of lncRNA UCA1 silencing on protein and mRNA expression of Cyclin D1, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)- 9, focal adhesion kinase (FAK) and Integrin β3 on lncRNA UCA1 silencing was measured by real-time PCR and Western blot assay. Results The expression of LncRNA UCA1 was higher in hepatic cancer tissues. The silencing of lncRNA UCA1 significantly inhibited the growth of HepG2 cells, and the abilities of cell invasion and migration were downregulated. Western blot assay and real-time PCR showed that expressions of Cyclin D1, VEGF, MMP-9, FAK and Integrin β3 were significantly inhibited. Conclusion The results suggest that the abnormal expression of lncRNA UCA1 is associated with the development of human hepatic cancer. The silencing of lncRNA UCA1 could suppress the cell proliferation, invasion and migration of hepatic carcinoma cells