Long noncoding RNAs ( lncRNAs ) are transcribed RNA molecules greater than 200 nucleotides in length. In recent years, studies have shown that lncRNAs have many important bi-ological functions. With the development of modern biological technology, lncRNAs transcripts can be easily detected and pre-dicted. However, unlike protein-coding genes whose sequence motifs usually have indicative function, lncRNA sequence infor-mation is currently uninformative for function prediction. Thus, how to decode the function of lncRNAs has gradually become a hot issue in genome research. The paper summarizes the studies regarding the methods to probe the function of lncRNAs.

Aim To study the protective effect of the naringin on chemotactic factor CX3 CL1 of human umbilical vein endothelial cells ( HUVEC) induced by high glucose. Methods The effect of different concen-trations of naringin on HUVEC cell viability was deter-mined by MTS. HUVECs were divided into 4 groups:① control group, ② high glucose group, ③ naringin group and④high glucose treated with naringin group. After treatment for 5 days, the concentration of nitric oxide ( NO ) in the culture medium was measured by nitrate reductase; intracellular reactive oxygen species ( ROS) was analyzed with fluorescence probe; the ex-pressions of CX3 CL1 mRNA and protein were deter-mined by the reverse transcription PCR ( RT-PCR ) and Western blot ( WB ) . Results NO content in the culture medium of high glucose group was markedly de-creased, which could be increased by naringin. Com-pared with the control group, intracellular ROS in the high glucose group was drastically elevated, but narin-gin decreased the elevated ROS induced by high glu-cose. The results of RT-PCR and WB showed that nar-ingin could downregulate the increased expressions of CX3CL1 mRNA and protein induced by high glucose. Conclusion Naringin has protective effect on the in-jury of the HUVEC induced by high glucose, which is associated with reducing the expression of CX3 CL1 and the antioxidative and anti-inflammatory action.

Objective To establish a rat model of chronic atrophic gastritis and explore the factors inducing atrophy.Methods In accordance with repeated orthogonal design of L8(27), 60% alcohol and 20mmol/L sodium deoxycholate (served as factor A), 0.05%-0.1% ammonia water (factor B), 0.05% indomethacin (factor C) were given, alone or in combination, to rats in three experiments for 3 months, 6 months or 9 months respectively. Then the rats were dissected, and their pathologic changes of the gastric mucosa were assessed.Results Typical signs of chronic atrophic gastritis (CAG) were found in all rats which were treated with factor A, B, C alone or in combination for 6 or 9 months. No significant difference of pathologic changes of gastric mucosa was found between the rats treated for 6 months and those for 9 months. No obvious CAG signs were found in the rats treated with factor A, B, C for 3 months.Conclusion Sixty percent of alcohol, 20mmol/L sodium deoxycholate, 0.05%-0.1% ammonia water and 0.05% indomethacin given to Sprague-Dawley rats for 6 months can successfully establish the animal model of CAG. Prolongation of the model-establishment time is not able to further facilitate the atrophy of gastric mucosa.