Background: To explore the effect of albiflorin (AL) on streptozotocin (STZ)-induced Alzheimer's disease (AD) in rats. Methods: A mouse model of diabetic encephalopathy was established by intraperitoneal injection of 1%STZ. Step down test and water maze test were used to test the cognitive function of rats. Congo Red Staining was used to detect the distribution of Aβ plaques in the hippocampus of rats. Cytokine levels in serum and hippocampus were measured using ELISA. Serum insulin, oral glucose tolerance (OGTT), serum superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured by commercial kits. And the content of Nrf-2/HO-1/HMGB1/NF-kB in the hippocampus of diabetic rats were detected by western blot. Results and Conclusion: Compared with the STZ model group, the average escape latency of rats in the AL group in the Morris water maze test was significantly shortened, and the average number of platform crossings and the ratio of distance/total swimming distance in the target quadrant were increased significantly. Staining of tissue sections and ELISA showed a decrease in Aβ plaque density in the hippocampus of rats in the AL group. And serum insulin levels of rats in the ALgroup were significantly reduced and OGTT was improved. In addition, AL could also regulate the Nrf-2/HO-1/HMGB1/NF-kB signal pathway in the hippocampus. Therefore, AL may ameliorate STZ-induced cognitive impairment in rats by regulating oxidative stress and inflammation in the brain.

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Long non-coding RNA (LncRNA) THOR (Lnc-THOR) is expressed in testis and multiple human malignancies. Lnc-THOR association with IGF2BP1 (IGF2 mRNA-binding protein 1) is essential for stabilization and transcription of IGF2BP1 targeted mRNAs. We tested its expression and potential functions in non-small cell lung cancer (NSCLC). In primary NSCLC cells and established cell lines, Lnc-THOR shRNA or CRISPR/Cas9-mediated knockout (KO) downregulated IGF2BP1 target mRNAs (IGF2, Gli1, Myc and SOX9), inhibiting cell viability, growth, proliferation, migration and invasion. Significant apoptosis activation was detected in Lnc-THOR-silenced/-KO NSCLC cells. Conversely, ectopic overexpression of Lnc-THOR upregulated IGF2BP1 mRNA targets and enhanced NSCLC cell proliferation, migration and invasion. RNA-immunoprecipitation and RNA pull-down assay results confirmed the direct binding between Lnc-THOR and IGF2BP1 protein in NSCLC cells. Lnc-THOR silencing and overexpression were ineffective in IGF2BP1-KO NSCLC cells. Forced IGF2BP1 overexpression failed to rescue Lnc-THOR-KO NSCLC cells. In vivo, intratumoral injection of Lnc-THOR shRNA adeno-associated virus potently inhibited A549 xenograft tumor growth in nude mice. At last we show that Lnc-THOR is overexpressed in multiple NSCLC tissues and established/primary NSCLC cells. Collectively, these results highlighted the ability of Lnc-THOR in promoting NSCLC cell growth by associating with IGF2BP1, suggesting that Lnc-THOR represents a promising therapeutic target of NSCLC.

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