Background Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes. Celastrol plays a certain role in the improvement of various diabetes complications. Therefore, this study aimed to explore whether celastrol inhibited the proliferation and angiogenesis of high glucose (HG)-induced human retinal endothelial cells (hRECs) by down-regulating the HIF1/VEGF signaling pathway. Methods The viability and proliferation of hRECs treated with glucose, celastrol or dimethyloxallyl glycine (DMOG) were analyzed by MTT assay. The invasion and tube formation ability of hRECs treated with glucose, celastrol or DMOG were in turn detected by transwell assay and tube formation assay. The expression of HIF1α and VEGF in hRECs after indicated treatment was analyzed by Western blot analysis and RT-qPCR analysis and ICAM-1 expression in hRECs after indicated treatment was detected by immunofluorescence assay Results HG induction promoted the proliferation, invasion and tube formation ability and increased the expression of HIF-1α and VEGF of hRECs, which were gradually suppressed by celastrol changing from 0.5 to 2.0 μM. DMOG was regarded as a HIF1α agonist, which attenuated the effect of celastrol on HG-induced hRECs. Conclusion Celastrol inhibited the proliferation and angiogenesis of HG-induced hRECs by down-regulating the HIF1α/VEGF signaling pathway.

As a glycophyte plant, pepper (Capsicum annuum L.) is widely cultivated worldwide, but its growth is susceptible to salinity damage, especially at the seedling stage. Here, we conducted a study to determine the physiological and transcriptional differences between two genotype seedlings (P300 and 323F3) with contrasting tolerance under salt stress. The P300 seedlings were more salt-tolerant and had higher K+ contents, higher antioxidase activities, higher compatible solutes, and lower Na+ contents in both their roots and their leaves than the 323F3 seedlings. During RNA-seq analysis of the roots, more up-regulated genes and fewer down-regulated genes were identified between salt-treated P300 seedlings and the controls than between salt-treated 323F3 and the controls. Many ROS-scavenging genes and several SOS pathway genes were significantly induced by salt stress and exhibited higher expressions in the salt-treated roots of the P300 seedlings than those of 323F3 seedlings. Moreover, biosynthesis of the unsaturated fatty acids pathway and protein processing in the endoplasmic reticulum pathway were deeply involved in the responses of P300 to salt stress, and most of the differentially expressed genes involved in the two pathways, including the genes that encode mega-6 fatty acid desaturases and heat-shock proteins, were up-regulated. We also found differences in the hormone synthesis and signaling pathway genes in both the P300 and 323F3 varieties under salt stress. Overall, our results provide valuable insights into the physiological and molecular mechanisms that affect the salt tolerance of pepper seedlings, and present some candidate genes for improving salt tolerance in pepper.