[Drought and Heat Stress-Mediated Modulation of Alternative Splicing in the Genes Involved in Biosynthesis of Metabolites Related to Tea Quality].

Alternative splicing (AS) regulates mRNAs at the post-transcriptional level to affect both their amounts and the protein function. However, little is known about the roles of AS in regulation of biosynthesis of amino acids, flavonoids, and volatile compounds in tea plants. In this study, we used Iso-seq and transcriptome deep sequencing (RNA-seq) to identify AS events, and analyzed the expression of respective mRNAs in tea plants under drought (DS), heat stress (HS), and their combination (HD). By RT-PCR, we validated the AS events in nine genes involved in the biosynthesis of amino acids and flavonoids. The genes accumulating AS transcripts under DS, HS, and HD conditions included those encoding for anthocyanidin reductase (ANR), dihydrofavonol-4-reductase-like (DFRA), and chalcone isomerase (CHI). Similarly, genes directly or indirectly involved in the biosynthesis of volatile compounds such as lipoxygenase (LOX), terpenoid/terpene synthase (TPS), and 1-deoxy-D-xylulose 5-phosphate reductoisomerase (DXR) also had AS events. Our study revealed that AS might specifically regulate the biosynthesis of amino acids in tea plants under stressful conditions. Moreover, we suggest that the AS events within the ANR and DFRA transcripts might play an important role in the regulation of flavonoid biosynthesis under DS, HS, and HD conditions. This study improved our understanding of the genetic drivers of the changes in the content of bioactive ingredients of tea plants subjected to abiotic stresses.

Diabetes mellitus abrogates the cardioprotection of sufentanil against ischaemia/reperfusion injury by altering glycogen synthase kinase-3ß.

BACKGROUND: Sufentanil is widely used in clinical anaesthesia because of its protective effects against ischaemia/reperfusion injury. Diabetes mellitus elevates the activity of glycogen synthase kinase-3ß (GSK-3ß), thereby increasing the permeability of mitochondrial transition pore. This study investigated the role of GSK-3ß in ameliorating the cardioprotective effect of sufentanil post-conditioning in diabetic rats. METHODS: Streptozotocin-induced diabetic rats and age-matched non-diabetic rats were subjected to 30 min of ischaemia and 120 min of reperfusion. Five minutes before reperfusion, rats were administered one of the following: a vehicle, sufentanil (1 µg/kg), or a GSK-3ß inhibitor SB216763 (0.6 mg/kg). Myocardial infarct size, cardiac troponin I, and the activity of GSK-3ß were then assessed. RESULTS: Sufentanil post-conditioning significantly reduced myocardial infarct size in the non-diabetic, but not in diabetic rats. SB216763 reduced infarct size in both diabetic and non-diabetic animals. Sufentanil-induced phospho-GSK-3ß was reduced 5 min after reperfusion in diabetic rats, but not in non-diabetic rats. CONCLUSIONS: Sufentanil treatment was ineffective in preventing against ischaemia/reperfusion in diabetic rats, which is associated with the activation of GSK-3ß. Our results also suggest that direct inhibition of GSK-3ß may provide a strategy to protect diabetic hearts against ischaemia/reperfusion injury.