GhbZIP30-GhCCCH17 module accelerates corm dormancy release by reducing endogenous ABA under cold storage in Gladiolus.

Gladiolus hybridus is one of the most popular flowers worldwide. However, its corm dormancy characteristic largely limits its off-season production. Long-term cold treatment (LT), which increases sugar content and reduces abscisic acid (ABA), is an efficient approach to accelerate corm dormancy release (CDR). Here, we identified a GhbZIP30-GhCCCH17 module that mediates the antagonism between sugars and ABA during CDR. We showed that sugars promoted CDR by reducing ABA levels in Gladiolus. Our data demonstrated that GhbZIP30 transcription factor directly binds the GhCCCH17 zinc finger promoter and activates its transcription, confirmed by yeast one-hybrid, dual-luciferase (Dual-LUC), chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) and electrophoretic mobility shift assay (EMSA). GhCCCH17 is a transcriptional activator, and its nuclear localisation is altered by surcose and cytokinin treatments. Both GhbZIP30 and GhCCCH17 positively respond to LT, sugars, and cytokinin treatments. Silencing GhbZIP30 or GhCCCH17 resulted in delayed CDR by regulating ABA metabolic genes, while their overexpression promoted CDR. Taken together, we propose that the GhbZIP30-GhCCCH17 module is involved in cold- and glucose-induced CDR by regulating ABA metabolic genes.

[Protective effects of gliclazide on myocardium of diabetic rats and its mechanism].

Objective: To investigate the protective effects of gliclazide on myocardium of diabetic rats and its possible mechanisms. Methods: Sixty healthy SD rats were randomly divided into two groups: normal group (NC, n=10) and model group (n=50). Rats in model group were fed with high glucose and high fat diet for 4 weeks and then intraperitoneally injected with STZ (45 mg/kg) to establish a diabetic model and randomly selected FBG ≥ 16.7 mmol / L as a successful diabetes model. Thirty-eight diabetic rats were randomly divided into model group (MC, n=9), gliclazide group (Glic, 80 mg/kg, n=10), glibenclamide group (Glib, 2.5 mg/kg, n=10) and fasudil group (Fas, 10 mg/kg, n=9). NC group and MC group were given equal volume distilled water by gavage, Glic group and Glib group were treated with gliclazide or glibenclamide by gavage, and the Fas group was treated with fasudil by intraperitoneal injection. Rats in each group were given once a day and recorded body mass and fasting blood glucose (FBG) weekly for 8 weeks. At the end of the experiment, the heart weight was measured, and the heart weight index (HWI) was calculated; the contents of glycosylated hemoglobin (HbA1c), total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL-C), low density lipoprotein (LDL-C), the level of serum malondialdehyde MDA) and the activity of superoxide dismutase (SOD) were measured; the pathological changes of myocardial tissue were observed by HE and Masson staining. The expressions of RhoA, ROCK1, eNOS, Bcl-2 and Bax protein were detected by Western blot. Results: Compared with NC group, in MC group, the levels of FBG, HWI, HbA1c, TC, TG, LDL-C, MDA, myocardial collagen deposition and cardiomyocyte apoptosis rate and RhoA, ROCK1, Bax protein in myocardial tissue were increased significantly, while the SOD activity, the levels of HDL-C, eNOS, Bcl-2 and body weight were decreased significantly (P＜0.01). Compared with MC group, Glic treatment decreased the levels of FBG, HWI, HbA1c, LDL-C, TG, TC and MDA, increased the levels of SOD activity and HDL-C (P＜0.01 or P＜0.05); decreased myocardial collagen deposition, inhibited cardiomyocyte apoptosis (P ＜ 0.01); decreased the expression levels of RhoA, ROCK1 and Bax protein; increased the levels of eNOS and Bcl-2 protein (P＜0.01 or P＜0.05). Compared with Glic group, in Glib group, the levels of blood lipids, BM, FBG, HWI, MDA, myocardial fibrosis and cardiomyocyte apoptosis rate were increased, the levels of SOD and Bcl-2 were decreased, and the expressions of RhoA, ROCK1 and Bax in myocardial tissue were upregulated (P＜0.01 or P＜0.05). Conclusion: Gliclazide significantly alleviates myocardial injury and reduces myocardial apoptosis in diabetic rats, and its mechanism may be related to lowering blood glucose, improving oxidative stress and regulating RhoA / ROCK1 / eNOS signaling pathway.