Molecular mechanism of geniposide in regulating GLUT2 glycosylation in pancreatic β cells / 中国中药杂志

Type 2 diabetes mellitus( T2 DM) is a common chronic metabolic disease characterized by persistent hyperglycemia and insulin resistance. In pancreatic β-cells,glucose-stimulated insulin secretion( GSIS) plays a pivotal role in maintaining the balance of blood glucose level. Previous studies have shown that geniposide,one of the active components of Gardenia jasminoides,could quickly regulate the absorption and metabolism of glucose,and affect glucose-stimulated insulin secretion in pancreatic β cells,but the specific mechanism needs to be further explored. Emerging evidence indicated that glycosylation of glucose transporter( GLUT) has played a key role in sensing cell microenvironmental changes and regulating glucose homeostasis in eucaryotic cells. In this study,we studied the effects of geniposide on the key molecules of GLUT2 glycosylation in pancreatic β cells. The results showed that geniposide could significantly up-regulate the mRNA and protein levels of Glc NAc T-Ⅳa glycosyltransferase( Gn T-Ⅳa) and galectin-9 but had no signi-ficant effect on the expression of clathrin,and geniposide could distinctively regulate the protein level of Gn T-Ⅳa in a short time( 1 h) under the conditions of low and medium glucose concentrations,but had no significant effect on the protein level of galectin-9. In addition,geniposide could also remarkably affect the protein level of glycosylated GLUT2 in a short-time treatment. The above results suggested that geniposide could quickly regulate the protein level of Gn T-Ⅳa,a key molecule of protein glycosylation in INS-1 rat pancreatic βcells and affect the glycosylation of GLUT2. These findings suggested that the regulation of geniposide on glucose absorption,metabolism and glucose-stimulated insulin secretion might be associated with its efficacy in regulating GLUT2 glycosylation and affecting its distribution on the cell membrane and cytoplasm in pancreatic β cells.

Effect of brain-derived neurotrophic factor on retinal Müller cells in diabetic rats / 眼科新进展

Objective To investigate the protective effect of brain derived neurotrophic factor (BDNF) on Müller cells in the retina of diabetic rats.Methods A total of 54 healthy male SD rats were recruited and randomly divided into control group,diabetic group and BDNF group.Then a diabetic model was established by intraperitoneal injection of streptozotocin in rats of diabetic and BDNF groups.Preparation of BDNF injection was performed using PBS balanced salt solution containing 0.1 g · L 1 BSA.The BDNF group was given BDNF injection,while the control and diabetic group were injected with equal dose of PBS balanced salt solution 4 weeks after successful modeling.And after 8 weeks,the expression of L-glutamate/L-aspartate transporter (GLAST),glutamine synthetase (GS) and synaptophysin (SYN) were detected by immunofluorescence technique and Western blot,and the content of glutamic acid in retina was determined by glutamic acid determination kit.Results Compared with the control group,the expression of GLAST,GS and SYN were significantly decreased in diabetic group,and the content of glutamic acid was increased significantly (all P ＜ 0.01).Compared with the diabetic group,the expression of GLAST,GS and SYN were increased in BDNF group,and the glutamate level was decreased significantly (all P ＜0.01).Conclusion In the early stage of diabetic retinopathy,administration of exogenous BDNF can unregulated the expression of GLAST,SYN and GS and improve the function of Müller cells to protect RGC against damage,suggesting that BDNF has neuroprotective effects on Müller cells in retina of rats with diabetic retinopathy.

Platelet-rich plasma combined with conventional surgery in the treatment of atrophic nonunion of femoral shaft fractures: study protocol for a prospective, randomized,controlled clinical trial / 中国组织工程研究

BACKGROUND:Internal and external fixation combined with autologous bone graft for treating atrophic nonunion has a long treatment cycle,and moreover,it cannot achieve a 100％ cure rate.Platelet-rich plasma contains a variety of growth factors and a large number of white blood cells,and contributes to tissue healing.However,there is no clinical study on the effectiveness of platelet-rich plasma combined with conventional surgery in the treatment of atrophic nonunion.OBJECTIVE:To investigate the effectiveness of platelet-rich plasma in the treatment of atrophic nonunion of femoral shaft fractures.METHODS:We conducted a prospective,open-label,randomized,controlled clinical trial at the Affiliated Hospital of Qinghai University,China.Ninety-two patients with atrophic nonunion of femoral shaft fractures were equally and randomly divided into control group and experimental group.Patients in the control group received conventional surgery.Patients in the experimental group were injected with autologous platelet-rich plasma on the basis of conventional surgery.The primary outcome was fracture healing rate at postoperative 9 months.The secondary outcomes were visual analogue scale scores in resting state and during passive motion,healing time,treatment costs,and adverse reactions.The study protocol was approved by the Ethics Committee of Affiliated Hospital of Qinghai University of China (approval number:QHG0223A) on May 20,2014.Written informed consent was provided by each patient and their family members after they fully understood the treatment plan.RESULTS AND CONCLUSION:Our partial results demonstrated that visual analogue scale scores and complications were similar between the two groups at postoperative 1-3 days.The healing rate was significantly higher in the experimental group than in the control group.The healing time was significantly shorter in the experimental group than in the control group.This trial will provide objective data for the clinical use of platelet-rich plasma combined with conventional surgery for the treatment of atrophic nonunion.