[Effects of Gui pi tang on myocardial ischemia in rats].

Objective: To investigate the effects of Guipitang (GPT) on myocardial ischemic (MI) injury of rats. Methods: Forty male SD rats were randomly divided into five groups as control, model, GPT low-dose and high-dose groups (7.52, 15.04 g/kg), and positive-drug trimetazidine group (2 mg/kg). Rat myocardial ischemia model was induced by feeding high fat forage and intraperitoneal injection of isoprenaline (ISO). After 15 days intragastric administration, rats were injected with ISO once a day for 3 days again. Subsequently, Electrocardiograph (ECG) was examined, serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and glucose (GLU) were detected using an automatic biochemical analyzer. The histopathological alterations of heart were assessed using HE and Masson staining. The protein expressions of Collagen I and Collagen III in heart were evaluated by Western blot. Results: Compared with control group, the electrocardiogram S-T segment of model rats moved down, the serum levels of TC, AST, CK, LDH and GLU in model group were increased significantly (P＜0.05), the expressions of collagen I and collagen III in heart were increased (P＜0.05), and the hearts were damaged severely. However, no significant changes of TG, HDL-C, LDL-C and ALT were observed (P＞0.05). Compared with the model group, the high and low dose groups of GPT and trimetazidine could inhibit the descent of S-T segment, reduced serum TC, AST, CK, LDH and GLU levels (P＜0.05), and decreased collagen III expression in heart (P＜0.05), and alleviated myocardial pathological damage as well. The high dose group of GPT could decrease the protein expression of collagen I. Conclusion: GPT could improve heart function and alleviate the injury of myocardial ischemia, especially the high lose.

Deletion of pancreatic ß-cell adenosine kinase improves glucose homeostasis in young mice and ameliorates streptozotocin-induced hyperglycaemia.

Severe reduction in the ß-cell number (collectively known as the ß-cell mass) contributes to the development of both type 1 and type 2 diabetes. Recent pharmacological studies have suggested that increased pancreatic ß-cell proliferation could be due to specific inhibition of adenosine kinase (ADK). However, genetic evidence for the function of pancreatic ß-cell ADK under physiological conditions or in a pathological context is still lacking. In this study, we crossed mice carrying LoxP-flanked Adk gene with Ins2-Cre mice to acquire pancreatic ß -cell ADK deficiency (Ins2-Cre± Adkfl/fl ) mice. Our results revealed that Ins2-Cre+/- Adkfl/fl mice showed improved glucose metabolism and ß-cell mass in younger mice, but showed normal activity in adult mice. Moreover, Ins2-Cre± Adkfl/fl mice were more resistant to streptozotocin (STZ) induced hyperglycaemia and pancreatic ß-cell damage in adult mice. In conclusion, we found that ADK negatively regulates ß-cell replication in young mice as well as under pathological conditions, such as STZ induced pancreatic ß-cell damage. Our study provided genetic evidence that specific inhibition of pancreatic ß-cell ADK has potential for anti-diabetic therapy.