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xie, h.

Publications and source records attributed to xie, h..

2 recordsLinked to original sources

ShenQi Compound improves diabetes by modulating pancreatic mitochondrial energy metabolism in GK rats

PurposeShenQi Compound (SQC) is a traditional herbal formula that has long been utilized in the treatment of type 2 diabetes and its complications. The purpose of this study was to investigate the effect of SQC on mitochondrial energy metabolism in pancreatic tissues of spontaneously type 2 diabetic Goto-Kakizaki (GK) rats. MethodsGK rats were induced into a diabetic model using a high-fat diet. They were randomly divided into 3 groups (n=8): diabetes model group, SQC group (14.4 g/kg/d) and metformin (Met) group (0.1 g/kg/d). Another 8 Wistar rats were taken as controls. Weight, Blood glucose was monitored weekly in each group,After 12 weeks of gavage. Fasting blood glucose and lipid levels were evaluated, and histopathological changes in the pancreas were assessed by hematoxylin-eosin (HE) staining, serum fasting insulin(FINS) and pancreatic mitochondrial respiratory chain complex I-V (complexI-V) levels were measured by enzyme-linked immunosorbent assay (ELISA), reactive oxygen species ((ROS)) levels were detected by chemiluminescence, superoxide dismutase (SOD) levels were detected by xanthine oxidase, and glutathione (GSH) and adenosine triphosphate (ATP) levels were detected by colorimetric assay. And the uncoupling protein(UCP-2) protein and mRNA expression levels were detected by protein blotting and real-time quantitative PCR. ResultsSQC treatment significantly decreased (P<0.01) the levels of FBS, FINS,triglyceride s(TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) (P<0.01) and significantly increased (P<0.01) the levels of denser lipoprotein cholesterol (HDL-C) in GK rats. Pancreatic histopathological damage was improved after SQC treatment, and complexI to complexIV significantly decreased (P<0.05) and complexV, SOD and GSH significantly increased (P<0.05) in pancreatic tissues. In addition, SQC reduced the content of ROS and ATP in pancreatic tissues (P<0.01) and down-regulated UCP-2 protein and mRNA expression (P<0.01). ConclusionSQC improves glucose-lipid metabolism and attenuates pathological damage of pancreatic tissues in T2DM rats, possibly by regulating mitochondrial energy metabolism in pancreatic tissues. The effects of SQC are not well understood. These findings provide new insights into the mechanism of action of SQC in the treatment of T2DM and its associated neurodegenerative effects.

zoology↗

Recurrent de novo single point mutation on the gene encoding Na+ /K+ pump results in epilepsy

The etiology of epilepsy remains undefined in two-thirds of patients. Here, we identified a de novo mutation of ATP1A2 (c.2426 T>G, p.Leu809Arg), which encodes the 2 subunit of Na+/K+-ATPase, from a family with idiopathic epilepsy. This mutation caused seizures in the study patients. We generated the point mutation mouse model Atp1a2L809R, which recapitulated the epilepsy observed in the study patients. In Atp1a2L809R/WT mice, convulsions were observed and cognitive and memory function was impaired. This mutation affected the potassium binding function of the protein, disabling its ion transport ability, thereby increasing the frequency of nerve impulses. Our work revealed that ATP1A2L809R mutations cause a predisposition to epilepsy. Moreover, we first provide a point mutation mouse model for epilepsy research and drug screening.

neuroscience↗