Biology subjects

xie, c.

Publications and source records attributed to xie, c..

3 recordsLinked to original sources

bioRxiv2025

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↗

bioRxiv2024

Artificial Intelligence-Enabled AlphaFold II Pipeline Guides Functional Fluorescence Labeling of Tubulin Across Species

Dynamic properties are essential for microtubule (MT) physiology. Current techniques for in vivo imaging of MTs present intrinsic limitations in elucidating the isotype-specific nuances of tubulins, which contribute to their versatile functions. Harnessing the power of AlphaFold II pipeline, we engineered a strategy for the minimally invasive fluorescence labeling of endogenous tubulin isotypes or those harboring missense mutations. We demonstrated that a specifically designed 16-amino acid linker, coupled with sfGFP11 from the split-sfGFP system and integration into the H1-S2 loop of tubulin, facilitated tubulin labeling without compromising MT dynamics, embryonic development, or ciliogenesis in C. elegans. Extending this technique to human cells and murine oocytes, we visualized MTs with the minimal background fluorescence and a pathogenic tubulin isoform with fidelity. The utility of our approach across biological contexts and species set an additional paradigm for studying tubulin dynamics and functional specificity, with implications for understanding tubulin-related diseases known as tubulinopathies.

cell biology↗

bioRxiv2021

Nrf2 mediated ER-phagy protects against oxidative damage in intervertebral disc degeneration

Intervertebral disc degeneration (IDD) increases the risk of low back pain (LBP). Oxidative stress may induce cellular damage and contribute to various diseases including IDD. Endoplasmic reticulum autophagy (ER-phagy) is a specific type of autophagy, its role in oxidative stress induced damage as well as in IDD is unknown. This study explores the role of ER-phagy in oxidative damage in intervertebral disc nucleus pulposus cells (NPCs), as well as the Nrf2/FAM134B axis in ER-phagy regulation and IDD therapy. We found ER-phagy was decreased in NPCs during oxidative stress; while FAM134B may promote ER-phagy and alleviate oxidative stress induced ER-stress and apoptosis. In addition, the nuclear transcription factor Nrf2 may promote the expression of FAM134B as well as ER-phagy, and suppress ER-stress and apoptosis in NPCs. Furthermore, overexpression of FAM134B and Nrf2 could effectively attenuate the progression of IDD in rats in vivo. These results suggest Nrf2/FAM134B mediated ER-phagy may combat oxidative damage in cells; meanwhile, ER-phagy as well as Nrf2 could be potential therapeutic targets for IDD. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/469451v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@188b390org.highwire.dtl.DTLVardef@1c4e4f6org.highwire.dtl.DTLVardef@193fe77org.highwire.dtl.DTLVardef@12770e2_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗