Current molecular medicine · 2026
Calycosin Attenuates Endoplasmic Reticulum Stress Injury in Human Renal Glomerular Endothelial Cells by Inhibiting SRC/SYKDependent Reactive Oxygen Species.
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Wang Yutian, Bai Xiaolin, Pei Ruixia, Lei Wen, Zhang Zequn, Dai Pei
Аннотация
INTRODUCTION: Diabetic Nephropathy (DN), a severe complication, involves endoplasmic reticulum stress. Calycosin, an isoflavone derived from Mongolian Milkvetch Root, may mitigate DN by targeting proto-oncogene tyrosine-protein kinase SRC (SRC)/Spleen Tyrosine Kinase (SYK)-dependent Reactive Oxygen Species (ROS)-mediated ER stress.
METHODS: Human Renal Glomerular Endothelial Cells (HRGECs) were exposed to high glucose to mimic DN, and then treated with calycosin or transfected with SRC overexpression plasmids. Quantitative real-time PCR was performed to assess transfection efficiency, and a western blot was conducted to examine the expression of proteins associated with endothelial dysfunction and endoplasmic reticulum stress. Cell viability, cytotoxicity, apoptosis, and ROS levels were assessed via cell counting kit-8, lactate dehydrogenase assay, flow cytometry, and DCFH-DA probes.
RESULTS: Calycosin barely affected HRGEC viability in normal glucose medium, but apparently reversed high glucose-induced suppression of viability. High glucose increased cytotoxicity, apoptosis, ROS content, and levels of intercellular cell adhesion molecule-1 (ICAM-1), Glucose-Regulated Protein 78 kD (GRP78), Phosphorylated (P)- Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK)/ total (t)-PERK ratio, C/EBP-Homologous Protein (CHOP), SYK, and SRC protein, which were all counteracted by calycosin. Overexpression of SRC attenuated the effects of calycosin on promoting cell viability and repressing apoptosis, ROS, ICAM-1, and endoplasmic reticulum stress-related proteins in high-glucose-treated HRGECs.
DISCUSSION: These findings are in line with prior research linking SRC/SYK-ROS signaling to endoplasmic reticulum stress in the context of DN, highlighting the therapeutic potential of calycosin, although the lack of in vivo evidence necessitates future investigation using animal models.
CONCLUSION: Calycosin attenuates high glucose-induced endoplasmic reticulum stress injury in HRGECs by inhibiting SRC/SYK-dependent ROS.
METHODS: Human Renal Glomerular Endothelial Cells (HRGECs) were exposed to high glucose to mimic DN, and then treated with calycosin or transfected with SRC overexpression plasmids. Quantitative real-time PCR was performed to assess transfection efficiency, and a western blot was conducted to examine the expression of proteins associated with endothelial dysfunction and endoplasmic reticulum stress. Cell viability, cytotoxicity, apoptosis, and ROS levels were assessed via cell counting kit-8, lactate dehydrogenase assay, flow cytometry, and DCFH-DA probes.
RESULTS: Calycosin barely affected HRGEC viability in normal glucose medium, but apparently reversed high glucose-induced suppression of viability. High glucose increased cytotoxicity, apoptosis, ROS content, and levels of intercellular cell adhesion molecule-1 (ICAM-1), Glucose-Regulated Protein 78 kD (GRP78), Phosphorylated (P)- Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK)/ total (t)-PERK ratio, C/EBP-Homologous Protein (CHOP), SYK, and SRC protein, which were all counteracted by calycosin. Overexpression of SRC attenuated the effects of calycosin on promoting cell viability and repressing apoptosis, ROS, ICAM-1, and endoplasmic reticulum stress-related proteins in high-glucose-treated HRGECs.
DISCUSSION: These findings are in line with prior research linking SRC/SYK-ROS signaling to endoplasmic reticulum stress in the context of DN, highlighting the therapeutic potential of calycosin, although the lack of in vivo evidence necessitates future investigation using animal models.
CONCLUSION: Calycosin attenuates high glucose-induced endoplasmic reticulum stress injury in HRGECs by inhibiting SRC/SYK-dependent ROS.