It is believed that hyperglycemia leads to increased aldose reductase activity and polyol metabolism in Schwann cells, and the resultant abnormal metabolites cause the organelle's damage and morphological changes such as swelling and vacuolation. Autophagy can remove the damaged organelles, but also provide the materials for cell survival under stressful conditions. Quercetin can reverse high glucose-induced inhibition of neural cell proliferation. Quercetin is also implicated in the mechanism underlying the reduction of apoptosis through autophagy induction. Whether or not quercetin protects Schwann cells through autophagy pathways remains unclear. Dr. Ling Qu and co-workers from Peking Union Medical College Hospital, Peking Union Medical College, China Academy of Medical Sciences, China show that under high glucose conditions, there are fewer autophagosomes in immortalized rat RSC96 cells and primary rat Schwann cells than under control conditions, the proliferative activity of both cell types is signifcantly impaired, and the expression of Beclin-1 and LC3, the molecular markers for autophagy, is significantly lower. After intervention with quercetin, the autophagic and proliferative activity of both cell types is rescued. These results, published in the Neural Regeneration Research (Vol. 9, No. 12, 2014), suggest that quercetin can alleviate high glucose-induced damage to Schwann cells by autophagy.
Article: "Quercetin alleviates high glucose-induced Schwann cell damage by autophagy" by Ling Qu1, Xiaochun Liang1, Bei Gu2, Wei Liu1 (1 Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College, China Academy of Medical Sciences, Beijing, China; 2 Cell Center, Institute of Basic Medical Science, Peking Union Medical College, China Academy of Medical Sciences, Beijing, China) Qu L, Liang XC, Gu B, Liu W. Quercetin alleviates high glucose-induced Schwann cell damage by autophagy. Neural Regen Res. 2014;9(12):1195-1203.
Contact: Meng Zhao
Neural Regeneration Research
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