A Study Of Protective Effect And Mechanism Of Lithium Chloride On Hypoglycemia Brain Injury

Object Hypoglycemia is one of the most common and terrible side effects in the course of antidiabetic treatment.Sustained and severe hypoglycemia events can cause irreversible neurological damage.However,the exact pathogenesis is not clear,and effective means of prevention and treatment are also lacking.This study explored the protective effect and mechanism of lithium chloride on hypoglycemia brain injury,aiming to provide theoretical reference for future scientific research and clinical work.Method To investigate the effect of lithium chloride on Wnt / ?-catenin signaling pathway and apoptosis in PC12 cell line using sugar-free medium in vitro;The effects of lithium chloride on cognitive function,neuronal death,glial cell activation and inflammatory response were observed in Wistar rats by injecting insulin to establish hypoglycemia brain injury model.Results(1)in vitro: The results of immunoblotting and polymerase chain reaction showed that hypoglycemia inhibited Wnt / ?-catenin signaling pathway via down-regulating the expression of wnt3 a,P-GSK3? and ?-catenin and up-regulating the expression of GSK-3?;MTT,LDH and ANNEXIN / FITC results show that hypoglycemia can induce significant apoptosis;The results of immunoblotting and immunofluorescence showed that hypoglycemia could upregulate the expression of caspase-2 and cleaved caspase-3;Lithium chloride attenuates hypoglycemia-induced Wnt / ?-catenin signaling inhibition and apoptosis.(2)in vivo: Morris water maze results show that hypoglycemia can lead to impaired learning and memory learning and memory capacity;The results of immunoblotting showed that hypoglycemia could inhibit Wnt / ?-catenin signaling pathway by downregulating the expression of wnt3 a,P-GSK3? and ?-catenin and up-regulating the expression of GSK-3?;The results of immunoblotting and immunofluorescence showed that hypoglycemia reduced the expression of NeuN and increased the expression of GFAP and CD11b;The results of enzyme-linked immunosorbent assay showed that hypoglycemia could up-regulate the expression of pro-inflammatory cytokines IL-1?,IL-6 and TNF-? and down-regulate the expression of IL-4,IL-10 and TGF?;Lithium chloride can attenuate hypoglycemia-induced cognitive impairment,Wnt / ?-catenin signaling inhibition,neuron death,glial cell activation and inflammatory response.Conclusion Hypoglycemia can induce neuronal apoptosis and ultimately lead to cognitive impairment,and lithium chloride can partially alleviate hypoglycemia hypoglycemiainduced nerve damage.Lithium chloride may play a neuroprotective role by activating the Wnt / ?-catenin signaling pathway and regulating the inflammatory response.