Hydrogen Sulfide Prevents Hippocampal Endoplasmic Reticulum Stress And Synapse Formation Disorder In Diabetic Rats And Up-regulates BDNF-TrkB Pathway

[Background and Objective] Diabetes causes the lesion of central nervous system, including endoplasmic reticulum(ER) stress and synaptic formation disorder. Hydrogen sulfide(H2S), the third gaseous transmitter, has neuroprotective and neuromodulatory effects. Brain derived neurotrophic factor(BDNF) involved in the growth of neurons and synaptic plasticity. The aim of this work is to investigate whether H2 S prevents ER stress and synaptic generated obstacles in the hippocampus of diabetic rats and whether BDNF-Trk B pathway is involved in this nerve protective effect of H2 S. [Methods] SD rats intraperitoneal injected with STZ were used as the animal model of diabetes. Expressions of Glucose regulated protein 78(GRP78), C/EBP homologous protein(CHOP), Cleaved caspase-12, SYN1, BDNF, and the receptor of BDNF, Tyrosine protein kinase B(Trk B), in hippocampus was measured by Western blot. [Results] Na HS(30,100 μmol/kg/d, ip) attenuated the expressions of GRP78, CHOP, and cleaved caspase-12 in the hippocampus of STZ-induced diabetic rats, which indicated that H2 S inhibitis hippocampal ER stress in diabetic rats. Na HS(30,100 μmol/kg/d, ip) increases the expressions of SYN1 in hippocampus of diabetic rats, which indicated that H2 S reverse synaptic formation obstacles. Na HS(30, 100 μmol/kg/d, ip) increases the expressions of BDNF and Trk B in the hippocampus of diabetic rats. [Conclusion] H2 S prevents hippocampal ER stress and synapase formation obstacles in STZ-induced diabetic rats, which may be involved in up-regulation of BDNF/Trk B pathway in the hippocampus.