| Background and ObjectiveDiabetes is one of the most common diseases in the world,which threateninghuman’s health at present, its incidence is increasing year by year.Leading to multipleorgan complications is its clinical characteristics, Dementia caused by diabetesattracts more and more attentions of people. Why Diabetes can causes dementia andhow to control is the focus of current medical.Hydrogen sulfide （H2S） as a new type gaseous signal molecule, has beendemonstrated to be involved in the regulation of organ function. It’s regulationfunction to central nervous system has been researched by a lots of scholar.Somereports has confirmed that H2S has an important role in some nerve protectionfunction such as anti-inflammatory, anti apoptosis of nerve cells and so on.Research shows that, there is a close relationship between diabetes and cognitivedysfunction. Diabetes is an independent risk factor through by causes Alzheimer’sdisease (AD). High blood sugar can reduces the expression of some neurotransmitter,changes hippocampal synaptic plasticity and reduces the oxygen free radicalscavenging. Neural protection function has been confirmed for improving thehippocampal synaptic plasticity and facilitating the induction of hippocampal longterm potentiation(LTP) by H2S. Does H2S can alleviate Cognitive dysfunctioninduced hyperglycemia? What dose of H2S is the best to improve the effectiveness ofdiabetes dementia? All of these need to be further discussed. In this study, we will observe the effect of H2S on diabetic rats through theestablishment of the model of diabetic rats, and evaluate the efficacy of H2S onpreventing cognitive dysfunction caused by diabetes.Methods75adult male Sprague Dawley(SD) rats were used for the experiments, to berandomized distributed to5groups: control, Simple diabetes group, low dose NaHStreatment, high dose NaHS treatment and simple NaHS treatment. In addition tocontrol group and the simple NaHS treatment group, the other groups were givenintraperitoneal injection of STZ. After the modeling, the simple NaHS treatmentgroup, low dose NaHS treatment and high dose NaHS treatment group were treatedwith different concentrations of NaHS by intraperitoneal injection for30days.Control group and simple diabetic group intraperitoneal injection of salineconsecutively for30days; Then we can evaluat the ability of learning and memorythrough Y maze, Morris water maze and novel object recognition test.Results1.The diabetic rat model was successfully established and diabetes can cause diabeticin model rats.The rats were fed normally for a week, in order to adapt to the environment.Afterrandomization, single cage feeding, weighing about (300±20) g, intraperitonealinjection with streptozotocin (STZ)-40mg/kg, after3days, the blood glucose≥16.7mmol/L, regarded as a successful model.After4weeks, the diabetic group compare to control group, Y maze correct ratewas lower than the control group.In Morris water maze,rats’s latency in search ofplatform was significantly longer.The times entering the target quadrant (dischargeplatform quadrant) is decreased and the retention time of percentage is reduction; thenew object recognition index about model rats are decreased significantly. Thus,diabetes can lead to dysfunction in diabetic behavior. 2. H2S can reduce cognitive dysfunction in diabetic model rats.After4weeks, Y-maze correct rate of the H2S treatment groups is higher than thesimple diabetic group; In the Morris water maze,rats in the experiment for shortlatency to platform than diabetic group,enter the target quadrant (discharge platformquadrant) more often than the diabetic group; the retention time of percent and a newobject recognition index diabetic groups were higher than that of the simple diabeticgroup. So, it is show that H2S can reduce the degree of cognitive impairment indiabetic rats.ConclusionH2S can reduce dementia in diabetes rats... |
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