The Molecular Pathogenesis Of Anesthetics Affect On Congnitive Function In Elderly Rats Via Pathway Of Inflammation And Oxidative Stress

Vascular cognitive impairment, caused by vascular injury and inflammation, affects brain function. Studies indicate that Vascular cognitive impairment is closely related with Vascular injury and inflammation, while the the degree of injury is positively correlated with inflammation and vascular injury. Studies show that the brain is playing a special role in cognitive function, thus comprehensive Brain Protection may be good for reducing vascular cognitive impairment under acute myocardial ischemia reperfusion injury. Sevoflurane can play a positive role on myocardial and brain injury, since it can reduce myocardial oxygen consumption, inhibit the movement of calcium ions in myocardium, activate mitochondrial signaling pathway and prevent the production of inflammatory factors. Present treatment for vascular injury primarily relies on combination therapy of surgery with anesthesia, however there is no direct evidence about the effect of sevoflurane in the treatment of vascular cognitive impairment. In this study, we sought to determine the effects of anesthetics, sevoflurane and fentanyl, on long-term cognitive function in brain tissue of rats, and potential correlations with inflammatory factors such as VEGF, IL-1?, TNF-?. We used shuttle box and water maze tests to study the cognitive function of Wistar rats. The results demonstrated that rats treated with sevoflurane or fentanyl performed less shock times and more active escape times compared with rats model undergoing vascular cognitive impairment. Treatment of anesthetics also shortened the periods of learning and memory incubation, suggesting a protective role in cognitive function. In addition, our results unraveled a reducing expression of TNF-? and IL-1? but an increasing level of VEGF in head tissues of rats implemented with anesthetics. These findings underscore the improving role of sevoflurane and fentanyl in the recovery of vascular cognitive impairment rats as well as the cognitive function in rats, by regulating the expression of inflammatory factors.Vascular injury and inflammation affect may cause vascular cognitive impairment of brain function. Ischemia reperfusion injury associated with microvascular injury is a direct consequence of the activation of the inflammatory response. The treatment of vascular injury uaually depends on the combination therapy of surgery and anesthesia. Conventional anesthetics such as propofol may cause autonomic cognitive dysfunction, which is not conducive to the rehabilitation of vascular cognitive impairment. However there is no direct evidence about the effect of sevoflurane in the treatment of vascular cognitive impairment. In the present study, we sought to determine the molecular pathogenesis of anesthetics affect on cognitive cognitive function in elderly rats via pathway of inflammation and oxidative stress, as well as and inflammatory cytokines such as vascular endothelial growth factor (VEGF), interleukin-l? (IL-1?) and tumor necrosis factor-? (TNF-?) potential, neuronal apoptosis and mitochondrial oxidative stress effect correlation.120 Wistar rats were randomly divided into four groups, group A of rats received sham surgery, group B of rats vascular cognitive impairment model, group C of rats vascular cognitive impairment model plus sevoflurane, group D of rats vascular cognitive impairment model plus fentanyl. Blood samples and brain tissue were collected, using the TUNEL assay hippocampal neurons apoptosis index, the rate of apoptosis was measured by flow cytometry and intracellular calcium ion levels in hippocampal neurons. Determination of membrane potential case of rat hippocampal neurons cytoplasm mitochondria recycling fluorescent probes. Enzyme-linked immunosorbent assay (ELISA) assay content of inflammatory factors in the blood.The simultaneous determination of the aforementioned methods of separation and purification Canon hippocampal neuronal cell homogenates groups mitochondrial respiratory chain complex activity. Results:The blood of rats using anesthetics in TNF-a,IL-1? expression and decrease VEGF expression increased. Anesthetic treatment reduced neuronal apoptosis rate and apoptosis index, reducing the transfer of calcium ions into the neuron cell ischemia, improves neuron cytoplasmic and mitochondrial membrane potential activity of mitochondrial respiratory chain complex ?-? active. Anesthetic can effectively reduce cognitive impairment in aged rats due to ischemia caused by the mechanism and enhance VEGF expression levels, and promote the formation of new blood vessels, reduce the inflammatory process damage hippocampal neurons caused by the inflammatory cytokines are involved in addition anesthetics also can reduce hippocampal neurons oxidative stress, thereby reducing the hippocampal neuronal apoptosis, thereby reducing the incidence of cognitive dysfunction.