ABSTRACT
Objective:To explore the effects of caffeine on the prevention of Alzheimer's disease (AD).Methods:Use Ethanol as a solvent to extract the caffeine in tea and then injecting 5％ D-galactose saline solution 1ml/d/kg to establish aging model mice.Divide mice randomly into experimental group (high-dose/low-dosecaffeine),positive control group,negative control group,and normal con-trol group (NS) and injecting appropriate drugs for consecutive four weeks.Test superoxyde dismutase (SOD) and malondialdehvde (MDA) periodically.Take mice's hippocampus and use Western blotting to detect the expression of brain derived neurotrophic factor (BDNF) and extracellular signal-regulated kinasesl/2 (p-ERK1/2).Results:The expression of BDNF and p-ERK1/2,negative control group is less than low-dose experimental group and positive control group (P＜0.01);The p-ERK1/2 expression of injecting D-galactose mice was significantly lower than normal group,negative control group compared weth the normal group,the differencd was significant (P＜0.05).The level of SOD in model group was significantly lower than that in normal control group,high,low dose caffeine group and positive control group (P＜0.01),but the level of MDA is opposite.Conclusions:Caffeine can delay aging process by increasing the level of SOD in aging mice,and enhancing the expression of BDNF and P-ERK1/2.Caffeine does a lot to prevent AD.
ABSTRACT
Objective To investigate the expression change of renal NLR family pyrin domain containing-3 protein(NALP3) in-flammasome in the nephrotic syndrome(NS) patients with focal segmental glomerulosclerosis(FSGS) and its relation with the tubu-lointerstitial pathogenic injury degree ,expression of inflammatory factors and clinical biochemical indexes .Methods Immunohisto-chemistry was used to detect the expressions of NALP3/ASC/caspase-1 and their downstream effector molecule IL-1β,IL-18 in re-nal tubular epithelial cells .The tubulointerstitial injury score and the activated macrophages F4/80 in renal interstitium of the FSGS patients and NS patiens were evaluated .The serum creatinine ,urea ,total protein ,albumin ,24 h urine protein and estimated glomer-ular filtration rate(eGFR) were observed .The correlation of tubulointerstitial injury with NALP3/ASC/caspase-1 ,IL-1β,IL-18 were respectively analyzed .Results The expression of NALP3/ASC/caspase-1 ,IL-1β,IL-18 in the renal tissue of the FSGS pa-tients was significantly increased compared with that in the control group (P<0 .01) .NALP3/ASC/capspase-1 expression was pos-itively correlated with the expression of IL-1β,IL-18(P< 0 .01) .NALP3/ASC/caspase-1 ,IL-1β,IL-18 expression was positively correlated with renal tubulointerstitial injury and the F4/80 expression intensity(P<0 .01) .NALP3/ASC/caspase-1 ,IL-1β,IL-18 was significantly positively correlated with 24 h urine protein and Scr ,and negatively correlated with the eGFR (P<0 .05) ,but had no obvious correlation with plasma urea ,plasma total protein and albumin concentrations .Conclusion The NALP3 inflammasome might participate in the pathogenic mechanism of FSGS through the activation of its downstream inflammatory factor of IL-1β,IL-18 ,the more higher its expression degree ,the more severe the renal tissue injury ,whether which could be served as the warning in-dex needs the further clinical verification .