One of the major reasons for studying chemical kinetics is to use measurements of the macroscopic properties of a system, Product Details of 1081-17-0, such as the rate of change in the concentration of reactants or products with time.In a article, mentioned the application of 1081-17-0, Name is 1-(4-Methoxyphenyl)-1H-pyrrole-2,5-dione, molecular formula is C11H9NO3
Corydalis edulis total alkaloids (CETA) ameliorates cognitive dysfunction in rat model of Alzheimer disease through regulation of the antioxidant stress and MAP2/NF-kappaB
Background: In recent years, the morbidity of Alzheimer’s disease in the world has become more and more serious. Therefore, it is an important means to find new drugs for treating AD from traditional medicines. It was found that Corydalis edulis Maxim. has a significant effect in the treatment of Alzheimer’s disease (AD) in traditional application. In this work, we evaluated the efficacy of Corydalis edulis Maxim. total alkaloids (CETA) in AD model rats. Methods: In this work, CETA was prepared by alkali extraction and acid precipitation, 11 alkaloids were identified by UPLC-MS/MS from CETA. AD model rats induced with D-galactose (D-gal) for 7 weeks. In modeling, the different doses of CETA (5, 20 mg/kg/Day) were continuously administered. Firstly, the change of the cognitive function, behavior, brain tissue pathology, and the activity of ROS, MDA, SOD, IL-1beta, TNF-alpha and CAT in rat hippocampal homogenate was measurement. Finally, the protein expression of Abeta, microtubule-associated protein 2 (MAP2) and nuclear factor (kappaBp65) in rat brain was measurement. Result: CETA was found to have the activity in regulating AD. Compared with the normal control group, the levels of SOD and CAT in the hippocampus of the AD model group were decreased, and the level of ROS, MDA, IL-1beta and TNF-alpha was increased. The protein expression of Abeta, and NF-kappaB were increased, and MAP2 were decreased. After treatment by CETA, the levels of SOD and CAT in hippocampus of AD model rats was significantly increased, ROS, MDA, IL-1beta and TNF-alpha were significantly decreased. The protein expression of Abeta, and NF-kappaB were decreased, and MAP2 were increased. Conclusion: CETA can improve the learning and memory ability in AD model. The mechanism may be achieved by regulating the oxidative stress and inflammatory of AD rats, inhibiting the protein expression levels of Abeta, and NF-kappaB, and promote the protein expression the levels of MAP2. Among them, 5 mg/kg is more effective than 20 mg/kg of CETA. Therefore, the therapeutic potential of CETA has been confirmed by our research, which may be a valuable drug for the treatment of AD.
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Reference£º
Pyrroline – Wikipedia,
1-Pyrroline | C4H7N – PubChem