In this work, CETA was prepared by alkali extraction and acid precipitation, 11 alkaloids were identified by UPLC-MS/MS from CETA. 
UPLC-MS/MS
Corydalis edulis total alkaloids (CETA) ameliorates cognitive dysfunction in rat model of Alzheimer disease through regulation of the antioxidant stress and MAP2/NF-κB.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.


 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-1β, TNF-α and CAT in rat hippocampal homogenate was measurement.  Finally, the protein expression of Aβ, microtubule-associated protein 2 (MAP2) and nuclear factor (κBp65) in rat brain was measurement.


 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-1β and TNF-α was increased.  The protein expression of Aβ, and NF-κB 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-1β and TNF-α were significantly decreased.  The protein expression of Aβ, and NF-κB 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 Aβ, and NF-κB, 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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