ABSTRACT
Objective: To observe the changes of behavior and mitochondria in Alzheimer's disease(AD) rats, and to explore the mechanism of Sijunzi Tang in the treatment of AD rats' behavior and the changes of mitochondrial energy metabolism in hippocampal neurons. Method: The 60 male SPF grade rats were randomly divided into normal group, model group, low, medium and high dose group of Sijunzi Tang(3.24, 6.48,12.56 g·kg-1), and dihydroergot group (0.27 mg·kg-1), 10 rats in each group. The normal group received no intervention and had a normal diet. The rest of the rats were injected with D-galactose to the abdomen at a dose of 200 mg·kg-1 once a day for 6 weeks. Morris water maze experiment was used to detect the cognitive function of rats. Tm-Vision behavioral experiment system was used to observe the behavioral changes of rats, and the hippocampal neuronal line structure was observed by transmission electron microscope. Mitochondrial complex colorimetry was adopted to detect rats CⅠ, CⅡ, CⅢ, CⅣ activity.Western blot was used to detect the expression of mitochondrial adenosine monophosphate-activated protein kinase(AMPK) protein in the hippocampus. Result: Compared with normal group, model group rats latent escape period time increasing, through fewer, movement distance, movement time increasing, center residence time increased (PPPPPPPPPPPPConclusion: The abnormal behavior of AD rats may be related to the decrease of central hippocampal energy metabolism and mitochondrial function. Sijunzi Tang has therapeutic effect.
ABSTRACT
The purpose of the study was to investigate the effect of sophoridine on the proliferation and apoptosis of human gastric cancer MKN45 cells and the possible mechanism. MKN45 cells were randomly divided into control and sophoridine (including 6 subgroups) groups. Cell proliferation was detected by methyl thiazolyl tetrazolium (MTT) colorimetric method. The protein expression of high mobility group-box 3 (HMGB3) was observed by immunocytochemical staining and Western blot. Hoechst 33342 staining method was used to observe the morphological changes of cells treated with sophoridine. Apoptosis was detected by flow cytometry. The results showed that the proliferation of cells was inhibited by 48-hour treatment of sophoridine in a dose-dependent manner. Compared with control group, sophoridine group showed decreased HMGB3 protein expression and increased apoptotic rate. These results suggest that sophoridine can inhibit the proliferation of MKN45 cells and promote their apoptosis, which may be related to down-regulation of HMGB3 protein expression.
