[Mongolian medicine Heisuga-25 promotes the expression of neuroskeletal protein, increases the content of neurotransmitter and improves the symptoms of Alzheimer's disease in mice].

Objective To investigate the effect and mechanism of Mongolian medicine Heisuga-25 on Alzheimer's disease (AD) mice. Methods Six month old SAMP8 mice were divided into model group, Heisuga-25 [360 mg/(kg.d), 90 mg/(kg.d)] treatment group, and donepezil control group[0.92 mg/(kg.d)], with 15 mice in each group. Another 15 6-month-old normal aging SAMR1 mice were selected as blank control group. The mice in the model group and blank control group were fed with normal saline, and the other groups were gavaged according to the dosage. All groups were gavaged once a day for 15 days. From Day 1 to Day 5 after administration, three mice in each group were taken and Morris water maze test was been used to detect the escape latency, times for crossing the platform and the residence time were detected. Nissl staining was used to observe the number of Nissl bodies. Western blot analysis and immunohistochemistry were used to detect the expression of microtubule associated protein 2 (MAP-2) and low molecular weight neurofilament protein (NF-L). ELISA was used to detect the contents of acetylcholine (ACh), 5-hydroxytryptamine (5-HT), norepinephrine (NE) and dopamine (DA) in cortex and hippocampus of mice. Results Compared with the blank control group, the escape latency was significantly prolonged, while the model group showed a decrease in the number of crossing the platform, residence time, Nissl bodies, and the protein expression of MAP-2 and NF-L. Compared with the model group, Heisuga-25 administration group exhibited an increase in the number of crossing the platform and residence time, Nissl bodies, and the protein expression of MAP-2 and NF-L, but a shortened escape latency. The effect of high-dose groupHeisuga-25 [360 mg /(kg.d)] on the above indexes was more obvious. Compared with the blank control group, the contents of ACh, NE, DA and 5-HT in hippocampus and cortex were decreased in the model group. Compared with the model group, the low-dose group, high-dose group and donepezil control group all observed an increase in the contents of ACh, NE, DA and 5-HT. Conclusion Mongolian medicine Heisuga-25 can improve learning and memory by protecting the neural function of AD model mice, which may be accounted for up-regulation of neuronal skeleton protein expression and increased content of neurotransmitters.

FBP2 and Talin-1 are potential protein markers for Mongolian medicine symptom evaluation in viral infectious diseases.

BACKGROUND: Influenza, measles, and mumps are common viral infectious diseases in Mongolia. The traditional Mongolian medicine (TMM) classified them as warm disease, and still plays a major role in the diagnoses and treatments. METHODS: To interpret the connotation of the complex theoretical system in TMM with scientific technique, in this study, a high throughput mass spectrometry was used to identify potential protein markers of TMM symptom types. Fifty venous blood samples were drawn from influenza, measles and mumps patients. Differential proteins between samples of patients diagnosed as immature and mature heat in TMM were detected by mass spectrometry. RESULTS: After proteomics analysis, 1500 proteins and 7619 polypeptides were identified and 1323 in total showed differential expression between those 2 symptom types; then enrichment analysis of the differentially expressed proteins revealed the significant biological functions related to the differentially expressed proteins, including cardiomyopathy, several bacterial and parasitic infections, bacterial invasion of epithelial cells, insulin signaling pathway, and regulation of actin cytoskeleton. The network analysis showed that FBP2 and Talin-1 were critical points and might determine the evolution directions of TMM warm disease symptom. CONCLUSIONS: This study suggests that the identified core differential proteins may be regarded as potential biomarkers, and benefit to evaluate the evolutionary tendency of TMM warm disease symptoms.