Effects of different components of Mao Dongqing's total flavonoids and total saponins on transient ischemic attack (TIA) model of rats.

Objective: To study the effects of the different components of the total flavonoids and total saponins from Mao Dongqing's active site on the rats of TIA model, determine the optimal reactive components ratio of Mao Dongqing on the rats of TIA. Methods: TIA rat model was induced by tail vein injection of tert butyl alcohol, the blank group was injected with the same amount of physiological saline, then behavioral score wasevaluated. Determination the level of glutamic acid in serum, the activity of Na+-K+-ATP enzyme, CA++-ATP enzyme and Mg++-ATP enzyme in Brain tissue, observe the changes of hippocampus in brain tissue, the comprehensive weight method was used to evaluate the efficacy of each component finally. Results: The contents of total flavonoids and total saponins in the active part of Mao Dongqing can significantly improve the pathological changes of brain tissue in rats, improve the activity of Na+-K+-ATP enzyme, Ca++-ATP enzyme and Mg++-ATP enzyme in the brain of rats, and reduce the level of glutamic acid in serum. The most significant of the contents was the ratio of 10:6. CONCLUSION: The different proportions of total flavonoids and total saponins in the active part of Mao Dongqing all has a better effect on the rats with TIA, and the ratio of 10:6 is the best active component for preventing and controlling TIA.

[Changes in electroencephalograph and somatosensory evoked potential and their relationship with neuron apoptosis in rat after ischemic insult to brain].

OBJECTIVE: To study the changes in electroencephalograph (EEG) and somatosensory evoked potential (SEP) and their relationship with neuron apoptosis in rat after ischemic insult to the brain. METHODS: Thirty-five SD rats were randomly divided into normal, sham operated and 3, 12, 24, 48, 72 hours after ischemia/reperfusion (I/R) groups with 5 rats in each group. The ischemia of brain was produced by clamping 4 vessels to the brain for various periods of time. Changes in EEG and SEP were recorded at different time after I/R, and the amounts of apoptotic neurons in hippocampus and cortex after I/R were assessed with terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) and acridine orange ethidium bromide (AO/EB) fluorescence examination techniques. RESULTS: Compared with sham operated group, EEG amplitude decreased significantly (all P<0.05), and the proportion of Delta wave increased significantly after ischemia of the brain (all P<0.05). The latent period of P1 wave crest extended markedly (all P<0.05), and P1-N1 amplitude decreased significantly after I/R (all P<0.05). EEG and SEP changes were correlated with the apoptosis and loss of neurons, which started in the hippocampus and extended to frontal cortex and parietal cortex. CONCLUSION: The combined analysis of EEG and SEP can reflect the process of neuron apoptosis, which is helpful for the diagnosis and evaluation of prognosis of patients suffering from cerebral ischemia.

Time window characteristics of cultured rat hippocampal neurons subjected to ischemia and reperfusion.

OBJECTIVE: To explore cell death and apoptosis in rat hippocampal neurons at different time points after ischemia, hypoxia and reperfusion injury and to elucidate time window characteristics in ischemia neuronal injury. METHODS: Hippocampal neurons were obtained from rat embryo and were cultured in vitro. The ischemia and reperfusion of cultured rat hippocampal neurons were simulated by oxygen-glucose deprivation (OGD) and recovery. OGD at different time points (0.25 h to 3.0 h) and then the same recovery (24 h) were prepared. Annexin V-PI staining and flow cytometry examined neuron death and apoptosis at different time after injury. RESULTS: After OGD and recovery, both necrosis and apoptosis were observed. At different times after OGD, there were statistically significant differences in neuron necrosis rate (P < 0.05), but not in apoptosis rate (P > 0.05). At recovery, survival rate of hippocampal neurons further decreased while apoptosis rate increased. Furthermore, apoptosis rates of different time differed greatly (P < 0.05). Apoptosis rate gradually increased with significant difference among those of different time points (P < 0.05). However, 2 h after ischemia, apoptosis rate decreased markedly. CONCLUSIONS: Apoptosis is an important pathway of delayed neuron death. The therapeutic time window should be within 2 h after cerebral ischemia and hypoxia.