Rats of vascular dementia were established with bilateral carotid artery ligation. After 30 days rats were treated nicergoline tablets 25, 12.5 and 6.25 mg/kg per day of total alkaloids of harmaline for 30 days. Learning and memory abilities were tested by Morris water maze, histomorphology in the hippocampal CA1 area was observed by HE staining, BAX and BCL-2 protein expression in the hippocampal CA1 area were detected by immunohistochemistry. 25 mg/kg of total alkaloids of harmaline shortened the incubation period in the third and fourth day significantly, and 12.5 mg/kg shortened the incubation period in the fourth day. Total alkaloids of harmaline improved the neurons pathological changes of the rats in the hippocampus CA1 area, 25 and 12.5 mg/kg of total alkaloids of harmaline downregulated the expression of apoptosis proteins BAX, upregulated the protein expression of BCL-2.

Human hepatoma HepG2 cells were maintained in Dulbecco's modified Eagle's medium, supplemented with 10% heat-inactivated fetal bovine serum, 2 mM L-glutamine, 100 IU/mL penicillin, and 100 micro-g/mL streptomycin and incubated at 37 deg-C under a 5% CO2 atmosphere. Cells were treated in serum-free medium with TCDD in presence of various concentrations of harmaline dissolved in up to 0.05% DMSO, and incubated for 24 hours. The effect of harmaline on HepG2 cell viability was determined by measuring the capacity of reducing enzymes present in viable cells to convert MTT to formazan crystals. At a concentration range of 0 25 micro-M, harmaline did not significantly affect cell viability when incubated with human hepatoma cells for 24 h either in presence or absence of TCDD.