ABSTRACT
Objective:To study the effect and underlying mechanism of BCG polysaccharide and nucleic acid ( BCG-PSN) in hy-persusceptibility in guinea pigs to explore the improvement method for the quality control model of BCG-PSN. Methods:The ovalbumin induced hypersusceptibility animal model was established, the effect of BCG-PSN on hypersusceptibility in guinea pigs was observed. According to the guideline for immunity toxicity study on Chinese traditional medicine and natural medicine, the hypersusceptibility tests were carried out. Serum IgE and histamine were determined by ELISA. Results:The guinea pigs in the model group and the low dosage BCG-PSN group showed strong anaphylactic symptoms, while the middle and high dosage BCG-PNS groups showed fewer symp-toms. The level of IgE in the model group was (1. 673 0 ± 0. 158 6) μg·ml-1 and (1. 683 1 ± 0. 228 1)μg·ml-1 before and after the attacking, respectively, which was higher than that in the control group(P<0. 01). The levels of IgE in the middle and high dos-age BCG-PNS groups were decreased compared with those in the model group before and after the attacking(P<0. 01). The same re-sults were observed in the levels of histamine. Before and after the attacking, the levels of histamine in the model group was (1. 499 7 ± 0. 133 1) ng·ml-1 and (1. 512 1 ± 0. 050 6) ng·ml-1 , respectively, while the levels of histamine in low, middle and high dos-age BCG-PNS groups were decreased compared with those in the model group before and after the attacking(P<0. 01). Conclusion:BCG-PSN can dose-dependently inhibit the anaphylactic reaction induced by ovalbumin.
ABSTRACT
The human immunodeficiency virus type 1 (HIV-1) protease mutation D30N is exclusively selected by the protease inhibitor (PI) nelfinavir and confers resistance to this drug. We demonstrate that D30N increases the susceptibility to saquinavir (SQV) and amprenavir in HIV-1 subtype B isolates and that the N88D mutation in a D30N background neutralizes this effect. D30N also suppresses indinavir (IDV) resistance caused by the M46I mutation. Interestingly, in patients with viruses originally containing the D30N mutation who were treated with IDV or SQV, the virus either reversed this mutation or acquired N88D, suggesting an antagonistic effect of D30N upon exposure to these PIs. These findings can improve direct salvage drug treatment in resource limited countries where subtype B is epidemiologically important and extend the value of first and second line PIs in these populations.