[Effects of Cinnabar and Realgar in Angong Niuhuang powder on heat shock protein, nitric oxide synthase and inflammatory cytokines in contusion cerebral edema].

Objective: To explore the pharmacological mechanism of Cinnabar and Realgar in Angong Niuhuang powder (ANP).
Methods: SD rats were randomly divided into six groups (12 rats/group): normal controls group (NS group), contusion cerebral edema model group( CCE group) , cerebral edema rats administrated by cinnabar 0. 15 g/kg 1h (CA group), cerebral edema rats administrated by realgar 0.15 g/kg 1h (RG group), cerebral edema rats administrated by Angong Niuhuang powder 1.5 g/kg 1h (ANP I group), cerebral edema rats administrated by Angong Niuhuang powder substracted cinnabar and realgar 1.2 g/kg 1h (ANP II group). Each group was divided into two subgroups (6 rats/subgroup). The rats in subgroups were killed at 8h and 24h after modeling respectively. Expression of heat shock protein 70 ( HSP 70) mRNA in brain tissues was measured by RT-PCR. Activities of nitric oxide synthase (NOS) and its isoenzymes (iNOS, cNOS) in brain tissues were tested by colorimetry. Levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) in serum were determined by radioimmunoassay (RIA).
Results: Expression of HSP 70 mRNA in ANP I group and ANP II group significantly increased as compared with CCE group 8h after being modeled (P < 0.05), and increase range in ANP I group were singificantly higher than that in ANP II group (P < 0.05). Activities of iNOS in CA group, RG group, ANP I group and ANP II group were lower than that in CCE group 8h after being modeled (P < 0.05) , and the activities in ANP I group were the lowest in the four groups. Levels of TNF-alpha in RG group, ANP I group and ANP II group decreased obviously as compared with CCE group 8h after being modeled (P < 0.05) , so did levels of IL-1beta in ANP I group and ANP II group (P < 0.05). But no significant difference was shown between ANP I group and ANP 11 group.
Conclusion: HSP 70, iNOS, TNF-alpha and IL-1beta are involved in contusion cerebral edema. ANP and CA, RG in ANP are protective against CCE in rats. It may be associated with the increase of HSP 70 mRNA expression, inhibition of iNOS activity, and the decreasae of inflammatory cytokines (TNF-alpha, IL-1beta) levels.