研究多巴胺受体拮抗剂左旋四氢巴马汀（l2THP）加强电针镇痛（EAA）的原理，阐明中枢神经系统内多巴胺（DA） 系统在EAA中的作用。方法：分别将D1受体激动剂SK&F-38393和D2受体激动剂quinpirole hydrochloride（Qui）注射入大鼠伏膈核，观察对EAA及ι-THP加强EAA的作用。结果：SK&F-38393（5μg，10μg）明显对抗了ι-THP加强EAA的作用，10μgSK&F-38393则减弱EAA；Qui（10μg，20μg）对EAA及ι-THP加强EAA的作用没有显著影响。结论：伏膈核内D1受体活动在EAA及ι-THP加强EAA中起重要作用，D2受体没有显著作用。

[Phe1ψ(CH2-NH) Gly2 nociceptin-(1-13)-NH2, a pseudopeptide analog of nociceptin, was originally seen as an antagonist of nociceptin receptors. In the present study, it was observed that intracerebroventricular (i. c. v.) injection of this pseudopeptide (1, 5, 10μg) significantly decreased the tail-flick latency of rats, indicating a hyperalgesic effect, while intrathecal (i. t.) injection of it (1, 2.5, 10μg) dramatically increased the tail-flick latency, indicating an analgesic effect. This strengthened the in vivo evidence that [Phe1ψ(CH2-NH) Gly2] nociceptin-1-13-NH might be an agonist of nociceptin receptors.

Interleukin-23 (IL-23), a novel cytokine composed of a newly identified p19 molecule and the p40 subunit of IL-12, can stimulate the proliferation in vitro of memory T cells. We examined whether Colon 26 murine colon carcinoma cells that were retrovirally transduced with the p19-linked p40 gene (Colon 26/IL-23) could produce antitumor effects in inoculated mice. The growth of Colon 26/IL-23 tumors developed in immunocompetent mice was significantly retarded and the tumors disappeared thereafter. Spleen cells from the mice that received Colon 26/IL-23 cells produced significant amounts of interferon-γ, when they were cultured with irradiated Colon 26 but not irrelevant cells. Depletion of CD8+T cells suppressed the production of interferon-γ. The mice that had rejected Colon 26/IL-23 tumors were resistant to subsequent challenge of parent but not irrelevant tumor cells. Colon 26/IL-23 tumors were not rejected in nude mice but the growth was retarded compared to parent tumors. Treatment of nude mice with anti-asialo GM1 antibody did not influence the growth of Colon 26/IL-23 tumors. These data suggest that expression of IL-23 in tumors produces T cell-dependent antitumor effects and induces systemic immunity.

We examined whether expression of monokine induced by IFN-γ(Mig, CXCL9) in tumors could produce antitumor effects. Murine lung carcinoma cells (A11) were retrovirally transduced with the murine Mig gene (A11/Mig) and were inoculated into syngeneic mice. Although proliferation in vitro of A11/Mig cells was not different from that of parent cells, the growth in vivo of A11/Mig tumors was significantly retarded compared with that of parent tumors. The antitumor effect was dependent on the amount of Mig produced. We compared the expression level of marker genes of lymphocytes and endothelial cells between parent and A11/Mig tumor masses with reverse transcription-polymerase chain reaction. Expression of CD4, CD8α, CD40, CD86, CD28, CD31 and vascular endothelial growth factor was not different between the two tumor groups but expression of CD40 ligand, CD80, NK1.1 and CXCR3 was relatively lower in A11/Mig tumors. Although Mig is a chemotactic factor for activated T and NK cells and an inhibitor for angiogenesis, the present data suggested that production of Mig in tumors did not recruit activated T and NK cells efficiently or suppress angiogenesis. The antitumor effects by Mig could be independent of anti-angiogenesis and recruitment of T and NK cells.