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应用ＲＴＰＣＲ及荧光探针标记技术观察大鼠腹腔巨噬细胞经内毒素活化后ＩＬ１２ｍＲＮＡ表达水平及细胞内信号传递系统和大黄酸对其调控作用。结果表明，内毒素能活化大鼠腹腔巨噬细胞使［Ｃａ２＋］ｉ水平及ＩＬ１２ｍＲＮＡ表达水平明显升高，并呈剂量依赖相关关系，随着ＬＰＳ剌激浓度的增加，ＩＬ１２ｍＲＮＡ表达水平及细胞内游离钙离子浓度逐渐增加。大黄酸能显著抑制ＬＰＳ活化的大鼠腹腔巨噬细胞ＩＬ１２ｍＲＮＡ表达水平及［Ｃａ２＋］ｉ的升高，亦呈剂量依赖相关关系，随着大黄酸浓度的增加ＩＬ１２ｍＲＮＡ表达水平及［Ｃａ２＋］ｉ逐渐降低。ＰＫＣ活化剂ＰＭＡ及Ａ２３１８７能显著提高ＩＬ１２ｍＲＮＡ的表达水平（与对照比较Ｐ＜０．００１，与ＬＰＳ组比较Ｐ＜０．０５）而ＰＫＣ抑制剂Ｃａｌ及ＳＰ能使经ＬＰＳ活化的大鼠腹腔巨噬细胞ＩＬ１２ｍＲＮＡ表达水平明显降低（与ＬＰＳ组比较Ｐ＜０．０１），大黄酸亦能显著抑制ＬＰＳ所至ＩＬ１２ｍＲＮＡ表达水平的升高。表明大鼠腹腔巨噬细胞经ＬＰＳ活化后其ＩＬ１２ｍＲＮＡ表达需经细胞内信号传递系统调控，大黄酸通过降低［Ｃａ２＋］ｉ使ＩＬ１２ｍＲＮＡ表达水平降低。
Application of RT PCR and fluorescent probe labeling technology observed peritoneal macrophages after endotoxin activation of IL 12mRNA expression and intracellular signaling system and rhein on its regulation. The results showed that endotoxin can activate rat peritoneal macrophages so that the level of [Ca2] i and IL 12 mRNA expression was significantly increased, and in a dose-dependent manner, with the LPS stimulated concentration increased, IL 12 mRNA expression levels And intracellular free calcium concentration gradually increased. Rhein can significantly inhibit LPS-activated rat peritoneal macrophages IL 12 mRNA expression and [Ca2 +] i increased, also showed a dose-dependent relationship with the rhein concentration increased IL 12 mRNA expression level and [Ca2 + ] I gradually decreased. PKC activators PMA and A23187 could significantly increase the expression of IL-12 mRNA (P <0.001 compared with the control, P <0.05 compared with LPS group), and PKC inhibitor Cal and SP could make LPS activated rats The expression of IL-12mRNA in peritoneal macrophages decreased significantly (compared with LPS group, P <0.01), rhein also significantly inhibited the expression of IL-12mRNA induced by LPS. These results indicated that the peritoneal macrophages of rat were activated by LPS, and the expression of IL-12mRNA was regulated by the intracellular signaling system. Rhein reduced the expression of IL-12mRNA by decreasing [Ca2 +] i.