AN IN-VIVO STUDY OF HEPATIC AND SPLENIC INTERLEUKIN-1-BETA MESSENGER-RNA EXPRESSION FOLLOWING ORAL PSK OR LEM ADMINISTRATION
AN IN-VIVO STUDY OF HEPATIC AND SPLENIC INTERLEUKIN-1-BETA MESSENGER-RNA EXPRESSION FOLLOWING ORAL PSK OR LEM ADMINISTRATION
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DOI：
10.1111/j.1349-7006.1994.tb02943.x
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发表时间：
1994-12-01
期刊：
影响因子：
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通讯作者：
FUJIMAKI, M
中科院分区：
文献类型：
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作者：
MORINAGA, H;TAZAWA, K;FUJIMAKI, M
在实验动物中研究了口服生物反应调节剂（BRM）在预防原发性结直肠癌术后微肝转移中的作用。测试的两种 BRM 是 Krestin (PSK) 和香菇菌丝体 (LEM)。在之前的实验中，我们发现口服PSK或LEM可以抑制肝转移并延长生存期。我们还发现这些药物可以提高肝脏自然杀伤细胞 (NK) 和肝脏巨噬细胞的活性。在本体内研究中，我们使用逆转录聚合酶链反应（RT-PCR）检查肝脏和脾脏是否具有诱导NK细胞和巨噬细胞的细胞因子，以及肝脏和脾脏是否具有由NK细胞或巨噬细胞诱导的细胞因子。我们重点检查体内肝脏和脾脏中白细胞介素（IL）-1β的表达。小鼠口服 PSK 或 LEM (1 g/kg) 2 至 6 小时后，肝脏和脾脏中的 IL-1 β 水平上升，24 小时后恢复到基线水平。这些发现提示了两种可能性：(1) 这些药物在给药后不久就会增强肝脏 IL-1 β，从而激活肝脏 NIC 细胞或巨噬细胞，或者 (2) 这些药物刺激肝脏巨噬细胞产生 IL-1 β，产生的 IL-1 β 会激活肝脏 NK 细胞或肝脏巨噬细胞（库普弗细胞）。这项体内研究的结果表明，PSK 和 LEM 对肝脏和脾脏 IL-1 β 的增强作用参与了结直肠癌微小肝转移的早期抑制。
The effects of orally administered biological response modifiers (BRMs) in preventing postoperative micro liver metastasis of primary colorectal cancer were examined in experimental animals. The two BRMs tested were Krestin (PSK) and Lentinus edodes mycelia (LEM). In previous experiments, we found that oral administration of PSK or LEM suppressed liver metastasis and prolonged the survival period. We also found that these agents elevated the liver natural killer (NK) and liver macrophage activities. In the present study in vivo, using reverse transcriptase-polymerase chain reaction (RT-PCR), we examined whether or not the liver and spleen have cytokines which would induce NK cells and macrophages, and whether or not the liver and spleen have cytokines induced by NK cells or macrophages. We placed emphasis on the examination of interleukin (IL)-1 beta expression in the liver and spleen in vivo. Two to six hours after oral administration of PSK or LEM (1 g/kg) to mice, IL-1 beta levels in the liver and spleen rose, and they returned to their baseline levels 24 h later. These findings suggest two possibilities: (1) hepatic IL-1 beta is potentiated by these agents soon after administration, resulting in activation of liver NIC cells or macrophages, or (2) these agents stimulate IL-1 beta production by liver macrophages, and the produced IL-1 beta activates liver NK cells or liver macrophages (Kupffer cells). The results of this in vivo study suggest that the potentiation of hepatic and splenic IL-1 beta by PSK and LEM is involved in the early phases of suppression of micro liver metastases of colorectal cancer.