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In vivo effects of dexmedetomidine on immune function and tumor growth in rats with ovarian cancer through inhibiting the p38MAPK/NF-κB signaling pathway
背景与目的
本研究旨在分析右美托咪啶(Dex)剂量与p38MAPK/NF-κB信号通路的相关性及其对卵巢癌（OC）大鼠免疫功能和肿瘤生长的影响。
方 法
本研究共选取了100只大鼠作为研究对象。正常组由20只大鼠组成，其余80只用于建立OC模型，并进一步分为模型组，0.2倍Dex组、1倍Dex组和5倍Dex组（根据Dex剂量分类，每组20只）。计算抑瘤率。应用免疫组织化学方法检测p38和NF-κB在卵巢组织中的阳性表达，MTT法测定细胞转化率和淋巴细胞增殖率，流式细胞术检测CD4+、CD8+的细胞周期和细胞凋亡，ELISA法检测血清IL-2和TNF-α水平，qRT-PCR和Western blotting法检测p38和NF-κB的mRNA和蛋白表达。
结 果
与正常组比较，其余4组血清IL-2、TNF-α水平升高，p38、NF-κB65 mRNA和蛋白表达上调；而CD4+和CD8+细胞的百分比则表现出下调的趋势。其它4组肿瘤重量和细胞凋亡均增加，细胞增殖和转化率降低。上述研究结果表明，与模型组相比，三个Dex组的有更大趋势。
结 论
研究结果提示，特定剂量的Dex可能通过抑制p38MAPK/NF-κB信号通路而增强OC大鼠的免疫功能。
原始文献摘要
Cai Q H, Tang Y, Fan S H, et al. In vivo effects of dexmedetomidine on immune function and tumor growth in rats with ovarian cancer through inhibiting the p38MAPK/NF-κB signaling pathway[J]. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2017, 95:1830.
OBJECTIVES:
During this study, we aimed to analyze the correlation between dosages of dexmedetomidine (DEX) and the p38MAPK/NF-κB signaling pathway, and their effects on immune function and tumor growth in rats with ovarian cancer (OC).
METHODS:
A total of 100 rats were selected for the purposes of the study. The normal group consisted of 20 rats, while the remaining 80 rats were utilized for OC model establishment purposes, and further assigned into the model, 0.2 DEX, 1 DEX and 5 DEX groups (based on respective dosages of DEX, n=20 per group). The tumor inhibition rate was calculated. Positive expressions of p38 and NF-κB in ovarian tissues were examined by means of immunohistochemical staining. Cell transformation as well as lymphocyte proliferation rates were measured using MTT. Cell cycle and apoptosis of CD4+ and CD8+ cells were determined by flow cytometry. Serum levels of IL-2 and TNF-α were detected using ELISA, while qRT-PCR and western blotting methods were used to analyze mRNA and protein expressions of p38 and NF-κB.
RESULTS:
Compared with the normal group, the other four groups exhibited up-regulated IL-2, TNF-α serum levels as well as up regulated expressions of p38, NF-κB65 mRNA and protein; while the respective percentages of both CD4+ and CD8+ T cells exhibited down-regulated rates. The other four groups displayed increases in tumor weight and cell apoptosis, as well as decreased levels of cell proliferation and transformation rates. The aforementioned findings of the study ultimately highlighted a greater tendency among the three DEX groups in comparison to the model group.
CONCLUSION:
The findings of the study suggest that a particular dosage of DEX may act to enhance the immune function of rats with OC by inhibiting the p38MAPK/NF-κB signaling pathway.
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