【原】右美托咪定通過p38MARKNF-κB信號通路影響卵巢癌大鼠免疫功能和腫瘤生長

罌粟花anesthGH 2021-07-21

展開全文

本公眾號每天分享一篇最新一期Anesthesia & Analgesia等SCI雜志的摘要翻譯，敬請關(guān)注并提出寶貴意見

In vivo effects of dexmedetomidine on immune function and tumor growth in rats with ovarian cancer through inhibiting the p38MAPK/NF-κB signaling pathway

背景與目的

本研究旨在分析右美托咪啶(Dex)劑量與p38MAPK/NF-κB信號通路的相關(guān)性及其對卵巢癌（OC）大鼠免疫功能和腫瘤生長的影響。

方法

本研究共選取了100只大鼠作為研究對象。正常組由20只大鼠組成，其余80只用于建立OC模型，并進一步分為模型組，0.2倍Dex組、1倍Dex組和5倍Dex組（根據(jù)Dex劑量分類，每組20只）。計算抑瘤率。應(yīng)用免疫組織化學(xué)方法檢測p38和NF-κB在卵巢組織中的陽性表達，MTT法測定細胞轉(zhuǎn)化率和淋巴細胞增殖率，流式細胞術(shù)檢測CD4+、CD8+的細胞周期和細胞凋亡，ELISA法檢測血清IL-2和TNF-α水平，qRT-PCR和Western blotting法檢測p38和NF-κB的mRNA和蛋白表達。

結(jié) 果

與正常組比較，其余4組血清IL-2、TNF-α水平升高，p38、NF-κB65 mRNA和蛋白表達上調(diào)；而CD4+和CD8+細胞的百分比則表現(xiàn)出下調(diào)的趨勢。其它4組腫瘤重量和細胞凋亡均增加，細胞增殖和轉(zhuǎn)化率降低。上述研究結(jié)果表明，與模型組相比，三個Dex組的有更大趨勢。

結(jié) 論

研究結(jié)果提示，特定劑量的Dex可能通過抑制p38MAPK/NF-κB信號通路而增強OC大鼠的免疫功能。

原始文獻摘要

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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