Qi-Hang Cai1, Yao Tang1, Shao-Hua Fan1, Zi-Feng Zhang1, Hong Li2, Shao-Qiang Huang2, Dong-Mei Wu3, Jun Lu4, Yuan-Lin Zheng5. 1. Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, PR China. 2. Department of Anesthesiology, Obstetrics & Gynecology Hospital of Fudan University, Shanghai 200090, PR China. 3. Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, PR China. Electronic address: wdm8610@jsnu.edu.cn. 4. Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, PR China. Electronic address: lu-jun75@163.com. 5. Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, PR China. Electronic address: ylzheng@jsnu.edu.cn.
Abstract
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.
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.