Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China (mainland).
Endoscopic Center of Nanjing Chest Hospital, Nanjing, Jiangsu, China (mainland).
Med Sci Monit. 2019 Oct 7;25:7538-7546. doi: 10.12659/MSM.917115.
BACKGROUND Lung cancer is the leading cause of cancer deaths in the world. Its major histopathological subtype is non-small cell lung cancer (NSCLC). Xiaoai Jiedu recipe (XJR) is a traditional Chinese medicine formula that can suppress growth and invasion of tumor cells. Here, we assessed the antitumor effect of XJR on NSCLC explored the underlying mechanisms. MATERIAL AND METHODS Three concentrations of XJR (low, middle, and high) were used to treat A549 cells. Cell Counting Kit-8 and colony formation assay were used to measure proliferation of A549 cells. Apoptosis was evaluated by Hoechst 33342 staining and flow cytometry. The expression of apoptosis-associated proteins was measured by Western blot analysis. Transwell and scratch wound healing assay were used to assess invasion and migration, respectively, of A549 cells. The expression of p38 MAPK pathway-associated proteins were measured using Western blot analysis. RESULTS XJR suppressed proliferation and promoted apoptosis of A549 cells, especially in the high-dose group. The expression of Bcl-2 was reduced with increasing expression of Bax, cleaved caspase-3, and cleaved caspase-9. Invasion and migration abilities of A549 cells were inhibited after XJR treatment. XJR treatment decreased the expression levels of phosphorylated p38 (p-p38), p-ERK, and p-JNK in a dose-dependent manner. CONCLUSIONS The results demonstrated that XJR can inhibit proliferation, invasion, and migration, and induce apoptosis of NSCLC by blocking the p38 MAPK pathway, which shows the potential of XJR as a new treatment of NSCLC.
肺癌是全球癌症死亡的主要原因。其主要组织病理学亚型是非小细胞肺癌（NSCLC）。消癌解毒方（XJR）是一种中药方剂，能抑制肿瘤细胞的生长和侵袭。在这里，我们评估了 XJR 对 NSCLC 的抗肿瘤作用，并探讨了其潜在的机制。
用三种浓度的 XJR（低、中、高）处理 A549 细胞。用细胞计数试剂盒-8 和集落形成实验来测量 A549 细胞的增殖。用 Hoechst 33342 染色和流式细胞术评估细胞凋亡。用 Western blot 分析测定凋亡相关蛋白的表达。用 Transwell 和划痕愈合实验分别评估 A549 细胞的侵袭和迁移。用 Western blot 分析测定 p38 MAPK 通路相关蛋白的表达。
XJR 抑制 A549 细胞的增殖并促进其凋亡，尤其是在高剂量组。Bcl-2 的表达减少，同时 Bax、cleaved caspase-3 和 cleaved caspase-9 的表达增加。XJR 处理后 A549 细胞的侵袭和迁移能力受到抑制。XJR 处理呈剂量依赖性地降低磷酸化 p38（p-p38）、p-ERK 和 p-JNK 的表达水平。
结果表明，XJR 通过阻断 p38 MAPK 通路抑制 NSCLC 的增殖、侵袭和迁移，并诱导其凋亡，显示了 XJR 作为 NSCLC 新治疗方法的潜力。
