肺癌（LC）是全球恶性肿瘤相关死亡的主要原因，现有的治疗干预措施与有害的副作用有关。在当前的研究中，我们评估了橙花叔醇（NRD）对人类非小细胞肺癌（NSCLC）细胞的抗肿瘤功效。橙花叔醇是一种从芳香植物精油中提取的倍半萜醇，具有已知的抗癌活性。 NRD 对 A549 细胞的抗增殖和凋亡作用的潜在作用尚不确定。因此，我们的工作旨在探索 NRD（20 和 25 μM/mL）对 A549 细胞的抗增殖和凋亡作用。使用MTT测试评估NRD对A549细胞的细胞毒性、细胞内活性氧（ROS）、线粒体膜电位（MMP）、细胞凋亡、抗凋亡蛋白以及MAPK/TAT3/NF-κB和P13K/AKT信号通路的活性、二氯二氢荧光素二乙酸酯（DCFH-DA）、双吖啶橙/溴化乙锭（AO/EB）、DAPI、Rh-123、逆转录聚合酶链反应（RT-PCR）和蛋白质印迹分析。我们发现NRD可以抑制NSCLC通过提高细胞内 ROS 和 MMP 损失来增强细胞活力，并以数量依赖性方式引发细胞凋亡。同样，NRD 可以减少炎症细胞因子和抗凋亡元件，并触发凋亡信号通路。我们的数据表明，NRD 通过 ROS 介导的细胞凋亡来减少 A549 细胞增殖，触发 MAPK/STAT3/NF-κB 和 P13K/AKT 通路，表明 NRD 是 NSCLC 的一种可能的保护性疗法。

Lung cancer (LC) is the leading cause of malignancy-related mortalities globally, and the existing treatment interventions are associated with harmful side effects. In the current study, we evaluated the anti-tumor efficiency of nerolidol (NRD) on human non-small cell lung cancer (NSCLC) cells.Nerolidol is a sesquiterpene alcohol extracted from the essential oils of aromatic flora with known anti-cancer activities.The latent action of NRD on antiproliferative and apoptotic effects in A549 cells is uncertain. Thus, our work is designed to explore the antiproliferative and apoptotic actions of NRD (20 and 25 μM/mL) against A549 cells. The activity of NRD on A549 cell cytotoxicity, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), apoptosis, anti-apoptotic proteins, and MAPK/TAT3/NF-κB and P13K/AKT signaling pathways were assessed using MTT tests, dichlorodihydrofluorescein diacetate (DCFH-DA), dual acridine orange/ethidium bromide (AO/EB), DAPI, Rh-123, reverse transciption polymerase chain reaction (RT-PCR), and western blot analyses.We found that NRD could inhibit NSCLC cell viability through elevated intracellular ROS and MMP loss and elicited apoptosis in a quantity-dependent manner. Similarly, NRD can reduce inflammatory cytokines and anti-apoptotic elements, as well as trigger apoptotic signaling pathways.Our data established that NRD decreases A549 cell proliferation through ROS-mediated apoptosis, triggering the MAPK/STAT3/NF-κB and P13K/AKT pathways, suggesting that NRD is a possible protective remedy for NSCLC.