Abstract
Lung cancer has one of the highest mortality rates among various types of cancer and is the most frequent cancer in the world. The incidence of lung cancer is increasing rapidly, in parallel with an increased incidence of smoking. Effective chemoprevention may be an alternative strategy to control the incidence of lung cancer. Thus, the objective of current work was to ascertain the possible preventive and therapeutic efficacies of Cuphea ignea extract in a mouse model of lung tumorigenesis and its cytotoxicity toward the A549 human lung cancer cell line. Lung tumorigenesis was induced by the oral administration of benzo(a)pyrene (50 mg/kg b.w.) twice per week to Swiss albino mice for 4 weeks. Benzo(a)pyrene-treated mice were orally administered C. ignea (300 mg/kg body weight, 5 days/week) for 2 weeks before or 9 weeks after the first benzo(a)pyrene dose, for a total of 21 weeks. At the end of the administration period, various parameters were measured in the serum and lung tissues. The results revealed that the oral administration of benzo(a)pyrene resulted in increases in relative lung weight, serum levels of tumor markers (ADA, AHH, and LDH), and the inflammatory marker NF-κB, and a decreased total antioxidant capacity compared with the control. In addition, decreased levels of enzymatic and non-enzymatic antioxidants, with a concomitant increase in lipid peroxidation, metalloproteinases (MMP-2 and MMP-12), and the angiogenic marker VEGF were detected in lung tissues. Moreover, benzo(a)pyrene administration induced the upregulation of PKCα, COX-2, and Bcl-2 expression, with the downregulation of BAX and caspase-3 expression. C. ignea treatment alleviated all alterations in these parameters, which was further confirmed by the histopathological analysis of lung tissues. The findings of the current work provide the first verification of the preventive and therapeutic potentials of C. ignea extract against benzo(a)pyrene-induced lung tumorigenesis in mice.
Highlights
Lung cancer is one of the most prevalent malignant tumors worldwide [1]
Our results revealed that the levels of Adenosine deaminase (ADA), aryl hydrocarbon hydroxylase (AHH), and lactate dehydrogenase (LDH) in the B(a)P group were significantly increased, by 62.36%, 39.32%, and 62.16%, respectively, compared with the control group
The results of the present study support the promising role of the aqueous ethanolic extract of the aerial parts of C. ignea as a chemopreventive agent against B(a)P-induced lung tumorigenesis in mouse model, and confirmed that pre-treatment was more efficacious than post-treatment
Summary
Lung cancer is one of the most prevalent malignant tumors worldwide [1]. It is a major cause of cancer-associated death, accounting for 18.4% of all cancer deaths, equivalent to approximately 1.76 million deaths in men and women, which represent a major public health problem [2]. Tobacco smoking is the most important etiological risk factor for lung cancer development. The consumption of cigarettes is responsible for the high incidence of lung cancer; an approximately 10fold increase in the risk of developing lung cancer is attributed to longterm smoking, compared with nonsmokers [3]. The major constituents of tobacco smoke, which has a prominent role in the induction of lung cancer induction, are polycyclic aromatic hydrocarbons (PAHs) [4]. It is often used to induce lung tumors in mouse models, as these tumors have molecular
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