AI Summary & Key Takeaways
AI InsightConclusion: CAPE may potentially represent a new therapeutic option in the prevention of CS-induced lung damages.
📌 3 Key Takeaways
Abstract
Background/aim: To evaluate the influence of caffeic acid phenethyl ester (CAPE) on cigarette smoke (CS)-induced cell damage, oxidative stress, and inflammation in human alveolar epithelial cells. Materials and methods: A549 alveolar epithelial cells were divided into control, CS exposure, CAPE, and CS+CAPE treatment groups. Undiluted CS-exposed medium (100%) and three dilutions (50%, 25%, and 10%) of CS-exposed media were applied to cultured A549 cells, which were analyzed after 3 h of incubation. Viability was measured by MTT assay, the gene expressions were evaluated by real-time PCR, and spectrophotometric techniques were used for biochemical assessments. Results: While CS exposure markedly reduced cellular viability by 32% after 3 h of incubation, 2.5 µM CAPE treatments prevented CS-induced cell death by 40% in the cells. CS exposure triggered lipid peroxidation and depleted antioxidant capacity through inhibiting catalase activity and depleting glutathione levels. Moreover, CS increased nitric oxide production via upregulation of iNOS expression. CAPE treatment significantly restored antioxidant capacity and prevented lipid peroxidation. Cigarette smoke exposure induced inflammation by significantly upregulating TNF-?, IL-1Ã, and COX-2 mRNA expressions (3-, 2- and 25-fold, respectively). CAPE treatment of A549 cells significantly reversed the inflammation. Conclusion: CAPE may potentially represent a new therapeutic option in the prevention of CS-induced lung damages.
Özet
Background/aim: To evaluate the influence of caffeic acid phenethyl ester (CAPE) on cigarette smoke (CS)-induced cell damage, oxidative stress, and inflammation in human alveolar epithelial cells. Materials and methods: A549 alveolar epithelial cells were divided into control, CS exposure, CAPE, and CS+CAPE treatment groups. Undiluted CS-exposed medium (100%) and three dilutions (50%, 25%, and 10%) of CS-exposed media were applied to cultured A549 cells, which were analyzed after 3 h of incubation. Viability was measured by MTT assay, the gene expressions were evaluated by real-time PCR, and spectrophotometric techniques were used for biochemical assessments. Results: While CS exposure markedly reduced cellular viability by 32% after 3 h of incubation, 2.5 µM CAPE treatments prevented CS-induced cell death by 40% in the cells. CS exposure triggered lipid peroxidation and depleted antioxidant capacity through inhibiting catalase activity and depleting glutathione levels. Moreover, CS increased nitric oxide production via upregulation of iNOS expression. CAPE treatment significantly restored antioxidant capacity and prevented lipid peroxidation. Cigarette smoke exposure induced inflammation by significantly upregulating TNF-?, IL-1Ã, and COX-2 mRNA expressions (3-, 2- and 25-fold, respectively). CAPE treatment of A549 cells significantly reversed the inflammation. Conclusion: CAPE may potentially represent a new therapeutic option in the prevention of CS-induced lung damages.