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Abstract
Luteolin significantly attenuates cigarette smoke-induced lung damage and inflammation in mouse models.
- Cigarette smoke exposure is a major risk factor for chronic obstructive pulmonary disease and is associated with cellular aging.
- Luteolin reduces histopathological changes and inflammatory cytokine release caused by cigarette smoke in mouse lung cells.
- Transcriptome analysis indicates that NQO1 and Fos may be key molecular targets in the context of cigarette smoke damage and luteolin treatment.
- Activation of the CREB pathway by luteolin may mitigate cellular aging effects without relying on PKA activation.
- Findings highlight the potential of luteolin as a therapeutic option for managing inflammation and cellular aging related to cigarette smoke.
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