COMBINED IMPACT OF PM2.5 AND CIGARETTE SMOKE ON GASTRIC MUCOSAL MORPHOLOGY: MECHANISMS OF INJURY AND MODERN APPROACHES TO CORRECTION
Abstract
ackground: Air pollution and cigarette smoking are among the most significant modifiable environmental risk factors affecting human health. Fine particulate matter (PM2.5) and cigarette smoke share similar physicochemical properties and biological effects, including oxidative stress, inflammation, and epithelial barrier disruption. However, their combined impact on the gastrointestinal system, particularly gastric mucosa, remains insufficiently explored.
Objective: This study aims to analyze the morphological and functional alterations in gastric tissues under the combined exposure to PM2.5 and cigarette smoke, and to summarize modern approaches for correcting these pathological changes.
Methods: A comprehensive literature review was conducted focusing on experimental and clinical studies investigating the effects of PM2.5 and cigarette smoke on gastric mucosa. Special attention was given to mechanisms of oxidative stress, inflammatory response, apoptosis, microcirculatory disturbances, and epithelial barrier dysfunction.
Results: Combined exposure to PM2.5 and cigarette smoke leads to pronounced morphological damage of gastric mucosa, including epithelial desquamation, glandular dystrophy, inflammatory infiltration, and mucosal barrier disruption. These effects are mediated through synergistic activation of oxidative stress pathways, pro-inflammatory cytokine release, mitochondrial dysfunction, and impairment of tight junction proteins. Furthermore, alterations in cell proliferation and apoptosis contribute to mucosal instability and impaired regeneration.
Conclusion: The combined effect of PM2.5 and cigarette smoke results in significant structural and functional impairment of gastric mucosa. Modern therapeutic strategies, including antioxidant therapy, anti-inflammatory agents, and barrier-protective interventions, show promising potential in mitigating these effects. Further experimental studies are required to develop targeted therapeutic approaches.
Keywords
PM2.5, cigarette smoke, gastric mucosa, oxidative stress, inflammation, apoptosis, epithelial barrier, morphology
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