ArticleHistology and histopathology2025
Melatonin inhibits the activation of microglia and cough sensitivity of guinea pigs exposed to PM2.5.
Article in Histology and histopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of supplementation with nutrients and dietary supplements on recovery and inflammatory response among patients with COVID-19: a network meta-analysis.Frontiers in nutrition · 2026Pooled it
- Effects of Melatonin Disorders on Parkinson's Disease: A Review of Mechanisms and Clinical Manifestations.Neuropsychiatric disease and treatment · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
objectiveThe study aimed to examine the impact of melatonin on mitigating brain inflammation and cough sensitivity resulting from exposure to particulate matter 2.5 (PM2.5).
methodsGuinea pigs were randomly assigned to the blank control group, normal saline group, PM2.5 exposure group, and PM2.5 exposure + melatonin group. The PM2.5 exposure and PM2.5 exposure + melatonin groups were given intranasal instillations of PM2.5 suspension twice daily for 28 consecutive days. Starting on day 21, the PM2.5 exposure + melatonin group was treated with an intraperitoneal injection of melatonin at 10 pm. Cough sensitivity to citric acid, microglia activation, IL-1β and TNF-α levels in the airway and dorsal vagal complex (DVC), and ultrastructural changes in neurons within the DVC were assessed.
resultsThe PM2.5 exposure group exhibited a significantly higher cough count to citric acid challenge (29.1±5.7 coughs) compared with the PM2.5 exposure + melatonin group (18.8±4.1 coughs), normal saline group (8.4±2.1 coughs), and blank control group (7.7±1.8 coughs). In addition, cough latency was shorter in the PM2.5 exposure group (26.9±6.5 seconds) than in the PM2.5 exposure + melatonin group (36.6±12.4 seconds), normal saline group (43.4±14.7 seconds), and blank control group (47.0±13.0 seconds). The PM2.5 exposure + melatonin group showed significantly reduced IL-1β (105.3±14.3 pg/ml) and TNF-α levels (113.0±23.5 pg/ml) in the DVC, as well as in the bronchoalveolar lavage fluid (IL-1β: 24.92±5.14 pg/ml, TNF-α: 12.72±3.99 pg/ml) compared with the PM2.5 exposure group (in the DVC: IL-1β: 132.7±17.6 pg/ml, TNF-α: 143.8±30.4 pg/ml; in the bronchoalveolar lavage fluid: IL-1β: 34.0±5.3 pg/ml; TNF-α: 15.8±0.8 pg/ml). Microglia in the DVC were less activated in the PM2.5 exposure + melatonin group (25.1±5.4) than in the PM2.5 exposure group (54.6±9.9). Furthermore, the PM2.5 exposure group exhibited an impaired blood-brain barrier in the DVC, which tended to alleviate the PM2.5 exposure + melatonin group.
conclusionsExposure to PM2.5 induces airway inflammation, central facilitation, and heightened cough sensitivity in guinea pigs. Melatonin significantly inhibits microglia activation and reduces airway and DVC inflammation, which might contribute to attenuated cough hypersensitivity.
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