ArticleFood science & nutrition2021
Potential of rosmarinic acid to ameliorate toxic effects of diethyl methoxy thio‑phosphoryl thio‑succinate on albino wistar rats' lung, mast cell infiltration inhibitory pathway.
Article in Food science & nutrition, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Protective effects of rosmarinic acid against carbaryl-exposed toxicity in honey bees (Apis mellifera): histopathological and molecular docking evidence.Veterinary research communications · 2026Article
- Advanced application of nanotechnology in active constituents of Traditional Chinese Medicines.Journal of nanobiotechnology · 2023Review
- Biomedical features and therapeutic potential of rosmarinic acid.Archives of pharmacal research · 2022Review
- Potential of rosmarinic acid to ameliorate toxic effects of diethyl methoxy thio‑phosphoryl thio‑succinate on albino wistar rats' lung, mast cell infiltration inhibitory pathway.Food science & nutrition · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malathion (MA) is a widely used pesticide in agriculture. It can cause toxicity in different organs of the body. Rosmarinic acid (RO) is found in rosemary extract that can be absorbed through gastrointestinal tract mucosa with potent antioxidant, and anti-inflammatory potential. The current study is designed to investigate the potential of RO to protect the lung after MA administration. Forty albino rats were allocated equally to four groups. C-group received corn oil. RO-group received RO orally. MA-group received MA. MA-RO-group received RO in addition to MA. After three weeks the lungs were dissected for histopathological and biochemical investigations. MA-group showed manifestations of severe inflammation with inflammatory cells infiltration in the lung. MA-RO-group showed limited inflammatory cell infiltration. C-group and RO-group appeared with weak anti-survivin immunoreactivity. MA-group showed strong positive immunoreactivity. The reactivity was weakly positive in MA-RO-group. MA-group showed a significant decrease in SP-D gene expression in comparison to the C-group, in addition, MA-RO-group showed a significant increase in SP-D expression. In conclusion, the current study approves that oral administration of MA causes lung injury as it has inflammatory effects, caused by oxidative stress and reports the potential of RO to protect lung tissue against toxic effects of MA through its anti-inflammatory, antioxidant, and anti-apoptotic potential.
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