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ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

Protective effects of Tanshinone IIA preconditioning against hypobaric hypoxia-induced lung injury in a rat model.

Seema Yadav, Somnath Singh, Mrinalini Singh

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Seema YadavExperimental Biology Division, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Lucknow Road, Timarpur, Delhi, 110 054, India.
Somnath SinghExperimental Biology Division, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Lucknow Road, Timarpur, Delhi, 110 054, India.
Mrinalini SinghExperimental Biology Division, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Lucknow Road, Timarpur, Delhi, 110 054, India. mrinalini.dipas@gov.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tanshinone IIA (Tan-IIA), derived from Salvia miltiorrhiza, has been used in traditional Chinese medicine to treat cardiovascular diseases and pulmonary hypertension. This study investigates the potential of Tan-IIA preconditioning as a protective strategy against hypoxia-induced lung injury. Male Sprague-Dawley rats (200 ± 25 g) were divided into four groups: normoxia, normoxia with Tan-IIA, hypobaric hypoxia, and hypobaric hypoxia with Tan-IIA. Tan-IIA was administered intraperitoneally at doses of 10, 20, and 40 mg/kg body weight one hour before exposure to hypobaric hypoxia (simulated altitude of 25,000 feet for 48 h). Pulmonary edema was assessed by measuring transvacuolar leakage of sodium fluorescein dye and lung water content. Exposure to hypoxia triggered redox imbalances, inflammation, and changes in levels of nitric oxide (NOx), endothelin- 1, and Na/K ATPase, which contributed to pulmonary edema. Tan-IIA preconditioning, particularly at 20 mg/kg, was effective in reversing these disturbances. Tan-IIA modulated the expression of key signaling molecules, including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38, as well as downstream activator protein- 1 (AP- 1) subunits (Jun and Fos), thus reducing inflammation. Its protective effects were partly due to increased NO levels and decreased endothelin, which lowered pulmonary vasoconstriction and permeability, respectively. Additionally, enhanced Na/K ATPase expression via hypoxia-inducible factor- 1 (HIF- 1) and AP- 1 pathways promoted alveolar fluid clearance, while interactions between nuclear factor erythroid 2-related factor 2 (Nrf2) and c-Jun highlighted the anti-oxidative properties of Tanshinone IIA. These findings demonstrate that Tanshinone IIA preconditioning protects against hypoxia-induced lung injury by mitigating pulmonary leakage. This highlights its potential therapeutic application in hypoxic lung conditions.

Indexed as

AbietanesHypoxiaLung InjuryAnimalsDisease Models, AnimalEndothelin-1LungMaleNitric OxidePulmonary EdemaRatsRats, Sprague-DawleySodium-Potassium-Exchanging ATPaseAbietanesEndothelin-1Nitric OxideSodium-Potassium-Exchanging ATPasetanshinoneHypobaric hypoxiaPulmonary edemaTanshinone IIA

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.