4.7 Article

Thalictrum minus L. ameliorates particulate matter-induced acute lung injury in mice

Journal

JOURNAL OF ETHNOPHARMACOLOGY
Volume 264, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2020.113379

Keywords

Thalictrum minus L.; Particulate matter; Acute lung injury; Homoorientin; Berberine; Inflammation; Oxidative stress

Funding

  1. National Natural Science Foundation of China [81774150, 81973506, 81603328]
  2. Natural Science Foundation of Jiangsu Province [BK20160761]
  3. China Postdoctoral Science Foundation [2016M600456, 2017T100425]
  4. Double First-Class University project [CPU2018GF06, CPU2018GF07]

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Thalictrum minus L., a traditional Mongolian folk medicinal plant, demonstrates effectiveness in attenuating particulate matter-induced acute lung injury by modulating inflammatory cytokines and oxidative damage signaling pathways.
Ethnopharmacological relevance: Thalictrum minus L., which is widespread across Eurasia, is utilized as a folk medicine for treating dysentery, bedsore, fungal infection and lung inflammation in China, Mongolia and Iran. Aim of the study: A Mongolian folk medicinal plant named Thalictrum minus L. (TML) has been extensively used for the treatment of lung inflammation, bacterial and fungal infection and tuberculosis. Our present study aims to investigate the effectiveness of TML against particulate matter (PM)-induced acute lung injury (ALI) and the potential underlying mechanisms. Materials and methods: Initially, HPLC-Q-TOF was applied for the qualitative analysis and HPLC was used for quantitative analysis of main components in TML. Then, the mice model of ALI was induced by PM via intratracheally instilled with 50 mg/kg body weight of Standard Reference Materia11648a (SRM1648a), and TML (10, 20, 40 mg/kg) were administered orally 1 h prior to PM. The efficacy and molecular mechanisms in the presence or absence of TML were elucidated. Results: Eleven main ingredients were detected in TML and the contents of homoorientin and berberine were quantified. Additionally, the results demonstrated that TML profoundly inhibited weight loss in mice and ameliorated lung pathological injury induced by PM. Furthermore, we also found that TML significantly decreased the lung wet to dry weight (W/D) ratios, reduced total protein in bronchoalveolar lavage fluid (BALF), and effectively attenuated PM-induced increased leukocyte and macrophages in BALF. Meanwhile, TML could pronouncedly inhibited myeloperoxidase (MPO) activity in lung tissues, decreased the PM-induced inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1 beta (IL-1 beta), reduced nitric oxide (NO) and increased superoxide dismutase (SOD) in BALF. In addition, TML markedly facilitated the expression of p-AMPK-Nrf2 and suppressed the expression of KEAP, prohibited the activation of the MAPKs-NLRP3/caspase-1 and cyclooxygenase-2 (COX2), and inhibited apoptotic pathways. Conclusion: These findings indicated that TML attenuated PM-induced ALI through suppressing the release of inflammatory cytokines and alleviating oxidative damage correlated with the AMPK-Nrf2/KEAP signaling pathways, MAPKs-NLRP3/caspase-1 signaling pathways, as well as apoptotic pathways.

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