Evidence map›Paper›PMID 30744607›Full record

ArticleBMC pulmonary medicine2019

Ligustrazin increases lung cell autophagy and ameliorates paraquat-induced pulmonary fibrosis by inhibiting PI3K/Akt/mTOR and hedgehog signalling via increasing miR-193a expression.

Ming-Wei Liu, Mei-Xian Su, Deng-Yun Tang, Li Hao, Xiang-Han Xun, Yun-Qiao Huang

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
9.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 94 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Ming-Wei LiuDepartment of Emergency, the First Affiliated Hospital of Kunming Medical University, 295 Xichang Road, Kunming, 650032, Yunan, People's Republic of China. lmw2004210@163.com.
Mei-Xian SuEmergency Intensive Care Unit, the Second Affiliated Hospital of Kunming Medical University, Kunming, 650106, China.
Deng-Yun TangSkin Disease Prevention Institute of Wenshan Zhuang and Miao autonomous prefecture, Wenshan, 655500, China.
Li HaoIntensive Care Unit, the Yan-an Affiliated Hospital of Kunming Medical University, Kunming, 650106, China.
Xiang-Han XunDepartment of Thoracic Surgery, People's Hospital of Fuyuan County, Qujing, 655500, China.
Yun-Qiao HuangDepartment of Emergency, the First Affiliated Hospital of Kunming Medical University, 295 Xichang Road, Kunming, 650032, Yunan, People's Republic of China. 15198852569@139.com.
Kunming Medical University · CNFourth People's Hospital of Taiyuan · CNPeople’s Hospital of Wenshan Prefecture · CN

Funding

Yunnan Applied Basic Research Project-Union Foundation of China 2017FE468 (-032)
6 · The paper itself

Abstract

backgroundReactive oxygen species (ROS) levels largely determine pulmonary fibrosis. Antioxidants have been found to ameliorate lung fibrosis after long-term paraquat (PQ) exposure. The effects of antioxidants, however, on the signalling pathways involved in PQ-induced lung fibrosis have not yet been investigated sufficiently. Here, we examined the impacts of ligustrazin on lung fibrosis, in particular ROS-related autophagy and pro-fibrotic signalling pathways, using a murine model of PQ-induced lung fibrosis.

methodsWe explored the effects of microRNA-193 (miR-193a) on Hedgehog (Hh) and PI3K/Akt/mTOR signalling and oxidative stress in lung tissues. Levels of miR-193a, protein kinase B (Akt), phosphoinositide 3-Kinase (PI3K), ceclin1, mammalian target of rapamycin (mTOR), sonic hedgehog (SHH), myosin-like Bcl2 interacting protein (LC3), smoothened (Smo), and glioma-associated oncogene-1 (Gli-1) mRNAs were determined with quantitative real-time PCR. Protein levels of PI3K, p-mTOR, p-Akt, SHH, beclin1, gGli-1, LC3, smo, transforming growth factor-β1 (TGF-β1), mothers against DPP homologue-2 (Smad2), connective tissue growth factor (CTGF), collagen I, collagen III, α-smooth muscle actin (α-SMA) nuclear factor erythroid 2p45-related factor-2 (Nrf2), and p-Smad2 were detected by western blotting. In addition, α-SMA, malondialdehyde, ROS, superoxide dismutase (SOD), oxidised and reduced glutathione, hydroxyproline, and overall collagen levels were identified in lung tissues using immunohistochemistry.

resultsLong-term PQ exposure blocked miR-193a expression, reduced PI3K/Akt/mTOR signalling, increased oxidative stress, inhibited autophagy, increased Hh signalling, and facilitated the formation of pulmonary fibrosis. Ligustrazin blocked PI3K/Akt/mTOR and Hh signalling as well as reduced oxidative stress via increasing miR-193a expression and autophagy, all of which reduced pulmonary fibrosis. These effects of ligustrazin were accompanied by reduced TGF-β1, CTGF, and Collagen I and III expression.

conclusionsLigustrazin blocked PQ-induced PI3K/Akt/mTOR and Hh signalling by increasing miR-193a expression, thereby attenuating PQ-induced lung fibrosis.

Indexed as

A549 CellsAnimalsAutophagyCollagen Type IFemaleHumansMiceMicroRNAsOxidative StressParaquatPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPulmonary FibrosisPyrazinesReactive Oxygen SpeciesSignal TransductionCollagen Type IMicroRNAsMIRN193 microRNA, humanMIRN193 microRNA, mouseParaquatPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazinesReactive Oxygen SpeciestetramethylpyrazineTOR Serine-Threonine KinasesTransforming Growth Factor beta1AktLigustrazinLung fibrosisMicemiR-193amTOROxidative stressParaquat

Identifiers

PMID30744607
PMCPMC6371511
OpenAlexW2919240155

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.