Oxymatrine exerts a protective effect in myocardial ischemia/reperfusion‑induced acute lung injury by inhibiting autophagy in diabetic rats

Zhou, Xiong; Xu, Jiali; Liu, Xin

doi:10.3892/mmr.2021.11822

Cited by 11 publications

(9 citation statements)

References 27 publications

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“… 42 In previous studies, the change in the levels of LC3B I, LC3B II, p62, ATG5, and Beclin-1 was evaluated to investigate autophagy. 43 , 44 , 45 In the present study, the levels of these autophagy-associated proteins in HSFs were also examined after ANGPT2 downregulation. The authors discovered that ANGPT2 knockdown reduced the levels of LC3B Ⅰ and P62, and increased the levels of LC3B II, ATG5, and Beclin-1, which demonstrated the activation of autophagy.…”

Section: Discussionmentioning

confidence: 97%

Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway

Chen

Xu²,

Sun³

et al. 2023

Anais Brasileiros de Dermatologia

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Section: Discussionmentioning

confidence: 97%

Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway

Chen

Xu²,

Sun³

et al. 2023

Anais Brasileiros de Dermatologia

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“…Neutrophil autophagy inhibition has a protective effect on LPS-induced ALI [ 50 ]. Autophagy inhibition can also improve ALI in diabetic rats [ 51 ]. However, autophagy inhibition following Beclin 1 knockdown can cause various types of cancers (such as lymphoma, liver cancer, and lung cancer) [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Preconditioning Alleviates Lipopolysaccharides-Induced Acute Lung Injury by Downregulating LC3‐II/I and Beclin 1 Expression

Sun

Zeng

Luo

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Our study aimed to investigate the effect of electroacupuncture pretreatment on the inflammatory response and expression levels of LC3-II/I and Beclin 1 using a model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Eighteen male Sprague-Dawley (SD) rats were randomly divided into three groups: normal control group (NC, n = 6), LSP modeling group (LM, n = 6), and electroacupuncture group (EA, n = 6). Rats in the EA group received electroacupuncture pretreatment at bilateral Zusanli (ST36) and Chize (LU5) points for five days (30 min each time daily, frequency; 3 Hz/15 Hz, intensity; 1 mA). Rats in the EA and LM groups were then injected with 5 mg/kg LPS (Beijing, Solarbio Company, concentration; 5 mg/mL) through the tail vein, while those in the NC group were injected with 5 mg/kg saline. The animals were sacrificed six hours after LPS or saline injection through cervical vertebrae by dislocation under deep anesthesia. Orbital blood was collected for the analysis of serum inflammatory factors including interleukin-1β (IL-1β) and transforming growth factor-β (TGF-β). The lower left lung was excised, stained with hematoxylin-eosin (HE), and subjected to histopathological analysis. The mRNA and protein expression of Beclin 1 and LC3 II/I in the lower right lung tissues were detected via RT-qPCR and Western blot analyses, respectively. The results showed that lung injury score was significantly higher in the LM group than that of the NC group ( P < 0.01 ) and EA group ( P < 0.01 ). The IL-1β contents were significantly decreased in the EA group ( P < 0.01 ) than in the LM group. In contrast, the GF-β contents were increased in the EA group significantly when compared with the LM group ( P < 0.01 ). RT-qPCR and Western blot detection showed that the relative gene expression of LC3‐II/I and Beclin 1 was significantly lower in the EA group than in the LM group ( P < 0.01 ). However, the relative protein expression level of LC3‐II/I and Beclin 1 was slightly lower in the EA group than the in LM group ( P > 0.05 ). These results show that electroacupuncture pretreatment reduces the inflammatory response in ALI and can protect lung tissue by inhibiting the gene and protein expression levels of LC3‐II/I and Beclin 1.

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“…The autophagy inhibitor 3-MA reversed these changes, while OMT inhibited autophagy in a dosedependent manner, suggesting that OMT ameliorated myocardial I/R-induced ALI in diabetic rats by inhibiting autophagy. 104 Hydroxytyrosol Hydroxytyrosol (HT) is a natural polyphenolic compound derived from Canarium album (Lour.) Rauesch.…”

Section: Oxyberberinementioning

confidence: 99%

Research Progress on Autophagy Regulation by Active Ingredients of Traditional Chinese Medicine in the Treatment of Acute Lung Injury

Dong¹,

Yin²,

Hao³

et al. 2023

JIR

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Autophagy is a highly conserved process that maintains cell stability in eukaryotes, participates in the turnover of intracellular substances to maintain cell function, helps to resist pathogen invasion, and improves cell tolerance to environmental changes. Autophagy has been observed in many diseases, and the symptoms of these diseases are significantly improved by regulating autophagy. Autophagy is also involved in the development of lung diseases. Studies have shown that autophagy may play a beneficial or harmful role in acute lung injury (ALI), and ALI has been treated with traditional Chinese medicine designed to promote or inhibit autophagy. In this paper, the molecular mechanism and common pathways regulating autophagy and the relationship between autophagy and ALI are introduced, and the active ingredients of traditional Chinese medicine that improve ALI symptoms by regulating autophagy are summarized.

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Oxymatrine exerts a protective effect in myocardial ischemia/reperfusion‑induced acute lung injury by inhibiting autophagy in diabetic rats

Cited by 11 publications

References 27 publications

Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway

Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway

Electroacupuncture Preconditioning Alleviates Lipopolysaccharides-Induced Acute Lung Injury by Downregulating LC3‐II/I and Beclin 1 Expression

Research Progress on Autophagy Regulation by Active Ingredients of Traditional Chinese Medicine in the Treatment of Acute Lung Injury

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