Astragaloside IV attenuates hypoxia/reoxygenation injury-induced apoptosis of type II alveolar epithelial cells through miR-21-5p

Li, Hang; Yao, Chen; Shi, Kai-Hu; Zhao, Yang; Du, Jin; Hu, Dinghui; Liu, Zuntao

doi:10.1080/21655979.2021.1982845

Cited by 10 publications

(7 citation statements)

References 17 publications

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“…For example, AS-IV inhibited lung cancer metastasis [ 29 ] and AS-IV took part in podocyte apoptosis of diabetic nephropathy [ 30 ]. Also, the previous reports indicated that AS-IV attenuated hypoxia/reoxygenation injury-induced cell apoptosis and inhibited cell progression of lung cancer [ 31 , 32 ]. However, there was no research for AS-IV in GC.…”

Section: Discussionmentioning

confidence: 98%

Astragaloside IV exhibits anti-tumor function in gastric cancer via targeting circRNA dihydrolipoamide S-succinyltransferase (circDLST)/miR-489-3p/ eukaryotic translation initiation factor 4A1(EIF4A1) pathway

Cao

Wang

et al. 2022

Bioengineered

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Astragaloside IV (AS-IV) is an inartificial saponin separated from astragalus membranaceus, which has exhibited key anti-tumor regulation in some cancers. Circular RNAs (circRNAs) are important regulators in malignant development of gastric cancer (GC). Herein, we focused on the molecular mechanism of AS-IV with circRNA dihydrolipoamide S-succinyltransferase (circDLST) in GC. CircDLST, microRNA-489-3p (miR-489-3p), and eukaryotic translation initiation factor 4A1 (EIF4A1) levels were detected by quantitative real-time polymerase-chain reaction and western blot. Cell functions were assessed by cell counting kit-8 assay, ethynyl-2’-deoxyuridine assay, colony formation assay, and transwell assay. The interaction between miR-489-3p and circDLST or EIF4A1 was analyzed by dual-luciferase reporter assay. Xenograft tumor assay was adopted to check the role of circDLST and AS-IV in vivo . CircDLST and EIF4A1 were upregulated but miR-489-3p was downregulated in GC cells. AS-IV restrained cell proliferation and metastasis in GC cells by downregulating circDLST. CircDLST served as a miR-489-3p sponge, and miR-489-3p inhibition reversed anti-tumor function of AS-IV. EIF4A1 was a target for miR-489-3p and circDLST sponged miR-489-3p to regulate EIF4A1. AS-IV suppressed GC cell progression via circDLST-mediated downregulation of EIF4A1. Also, AS-IV recued tumor growth in vivo via targeting circDLST to regulate miR-489-3p/EIF4A1 axis. AS-IV inhibited the development of GC through circDLST/miR-489-3p/EIF4A1 axis.

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Section: Discussionmentioning

confidence: 98%

Astragaloside IV exhibits anti-tumor function in gastric cancer via targeting circRNA dihydrolipoamide S-succinyltransferase (circDLST)/miR-489-3p/ eukaryotic translation initiation factor 4A1(EIF4A1) pathway

Cao

Wang

et al. 2022

Bioengineered

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“…A study by Qi H et al reported miR-21 protects cardiomyocytes from ROS oxidative stress [ 53 ]. Another study by Li H et al indicated that the regulation of miR-21-5p suppresses hypoxia/reoxygenation injury-induced apoptosis of type II alveolar epithelial cells [ 54 ]. All these evidences support the possibility of miR-21 becoming a downstream target of MEG3 in our study.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA MEG3 promotes tumor necrosis factor-alpha induced oxidative stress and apoptosis in interstitial cells of cajal via targeting the microRNA-21 /I-kappa-B-kinase beta axis

Bai

Tuerdi

et al. 2022

Bioengineered

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Interstitial Cells of Cajal (ICC) plays a critical role in the peristaltic contractions of the gastrointestinal and urinary tract. The dysfunction and loss of ICC contributes to hypokinetic disease, such as gallstoneand ureteropelvic junction obstruction . In the present study, we identified the underlying driving molecular signals of oxidative stress and apoptosis in ICC. ICC was isolated from small intestine of Balb/c mice, and stimulated with tumor necrosis factor-alpha (TNF-α). MTT and flow cytometry were performed to assess cell viability, apoptosis, and the level of reactive oxygen species in ICC, respectively. The level of malondialdehyde, superoxide dismutase, and glutathione peroxidase in cells were measured to assess oxidative stress. The expression of inflammatory factors (interleukin, IL-1 and IL-6) and apoptosis-related proteins were detected by western blot. We observed that TNF-αinduced inflammation, oxidative stress and cell apoptosis in ICC. By using quantitative real-time PCR , we verified that the expression of long non-coding RNAMEG3 was elevated by TNF-α in ICC. Silencing MEG3 reversed inflammation, oxidative stress, and cell apoptosisin TNF-α-treated ICC. Subsequently, we confirmed that MEG3 sponged cytoprotective miR-21 to upregulate the expression of I-kappa-B-kinase beta (IKKB) and activate the nuclear factor kappa-B (NF-κB) pathway. Both miR-21 overexpression and IKKB knockdown reduced TNF-α-induced above symptoms in ICC. Taken together, we can conclude that MEG3 mediates inflammation, oxidative stress and apoptosis in TNF-α-treated ICC via the miR-21/IKKB-NF-κB axis. The study improves our understanding of the molecular mechanism of ICC reduction related diseases.

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“…For experiment 2, the cells were divided into five groups: normoxia, hypoxia, hypoxia + VD3, hypoxia + VD3 + mitochondrial autophagy inhibitor (5 μM Mdivi-1), and hypoxia + VD3 + mitochondrial autophagy agonist (50 μM CCCP). The Rat type II alveolar epithelial cells were incubated under normoxic (95% O 2 , 5% CO 2 , 37 °C) conditions for 1 h and then in hypoxia (1% O 2 , 94% N 2 , 5% CO 2 , 37 °C) for 24 h, as the previously described [ 33 ]. For VD3 treatment, rat type II alveolar epithelial cells were treated with low VD3 (20 nM) or high VD3 (40 nM) for 24 h. For the mitochondrial fission inhibitor Mdivi-1 (Beyotime, Shanghai, China), rat type II alveolar epithelial cells were treated with 5 μM Mdivi-1.…”

Section: Methodsmentioning

confidence: 99%

Vitamin D3 improved hypoxia-induced lung injury by inhibiting the complement and coagulation cascade and autophagy pathway

Dai,

Lin,

et al. 2024

BMC Pulm Med

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Background Pulmonary metabolic dysfunction can cause lung tissue injury. There is still no ideal drug to protect against hypoxia-induced lung injury, therefore, the development of new drugs to prevent and treat hypoxia-induced lung injury is urgently needed. We aimed to explore the ameliorative effects and molecular mechanisms of vitamin D3 (VD3) on hypoxia-induced lung tissue injury. Methods Sprague–Dawley (SD) rats were randomly divided into three groups: normoxia, hypoxia, and hypoxia + VD3. The rat model of hypoxia was established by placing the rats in a hypobaric chamber. The degree of lung injury was determined using hematoxylin and eosin (H&E) staining, lung water content, and lung permeability index. Transcriptome data were subjected to differential gene expression and pathway analyses. In vitro, type II alveolar epithelial cells were co-cultured with hepatocytes and then exposed to hypoxic conditions for 24 h. For VD3 treatment, the cells were treated with low and high concentrations of VD3. Results Transcriptome and KEGG analyses revealed that VD3 affects the complement and coagulation cascade pathways in hypoxia-induced rats, and the genes enriched in this pathway were Fgb/Fga/LOC100910418. Hypoxia can cause increases in lung edema, inflammation, and lung permeability disruption, which are attenuated by VD3 treatment. VD3 weakened the complement and coagulation cascade in the lung and liver of hypoxia-induced rats, characterized by lower expression of fibrinogen alpha chain (Fga), fibrinogen beta chain (Fgb), protease-activated receptor 1 (PAR1), protease-activated receptor 3 (PAR3), protease-activated receptor 4 (PAR4), complement (C) 3, C3a, and C5. In addition, VD3 improved hypoxic-induced type II alveolar epithelial cell damage and inflammation by inhibiting the complement and coagulation cascades. Furthermore, VD3 inhibited hypoxia-induced autophagy in vivo and in vitro, which was abolished by the mitophagy inducer, carbonyl cyanide-m-chlorophenylhydrazone (CCCP). Conclusion VD3 alleviated hypoxia-induced pulmonary edema by inhibiting the complement and coagulation cascades and autophagy pathways.

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Astragaloside IV attenuates hypoxia/reoxygenation injury-induced apoptosis of type II alveolar epithelial cells through miR-21-5p

Cited by 10 publications

References 17 publications

Astragaloside IV exhibits anti-tumor function in gastric cancer via targeting circRNA dihydrolipoamide S-succinyltransferase (circDLST)/miR-489-3p/ eukaryotic translation initiation factor 4A1(EIF4A1) pathway

Astragaloside IV exhibits anti-tumor function in gastric cancer via targeting circRNA dihydrolipoamide S-succinyltransferase (circDLST)/miR-489-3p/ eukaryotic translation initiation factor 4A1(EIF4A1) pathway

Long non-coding RNA MEG3 promotes tumor necrosis factor-alpha induced oxidative stress and apoptosis in interstitial cells of cajal via targeting the microRNA-21 /I-kappa-B-kinase beta axis

Vitamin D3 improved hypoxia-induced lung injury by inhibiting the complement and coagulation cascade and autophagy pathway

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