FOOD SCIENCE AND BIOTECHNOLOGY
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2022
·Vol. 31
·期 13
·1741-1751
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IF 3.231
Ding Haomiao,Zhang Yuzhe,Zha Yue,Zhou Sijia,Cao Chaoqing,Zhu Huajian,Xu Feng,Zhang Xiuqiang,Wang Caisheng
The cytoprotective and potential molecular mechanisms of Hylocereus polyrhizus protein (RFPP) were investigated on the hydrogen peroxide (H 2 O 2 )-triggered damage in normal human embryonic lung (MRC-5) cells. An MTT assay was conducted to assess the MRC-5 cell viability after exposure to H 2 O 2 or RFPP. Cell cycle distribution and apoptosis were explored via flow cytometry. The contents of related proteins were assessed via western blot. MRC-5 cells exhibited markedly decreased cellular viability after treatment with H 2 O 2 ; however, treatment with RFPP suppressed this decrease. Additionally, RFPP interference dampened H 2 O 2 -triggered intracellular apoptosis levels and increased H 2 O 2 -triggered intracellular S phase. In these processes, the contents of phosphorylated ( p )-AKT along with p -mTOR proteins were downregulated in 120 µM H 2 O 2 -treated cells compared with vehicle-treated cells. Nevertheless, in MRC-5 cells inoculated with RFPP, the levels expression of these proteins were reversed. To conclude, RFPP protected MRC-5 cells from H 2 O 2 -triggered damage via activation of the PI3K/AKT/mTOR cascade.
研究领域:
细胞生物学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
Journal of Translational Medicine
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2024
·Vol. 22
·期 1
·1-19
·
IF 6.1
Liu Nannan,Fan Xuefei,Shao Yubao,Chen Suhuan,Wang Taorong,Yao Tao,Chen Xiaoyu
Background and purposeInterstitial lung disease (ILD) represents a significant complication of rheumatoid arthritis (RA) that lacks effective treatment options. This study aimed to investigate the intrinsic mechanism by which resveratrol attenuates rheumatoid arthritis complicated with interstitial lung disease through the AKT/TMEM175 pathway.Methods We established an arthritis model by combining chicken type II collagen and complete Freund’s adjuvant. Resveratrol treatment was administered via tube feeding for 10 days. Pathological changes in both the joints and lungs were evaluated using HE and Masson staining techniques. Protein expression of TGF-β1, AKT, and TMEM175 was examined in lung tissue. MRC-5 cells were stimulated using IL-1β in combination with TGF-β1 as an in vitro model of RA-ILD, and agonists of AKT, metabolic inhibitors, and SiRNA of TMEM175 were used to explore the regulation and mechanism of action of resveratrol RA-ILD.Results Resveratrol mitigates fibrosis in rheumatoid arthritis-associated interstitial lung disease and reduces oxidative stress and inflammation in RA-ILD. Furthermore, resveratrol restored cellular autophagy. When combined with the in vitro model, it was further demonstrated that resveratrol could suppress TGF-β1 expression, and reduce AKT metamorphic activation, consequently inhibiting the opening of AKT/MEM175 ion channels. This, in turn, lowers lysosomal pH and enhances the fusion of autophagosomes with lysosomes, ultimately ameliorating the progression of RA-ILD.Conclusion In this study, we demonstrated that resveratrol restores autophagic flux through the AKT/MEM175 pathway to attenuate inflammation as well as fibrosis in RA-ILD by combining in vivo and in vitro experiments. It further provides a theoretical basis for the selection of therapeutic targets for RA-ILD.Graphical Abstract
研究领域:
药理学
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免疫学
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肺科学
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风湿病学
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细胞生物学
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DOI
PubMed
高影响因子
TALANTA
·
2018
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IF 4.244
JingHong Li,Nan Chen,YiPing Tian,Hui Xu
The exploration of volatile organic compounds (VOCs) produced by cell lines may be a powerful and non-invasive tool for the study of the health risk of human exposure to atmospheric particulate matter (PM). In this work, we developed a sensitive solid phase microextraction-gas chromatography-mass spectrometry method (SPME-GC-MS) to analyze VOCs in breathed gas of PM2.5-induced human embryonic fibroblast cell line (MRC-5). A novel graphene oxide/polyaniline/polydopamine (GO/PANI/PDA) coating was prepared on a stainless steel wire via electrochemical deposition and self-polymerization for the first time. The GO/PANI/PDA coating exhibited high extraction efficiency, good thermal stability (> 380 ℃), excellent mechanical stability as well as long service time (> 150 times). Parameters that may affect the results were optimized systematically. Under the optimal conditions, VOCs including benzene series, aldehydes and alkane were detected with low limit of detection (0.2–2.0 μg L −1 ) and good correlation (correlation coefficients above 0.9922). The relative standard deviations of within-day and between-day were 1.1–8.4% and 0.2–11.2%, respectively. Satisfactory recoveries of 82–117% indicated good repeatability of the method. The method has been successfully applied for the determination of target VOCs in the headspace gas of PM2.5-induced MRC-5 cell. And it is expected to provide an alternative tool for the study of cytotoxicology of atmospheric particulates.
研究领域:
环境生物学
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毒理学
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分析化学
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DOI
PubMed
高影响因子
AMERICAN JOURNAL OF CHINESE MEDICINE
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2024
·
IF 4.8
Qing Zheng,Feng-Ping Lei,Shan Hui,Ming Tong,Li-Hui Liang
Cellular senescence is an adverse factor in the development of pulmonary fibrosis (PF). Ginsenoside Rb1 has been found to inhibit both cellular senescence and PF. This study aimed to elucidate the molecular mechanisms by which ginsenoside Rb1 regulates cellular senescence and PF. A PF mouse model was established by Bleomycin (BLM) administration, and a cell model of senescence was constructed using MRC-5 cells treated with Adriamycin RD (ARD) administration. Hematoxylin and Eosin (HE) staining and Masson staining were employed to evaluate cellular structure and collagen fiber content. RT-qPCR and western blotting were used to detect mRNA and protein expression of the target genes. Enzyme-linked Immunosorbent Assay (ELISA) was applied to measure the protein concentration of IL-1 β and IL-18. SA- β -gal staining was used to evaluate cellular senescence. Our results show that ginsenoside Rb1 effectively suppressed BLM-induced PF in mice. ARD administration to induce cellular senescence reduced NRF2, QKI, and SMAD7 expression in MRC-5 cells. By inducing NRF2 overexpression, ARD-induced cellular senescence and fibrosis in MRC-5 cells were relieved. Notably, NRF2 knockdown abolished the mitigating effects of ginsenoside Rb1 on ARD-induced cellular senescence and fibrosis in MRC-5 cells. Mechanistically, NRF2 increased SMAD7 mRNA stability through the transcriptional regulation of QKI. As expected, ginsenoside Rb1 alleviated ARD-induced senescence and fibrosis in MRC-5 cells by activating the NRF2/QKI/SMAD7 axis. Therefore, it was found that ginsenoside Rb1 mitigates cellular senescence and fibrosis during PF progression by activating the NRF2/QKI/SMAD7 axis. This study provides a potential therapeutic strategy for the treatment of PF and elucidates its mechanism of action.
研究领域:
药理学
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呼吸病学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
Experimental and Therapeutic Medicine
·
2023
·Vol. 25
·期 4
·1-11
·
IF 2.7
Chun-Lian Liang,Xiu-Li Li,Xiao-Juan Quan,Lin Zhang
Idiopathic pulmonary fibrosis (IPF) is a heterogeneous lung disease associated with high mortality. Disabled‑2 (DAB2), an adapter protein, regulates cell‑fibrinogen adhesion and fibrinogen uptake. DAB2 is differentially expressed in mouse fibrotic lungs induced by bleomycin according to a genome microarray analysis based on Gene Expression Omnibus database. However, the role of DAB2 in IPF has not been revealed. A bleomycin‑induced mouse model of pulmonary fibrosis was constructed in the present study. It found that the expression of DAB2 was upregulated in bleomycin‑induced fibrotic lung tissue with collagen fiber deposition and pulmonary interstitium thickening. Colocalization of DAB2 with α‑smooth muscle actin (SMA) was observed in lung tissue sections. In vitro, human lung fibroblast MRC‑5 cells were treated with TGF‑β1 and the expression of DAB2 was increased. Knockdown of DAB2 suppressed cell proliferation and the expression of α‑SMA, collagen I, collagen IV and fibronectin in TGF‑β1‑treated MRC‑5 cells. The phosphorylation levels of PI3K and AKT were suppressed in DAB2‑knockdown cells. IGF‑1/IGF‑1R has been reported to promote pulmonary fibrosis and activate the PI3K/Akt signaling. In the present study, the activation of IGF‑1/IGF‑1R signaling pathways in bleomycin‑induced fibrotic lung tissues were positively associated with DAB2 expression. The phosphorylation level of IGF‑1R was increased in MRC‑5 cells with TGF‑β1 treatment, and DAB2 expression was decreased by silencing of IGF‑1R. This suggested that DAB2 might be a downstream target of the IGF‑1R pathway and thus induced PI3K/AKT signaling activation and fibrogenesis. The current study demonstrated the importance of DAB2 in pulmonary fibrosis and suggested the potential of IGF‑1R/DAB2/PI3K in the pathogenesis of IPF.
研究领域:
肺科学
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细胞生物学
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分子生物学
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病理学
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产品关联
DOI
PubMed
高影响因子
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