Cryptotanshinone attenuates LPS-induced acute lung injury by regulating metabolic reprogramming of macrophage

Ye, Zesen; Wang, Panxia; Guo, Feng; Wang, Quan; Liu, Cui; Lü, Jing; Chen, Jianwen; Liu, Peiqing

doi:10.3389/fmed.2022.1075465

Cited by 6 publications

(4 citation statements)

References 63 publications

(59 reference statements)

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“…However, effective therapeutic agents for BPD treatment are scarce ( Poets and Lorenz, 2018 ). Previous studies have shown that CTS plays an important role in lung injury ( Jiang et al, 2019 ; Ye et al, 2022 ), and the anti-inflammatory and anti-fibrotic effects of CTS are gradually being explored ( Li et al, 2021 ). Accordingly, this study aimed to explore the anti-inflammatory and anti-fibrotic effects of CTS in a BPD model.…”

Section: Discussionmentioning

confidence: 99%

“…Six fields of view were randomly selected for each stained section for observation under a light microscope (magnification, ×40). Ye et al (2022) assessed the degree of inflammatory damage in the lung using a score based on four parameters: the degree of interstitial oedema, inflammatory cell infiltration, alveolar septal thickness and alveolar congestion level. The score was graded as follows: Level 0 was normal; Level 1 was 25%; Level 2 was 25%–50%; Level 3 was 50%–75%; and Level 4 was ≥75%.…”

Section: Methodsmentioning

confidence: 99%

“…Cryptotanshinone (CTS) is a bioactive ingredient extracted from the traditional Chinese medicine Salvia miltiorrhiza , which possess the pharmacological activities such as anti-inflammatory ( Li et al, 2011 ; Nagappan et al, 2019 ), anti-tumour ( Dalil et al, 2022 ), anti-fibrotic ( Wang et al, 2022 ; Wei et al, 2023 ) and neuroprotective ( Mao et al, 2021 ) effects. Recently, it was reported that CTS showed potent anti-inflammatory properties by modulating macrophage polarization in vitro ( Ye et al, 2022 ) and attenuated lipopolysaccharide-induced acute lung injury in mice by inhibiting the TLR4-mediated NF-κB signaling pathway ( Tang et al, 2014 ). In a radiation-induced lung injury model in rats, CTS ameliorated lung injury by regulating TGF-β signaling as well as NOX4 expression ( Jiang et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

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Cryptotanshinone affects HFL-1 cells proliferation by inhibiting cytokines secretion in RAW264.7 cells and ameliorates inflammation and fibrosis in newborn rats with hyperoxia induced lung injury

Ma¹,

Bao²,

Li³

et al. 2023

Front. Pharmacol.

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Objective: Bronchopulmonary dysplasia (BPD) is a common complication of prematurity and has no specific treatment option. Moreover, inflammation and fibrosis play a vital role in the development of BPD. Thus, this study aimed to explore the role of the anti-inflammatory and anti-fibrotic drug cryptotanshinone (CTS) in the treatment of inflammation and fibrosis in BPD.Methods:In vivo, Sprague–Dawley rats (male) were divided into air, hyperoxia and CTS groups with different dose interventions (7.5, 15, and 30 mg/kg). A BPD rat model was induced by continuous inhalation of hyperoxia (95%) for 7 days, during which different doses of CTS were injected intraperitoneally. Furthermore, histological examination, hydroxyproline content measurement, Western blot and real-time quantitative polymerase chain reaction were used to detect the levels of inflammation and fibrosis in the tissues. RAW264.7 cells exposed to 95% oxygen were collected and co-cultured with fibroblasts to determine the expression levels of α-SMA, collagen-Ⅰ and MMPs. The levels of pro-inflammatory cytokines such as TNF-α, IL-6 and pro-fibrotic factor TGF-β1 in the supernatants were measured using enzyme-linked immunosorbent assay.Results: Haematoxylin and eosin staining revealed that CTS reduced the inflammatory response in rat lungs. Masson staining revealed that CTS alleviated the level of pulmonary fibrosis. CTS also reduced the levels of TNF-α, IL-6 and TGF-β1 along with the expression of the fibrosis marker α-SMA in lung tissue. Similarly, in vitro analysis revealed that CTS decreased the levels of TNF-α, IL-6 and TGF-β1 expressed in RAW 264.7 cells, and reduced α-SMA, collagen-Ⅰ, MMPs concentrations in HFL-1 cells co-cultured with the supernatant of RAW264.7 cells after hyperoxia.Conclusion: CTS can attenuate the hyperoxia-induced inflammatory response and the level of fibrosis by regulating the levels of inflammatory factors and fibrotic factor TGF-β1 expressed by macrophages, thereby highlighting the therapeutic potential of CTS in the treatment of BPD.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cryptotanshinone affects HFL-1 cells proliferation by inhibiting cytokines secretion in RAW264.7 cells and ameliorates inflammation and fibrosis in newborn rats with hyperoxia induced lung injury

Ma¹,

Bao²,

Li³

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

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“…HE lung injury scores were calculated by light microscopic analysis of 4 parameters including alveolar septal thickness, interstitial edema, infiltration of inflammatory cells, and alveolar congestion/collapse. Each parameter was categorized into four grades: 0 = normal, 1 ≤ 25%, 2 = 25–50%, 3 = 50–75%, and 4 ≥ 75%, and the mean score of the four parameters was used to represent the overall lung injury [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

Fibroblast Growth Factor 21 Relieves Lipopolysaccharide-Induced Acute Lung Injury by Suppressing JAK2/STAT3 Signaling Pathway

Cai,

Ye,

Zhu

et al. 2023

Inflammation

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Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a life‐threatening disease without an effective drug at present. Fibroblast growth factor 21 (FGF21) was reported to be protective against inflammation in metabolic disease in recent studies. However, the role of FGF21 in ALI has been rarely investigated. In this study, it was found that the expression of FGF21 was markedly increased in lung tissue under lipopolysaccharide (LPS) stimulation in vivo, whereas it was decreased in lung epithelial cells under LPS stimulation in vitro. Therefore, our research aimed to elucidate the potential role of FGF21 in LPS-induced ALI and to detect possible underlying mechanisms. The results revealed that the deficiency of FGF21 aggravated pathological damage, inflammatory infiltration, and pulmonary function in LPS-induced ALI, while exogenous administration of FGF21 improved these manifestations. Moreover, through RNA sequencing and enrichment analysis, it was unveiled that FGF21 might play a protective role in LPS-induced ALI via JAK2/STAT3 signaling pathway. The therapeutic effect of FGF21 was weakened after additional usage of JAK2 activator in vivo. Further investigation revealed that FGF21 significantly inhibited STAT3 phosphorylation and impaired the nuclear translocation of STAT3 in vitro. In addition, the aggravation of inflammation caused by silencing FGF21 can be alleviated by JAK2 inhibitor in vitro. Collectively, these findings unveil a potent protective effect of FGF21 against LPS-induced ALI by inhibiting the JAK2/STAT3 pathway, implying that FGF21 might be a novel and effective therapy for ALI.

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Sex differences in CXCL4‐mediated lung damage in the bleomycin‐induced systemic sclerosis mice model

Tian,

Li,

et al. 2024

Rheumatology & Autoimmunity

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BackgroundSex is an independent risk factor for systemic sclerosis (SSc). Chemokine ligand 4 (CXCL4) participates in SSc via multiple mechanisms. In the present study, we investigated the role of CXCL4 in sex‐specific lung injury in the bleomycin‐induced systemic sclerosis (BLM‐SSc) mouse model.MethodsThirty‐two 6‐week‐old CXCL4–/– C57BL/6J and wild‐type (WT) mice were divided into CXCL4–/– male, CXCL4–/– female, wild‐type male (WT male), and wild‐type female (WT female) groups (n = 8 each). BLM‐SSc mice were established by subcutaneous injections of 100 µL (2 mg/mL of bleomycin, once every other day) for 4 weeks. Thereafter, all mice were sacrificed and the extracted lung tissues were stained with hematoxylin and eosin and Masson's trichrome to evaluate the degree of inflammation and fibrosis. Enzyme‐linked immunosorbent assay was used to measure the levels of tumor necrosis factor‐α and interleukin‐6 in the lung tissue homogenate. In addition, immunofluorescence double staining detected the coexpression of S100 calcium‐binding protein A8 and matrix metalloproteinase 7. Two‐way analysis of variance was used to examine the independent effects of sex, CXCL4, and their interactions.ResultsCompared to CXCL4–/– mice, WT mice had significantly higher infiltration of macrophages and neutrophils, inflammation scores, and fibrosis scores (all p < 0.05). Specifically, the degree of macrophage infiltration and fibrosis scores were higher in male mice than those in female mice (all p < 0.05). In CXCL4–/– mice, fibrosis scores were higher in males than those in females (p < 0.05); however, no significant difference was observed in inflammation scores between the two groups (p > 0.05). Compared with that of the CXCL4–/– mice, the levels of tumor necrosis factor‐α and interleukin‐6 in the lung tissue homogenate were increased in the WT mice with higher levels in the male group. No significant sex‐based differences were observed in CXCL4–/– mice (p > 0.05). Immunofluorescence double staining revealed a significantly higher number of positive double‐stained cells in the WT male than the WT female group; however, no such cells were observed in CXCL4–/– groups.ConclusionCXCL4 may participate in the pathogenesis of sex‐based differential lung injury in the BLM‐SSc model by inducing the macrophage subtype M4.

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Cryptotanshinone attenuates LPS-induced acute lung injury by regulating metabolic reprogramming of macrophage

Cited by 6 publications

References 63 publications

Cryptotanshinone affects HFL-1 cells proliferation by inhibiting cytokines secretion in RAW264.7 cells and ameliorates inflammation and fibrosis in newborn rats with hyperoxia induced lung injury

Cryptotanshinone affects HFL-1 cells proliferation by inhibiting cytokines secretion in RAW264.7 cells and ameliorates inflammation and fibrosis in newborn rats with hyperoxia induced lung injury

Fibroblast Growth Factor 21 Relieves Lipopolysaccharide-Induced Acute Lung Injury by Suppressing JAK2/STAT3 Signaling Pathway

Sex differences in CXCL4‐mediated lung damage in the bleomycin‐induced systemic sclerosis mice model

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