Yangqing Chenfei formula attenuates silica-induced pulmonary fibrosis by suppressing activation of fibroblast via regulating PI3K/AKT, JAK/STAT, and Wnt signaling pathway

Yang, Fan; Hou, Runsu; Liu, Xinguang; Tian, Yange; Bai, Yunping; Li, Jiansheng; Zhao, Peng

doi:10.1016/j.phymed.2022.154622

Cited by 9 publications

(3 citation statements)

References 29 publications

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“…Its key compounds, identified as tangeretin, L‐Malic acid, and 2‐Monolinolein, showed good drug absorption, targeting the TGF‐β/Smad3 signaling pathway in pulmonary fibrosis tissue. [ 63 ] Therefore, these seven compounds may contribute to the anti‐inflammatory activity of the WA subfractions. Furthermore, this experiment extended the analysis through molecular docking techniques to compare the effects of single molecules and multiple molecules in the extract on inhibiting the p65 protein.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of the amelioration effect of Ganoderma formosanum extract on delaying PM2.5 damage to lung macrophages

Hou,

Hsieh,

Hung

et al. 2024

Molecular Nutrition Food Res

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ScopeParticulate matter (PM) contains toxic organic matter and heavy metals that enter the entire body through blood flow and may cause mortality. Ganoderma formosanum mycelium, a valuable traditional Chinese medicine that has been used since ancient times, contains various active ingredients that can effectively impede inflammatory responses on murine alveolar macrophages induced by PM particles.Methods and ResultsAn experimental study assessing the effect of G. formosanum mycelium extract's water fraction (WA) on PM‐exposed murine alveolar macrophages using ROS measurement shows that WA reduces intracellular ROS by 12% and increases cell viability by 16% when induced by PM particles. According to RNA‐Sequencing, western blotting, and real‐time qPCR are conducted to analyze the metabolic pathway. The WA reduces the protein ratio in p‐NF‐κB/NF‐κB by 18% and decreases the expression of inflammatory genes, including IL‐1β by 38%, IL‐6 by 29%, and TNF‐α by 19%. Finally, the identification of seven types of anti‐inflammatory compounds in the WA fraction is achieved through UHPLC‐ESI‐Orbitrap‐Elite‐MS/MS analysis. These compounds include anti‐inflammatory compounds, namely thiamine, adenosine 5ʹ‐monophosphate, pipecolic acid, L‐pyroglutamic acid, acetyl‐L‐carnitine, D‐mannitol, and L‐malic acid.ConclusionsThe study suggests that the WA has the potential to alleviate the PM ‐induced damage in alveolar macrophages, demonstrating its anti‐inflammatory properties.

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Section: Resultsmentioning

confidence: 99%

Evaluation of the amelioration effect of Ganoderma formosanum extract on delaying PM2.5 damage to lung macrophages

Hou,

Hsieh,

Hung

et al. 2024

Molecular Nutrition Food Res

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“…In addition, the other pathways enriched by KEGG can also be supported by the previous studies. For instance, TNF and IL-17 can play a role in tissue inflammation and fibrosis caused by NLRP3 inflammatory activation, [60][61][62][63] PI3K-Akt signaling pathway is involved in tissue NLRP3 inflammation and fibrosis, 64,65 PPARγ is also a major regulator of tissue inflammation and fibrosis like TGF-β, 66,67 Th1, and Th2 cell differentiation has also taken parting in tissue fibrosis, 68,69 and AMPK signaling pathway is associated with tissue NLRP3 inflammation and fibrosis. [70][71][72] In summary, the present study revealed that arsenic exposure induced mitochondrial damage, inflammation, and fibrosis in the kidney of SD rats and HK2 cells.…”

Section: Discussionmentioning

confidence: 99%

Arsenic exposure induced renal fibrosis via regulation of mitochondrial dynamics and the NLRP3‐TGF‐β1/SMAD signaling pathway

Ren,

Li,

et al. 2024

Environmental Toxicology

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Environmental arsenic exposure is one of the major global public health problems. Studies have shown that arsenic exposure can cause renal fibrosis, but the underlying mechanism is still unclear. Integrating the in vivo and in vitro models, this study investigated the potential molecular pathways for arsenic‐induced renal fibrosis. In this study, SD rats were treated with 0, 5, 25, 50, and 100 mg/L NaAsO2 for 8 weeks via drinking water, and HK2 cells were treated with different doses of NaAsO2 for 48 h. The in vivo results showed that arsenic content in the rats' kidneys increased as the dose increased. Body weight decreased and kidney coefficient increased at 100 mg/L. As a response to the elevated NaAsO2 dose, inflammatory cell infiltration, renal tubular injury, glomerular atrophy, tubulointerstitial hemorrhage, and fibrosis became more obvious indicated by HE and Masson staining. The kidney transcriptome profiles further supported the protein–protein interactions involved in NaAsO2‐induced renal fibrosis. The in vivo results, in together with the in vitro experiments, have revealed that exposure to NaAsO2 disturbed mitochondrial dynamics, promoted mitophagy, activated inflammation and the TGF‐β1/SMAD signaling pathway, and finally resulted in fibrosis. In summary, arsenic exposure contributed to renal fibrosis via regulating the mitochondrial dynamics and the NLRP3‐TGF‐β1/SMAD signaling axis. This study presented an adverse outcome pathway for the development of renal fibrosis due to arsenic exposure through drinking water.

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“…Exogenous TGF-β1 significantly increased the levels of Smad2 and Smad3 phosphorylation, but the administration of Trig upregulated Smad7, a negative regulator of the TGF-β1 signaling pathway, and inhibited TGF-β1-induced Smad2/3 phosphorylation. Although the PI3K/AKT signaling pathway is also involved in silicosis pulmonary fibrosis [ 48 ]. No conspicuously differences were detected in the phosphorylated forms of PI3K, Akt, and mTOR.…”

Section: Discussionmentioning

confidence: 99%

Trigonelline hydrochloride attenuates silica-induced pulmonary fibrosis by orchestrating fibroblast to myofibroblast differentiation

Zhang,

Yue,

Dong

et al. 2024

Respir Res

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Background Silicosis represents a paramount occupational health hazard globally, with its incidence, morbidity, and mortality on an upward trajectory, posing substantial clinical dilemmas due to limited effective treatment options available. Trigonelline (Trig), a plant alkaloid extracted mainly from coffee and fenugreek, have diverse biological properties such as protecting dermal fibroblasts against ultraviolet radiation and has the potential to inhibit collagen synthesis. However, it’s unclear whether Trig inhibits fibroblast activation to attenuate silicosis-induced pulmonary fibrosis is unclear. Methods To evaluate the therapeutic efficacy of Trig in the context of silicosis-related pulmonary fibrosis, a mouse model of silicosis was utilized. The investigation seeks to elucidated Trig's impact on the progression of silica-induced pulmonary fibrosis by evaluating protein expression, mRNA levels and employing Hematoxylin and Eosin (H&E), Masson's trichrome, and Sirius Red staining. Subsequently, we explored the mechanism underlying of its functions. Results In vivo experiment, Trig has been demonstrated the significant efficacy in mitigating SiO2-induced silicosis and BLM-induced pulmonary fibrosis, as evidenced by improved histochemical staining and reduced fibrotic marker expressions. Additionally, we showed that the differentiation of fibroblast to myofibroblast was imped in Trig + SiO2 group. In terms of mechanism, we obtained in vitro evidence that Trig inhibited fibroblast-to-myofibroblast differentiation by repressing TGF-β/Smad signaling according to the in vitro evidence. Notably, our finding indicated that Trig seemed to be safe in mice and fibroblasts. Conclusion In summary, Trig attenuated the severity of silicosis-related pulmonary fibrosis by alleviating the differentiation of myofibroblasts, indicating the development of novel therapeutic approaches for silicosis fibrosis.

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Yangqing Chenfei formula attenuates silica-induced pulmonary fibrosis by suppressing activation of fibroblast via regulating PI3K/AKT, JAK/STAT, and Wnt signaling pathway

Cited by 9 publications

References 29 publications

Evaluation of the amelioration effect of Ganoderma formosanum extract on delaying PM2.5 damage to lung macrophages

Evaluation of the amelioration effect of Ganoderma formosanum extract on delaying PM2.5 damage to lung macrophages

Arsenic exposure induced renal fibrosis via regulation of mitochondrial dynamics and the NLRP3‐TGF‐β1/SMAD signaling pathway

Trigonelline hydrochloride attenuates silica-induced pulmonary fibrosis by orchestrating fibroblast to myofibroblast differentiation

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