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- 저자 : Lifang Xi (검색결과 2 건)
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Flavonoids in Resina Draconis protect against pulmonary fibrosis via the TGF‑β1/NOTCH1 pathway
Liteng Yang,Xin Liu,Ning Zhang,Gaohui Wu,Lifang Chen,Jingyi Xu,Xi Ren,Xiaoming Jiang,Zhijing Huang 대한독성 유전단백체 학회 2020 Molecular & cellular toxicology Vol.16 No.2
Background It is known that flavonoids in Resina Draconis (FRD) have anti-inflammatory and analgesic effects, but the function and mechanisms of FRD against pulmonary fibrosis remain unknown. Objective The study aimed to study the effect and mechanism of FRD on pulmonary fibrosis. Methods Pulmonary fibroblasts were isolated and identified. After treatment with transforming growth factor (TGF)-β1 and FRD-containing serum, expressions of TGF-β1, Jagged1, Notch1, alpha-smooth muscle actin, and collagen I were examined using real-time quantitative PCR and Western blot. Besides, the related proteins were verified in rats with bleomycin-induced pulmonary fibrosis. Results We successfully isolated and identified pulmonary fibroblasts and proved that FRD-containing serum inhibits proliferation and downregulates Notch1 expression in TGF-β1-induced fibroblasts. Moreover, our results indicate that FRD might alleviate pulmonary fibrosis via the Jagged1/Notch1 signaling pathways in vivo. Conclusion Flavonoids in Resina Draconis might play a key role in pulmonary fibrosis via critical pathways, especially the TGF-β1 and NOTCH1 signaling pathways.
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Youmei Xiao,Zhanxue Xu,Yuan Cheng,Rufan Huang,Yuan Xie,Hsiang‑i Tsai,Hualian Zha,Lifang Xi,Kai Wang,Xiaoli Cheng,Yanfeng Gao,Changhua Zhang,Fang Cheng,Hongbo Chen 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00
Background Ferroptosis, iron-dependent cell death, is an established mechanism for cancer suppression, particularly in hepatocellular carcinoma (HCC). Sorafenib (SOR), a frontline drug for the treatment of HCC, induces ferroptosis by inhibiting the Solute Carrier family 7 member 11 (SLC7A11), with inadequate ferroptosis notably contributing to SOR resistance in tumor cells. Methods To further verify the biological targets associated with ferroptosis in HCC, an analysis of the Cancer Genome Atlas (TCGA) database was performed to find a significant co-upregulation of SLC7A11 and transferrin receptor (TFRC), Herein, cell membrane-derived transferrin nanovesicles (TF NVs) coupled with Fe3+ and encapsulated SOR (SOR@TF-Fe3+ NVs) were established to synergistically promote ferroptosis, which promoted the iron transport metabolism by TFRC/TF-Fe3+ and enhanced SOR efficacy by inhibiting the SLC7A11. Results In vivo and in vitro experiments revealed that SOR@TF-Fe3+ NVs predominantly accumulate in the liver, and specifically targeted HCC cells overexpressing TFRC. Various tests demonstrated SOR@TF-Fe3+ NVs accelerated Fe3+ absorption and transformation in HCC cells. Importantly, SOR@TF-Fe3+ NVs were more effective in promoting the accumulation of lipid peroxides (LPO), inhibiting tumor proliferation, and prolonging survival rates in HCC mouse model than SOR and TF- Fe3+ NVs alone. Conclusions The present work provides a promising therapeutic strategy for the targeted treatment of HCC.
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