| 本文已被：浏览 171次 下载 132次 |
码上扫一扫！ |
|
|
| 华山参通过TGF-β1/Smad3通路对体外纤维化的调节作用 |
|
商丹丹1, 周鸿2, 黄蔓如1, 江永萍2, 刘彩艳1, 刘锐3, 张思祺1, 于海洋1, 王涛1
|
|
1.天津中医药大学, 天津 301617;2.津药达仁堂集团股份有限公司第六中药厂, 天津 300401;3.津药达仁堂集团股份有限公司中药研究院 植化研究室, 天津 300457
|
|
| 摘要: |
| [目的] 研究华山参对重组小鼠转化生长因子 β1 以及香烟提取物（CSE）对小鼠胚胎成纤维细胞（NIH-3T3）和人源支气管上皮细胞（BEAS-2B）的影响及相关机制。[方法] 噻唑蓝（MTT）法筛选华山参生物碱、非生物碱、总提取物对 NIH-3T3 细胞的安全浓度；重组小鼠转化生长因子 β1 诱导 NIH-3T3 细胞 24 h，进行天狼猩红染色，并计算相对胶原沉积率；MTT 法分别筛选 7 种华山参生物碱单体对 BEAS-2B 细胞的安全浓度；CSE 处理 BEAS-2B细胞 24 h 后，进行 β-半乳糖苷酶（β-Gal）染色；蛋白免疫印迹法（Western Blot）检测 TGF-β1、Smad3、NLRP3 蛋白的表达水平。[结果] 华山参生物碱、非生物碱、总提取物均能抑制重组小鼠转化生长因子 β1 诱导的 NIH-3T3 细胞发生胶原沉积（P 均<0.05）；东莨菪碱和去水阿托品可以显著抑制 CSE 诱导的 BEAS-2B 细胞发生衰老（P 均<0.05），并且能够显著抑制 TGF-β1、Smad3、NLRP3 蛋白的表达（P 均<0.05）。[结论] 华山参可能通过抑制 TGF-β1/Smad3 通路来调节体外肺纤维化的进程。 |
| 关键词: 华山参 肺纤维化 TGF-β1/Smad3 |
| DOI：10.11656/j.issn.1673-9043.2024.06.09 |
| 分类号:R563 |
| 基金项目: |
|
| Study on the in vitro mechanism of Physochlaina infundibularis Kuang in intervening pulmonary fibrosis |
|
SHANG Dandan1, ZHOU Hong2, HUANG Manru1, JIANG Yongping2, LIU Caiyan1, LIU Rui3, ZHANG Siqi1, YU Haiyang1, WANG Tao1
|
|
1.Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China;2.The Sixth Chinese Medicine Factory of Tianjin Darentang Group Co., Tianjin 300401, China;3.Phytochemical Research Department, Research Institute of Traditional Chinese Medicine, Tianjin 300457, China
|
| Abstract: |
| [Objective] To study the effects of Physochlaina infundibularis Kuang on Recombinant Mouse TGF-β1 （TGF-β1） as well as cigarette smoke extract（CSE） on mouse embryonic fibroblasts（NIH-3T3） and human bronchial epithelial cells（BEAS-2B） and related mechanisms. [Methods] MTT method was used to screen the safe concentrations of Physochlaina infundibularis Kuang alkaloids，non-alkaloids，and total extracts on NIH-3T3 cells；NIH-3T3 cells were induced by TGF-β1 for 24 h，stained with Sirius Scarlet，and the relative collagen deposition rate was calculated；MTT method was used to screen the safe concentrations of 7 Physochlaina infundibularis Kuang alkaloidal monomers on BEAS-2B cells，respectively；BEAS-2B cells were treated with CSE After 24，βgalactosidase staining was performed；Western blot method was used to detect the expression levels of TGF-β1， Smad3 and NLRP3 proteins. [Results] Physochlaina infundibularis Kuang alkaloids，non-alkaloids，and total extracts significantly inhibited TGF-β1-induced collagen deposition in NIH-3T3 cells（all P<0.05）；scopolamine and dehydro-atropine significantly inhibited CSE-induced senescence in BEAS-2B cells （all P<0.05），and were able to significantly inhibit the expression of TGF-β1，Smad3，and NLRP3 proteins （all P <0.05）. [Conclusion] Physochlaina infundibularis Kuang may regulate the progression of pulmonary fibrosis in vitro by inhibiting the TGFβ1/Smad3 pathway. |
| Key words: Physochlaina infundibularis Kuang pulmonary fibrosis TGF-β1/Smad3 |
