| 曹 倩,王鹏来,姜艳秋,李 娜,倪 哲.葛根素调节Nrf2/HO-1信号通路对脂多糖诱导的人牙龈成纤维细胞炎症反应的影响[J].,2024,(18):3422-3428 |
| 葛根素调节Nrf2/HO-1信号通路对脂多糖诱导的人牙龈成纤维细胞炎症反应的影响 |
| Effect of Puerarin on Lipopolysaccharide-Induced Inflammatory Response in Human Gingival Fibroblasts by Regulating Nrf2/HO-1 Signaling Pathway |
| 投稿时间：2024-02-28 修订日期：2024-03-24 |
| DOI：10.13241/j.cnki.pmb.2024.18.004 |
| 中文关键词: 葛根素 Nrf2/HO-1信号通路 脂多糖 人牙龈成纤维细胞 炎症反应 |
| 英文关键词: Puerarin Nrf2/HO-1 signaling pathway Lipopolysaccharide Human gingival fibroblasts Inflammatory response |
| 基金项目:江苏省基础研究计划青年基金项目（BK20210080） |
|
| 摘要点击次数: 139 |
| 全文下载次数: 76 |
| 中文摘要: |
| 摘要 目的：探讨葛根素（GGS）调节核因子E2相关因子2（Nrf2）/血红素氧合酶-1（HO-1）信号通路对脂多糖（LPS）诱导的人牙龈成纤维细胞（HGFs）炎症反应的影响。方法：体外培养HGFs细胞，将HGFs细胞分为空白对照（CK）组（0.9%氯化钠）、LPS组（100 nM LPS）、LPS+GGS低剂量（LPS+GGS-L）组（100 nM LPS+50 μM GGS）、LPS+GGS高剂量（LPS+GGS-H）组（100 nM LPS+100 μM GGS）、LPS+GGS-H+ML385（Nrf2/HO-1信号通路抑制剂）组（100 nM LPS+100 μM GGS+10 μM ML385）。采用细胞计数试剂盒-8（CCK-8）检测细胞增殖能力；酶联免疫吸附法（ELISA）检测白细胞介素（IL）-6、乳酸脱氢酶（LDH）、IL-10、IL-1β水平；试剂盒检测丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）水平；流式细胞术检测HGFs细胞凋亡率；碘化丙啶（PI）染色法检测细胞膜孔的形成；Western blot法检测B淋巴细胞瘤-2（Bcl-2）、B细胞淋巴瘤-2相关X蛋白（Bax）、NOD样受体蛋白3（NLRP3）、Nrf2、HO-1蛋白表达。结果：与CK组相比，LPS组HGFs细胞OD450（24、48 h）值、IL-10水平、GSH-Px和SOD活性、Bcl-2、Nrf2和HO-1蛋白表达显著降低，IL-6、LDH、IL-1β水平、MDA含量、细胞凋亡率、细胞PI染色阳性率、Bax和NLRP3蛋白表达显著升高（P<0.05）；与LPS组相比，LPS+GGS-L组和LPS+GGS-H组HGFs细胞OD450（24、48 h）值、IL-10水平、GSH-Px和SOD活性、Bcl-2、Nrf2和HO-1蛋白表达显著升高，IL-6、LDH、IL-1β水平、MDA含量、细胞凋亡率、细胞PI染色阳性率、Bax和NLRP3蛋白表达显著降低（P<0.05）；ML385可减轻GGS对LPS诱导的HGFs细胞炎症损伤的改善作用（P<0.05）。结论：GGS可能通过激活Nrf2/HO-1信号通路减轻LPS诱导的HGFs细胞炎症和氧化应激反应，降低细胞凋亡。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect of puerarin (GGS) on lipopolysaccharide (LPS) -induced inflammatory response in human gingival fibroblasts (HGFs) by regulating nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. Methods: HGFs cells were cultured in vitro, HGFs cells were divided into blank control (CK) group (0.9% sodium chloride), LPS group (100 nM LPS), LPS+GGS low dose (LPS+GGS-L) group (100 nM LPS+50 μM GGS), LPS+GGS high dose (LPS+GGS-H) group (100 nM LPS+100 μM GGS), LPS+GGS-H+ML385 (Nrf2/HO-1 signaling pathway inhibitor) group (100 nM LPS+100 μM GGS+10 μM ML385). The cell proliferation ability was detected by cell counting kit-8 (CCK-8). The levels of interleukin (IL) -6, lactate dehydrogenase (LDH), IL-10 and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). The levels of malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were detected by kits. The apoptosis rate of HGFs was detected by flow cytometry. The formation of cell membrane pores was detected by propidium iodide (PI) staining. The expressions of B-cell lymphoma-2 (Bcl-2), B-cell lymphoma-2 associated X protein (Bax), NOD-like receptor protein 3 (NLRP3), Nrf2 and HO-1 were detected by Western blot. Results: Compared with CK group, the OD450 (24 and 48 h) value, IL-10 level, GSH-Px and SOD activity, Bcl-2, Nrf2 and HO-1 protein expression of HGFs cells in LPS group were significantly decreased, and the levels of IL-6, LDH, IL-1β, MDA content, apoptosis rate, positive rate of PI staining, Bax and NLRP3 protein expression were significantly increased (P<0.05). Compared with LPS group, the OD450 (24 and 48 h) value, IL-10 level, GSH-Px and SOD activity, Bcl-2, Nrf2 and HO-1 protein expression of HGFs cells in LPS+GGS-L group and LPS+GGS-H group were significantly increased, and the levels of IL-6, LDH, IL-1β, MDA content, apoptosis rate, positive rate of PI staining, Bax and NLRP3 protein expression were significantly decreased(P<0.05). ML385 could reduce the improvement of GGS on LPS-induced inflammatory injury in HGFs cells(P<0.05). Conclusion: GGS may alleviate LPS-induced inflammation and oxidative stress in HGFs cells by activating Nrf2/HO-1 signaling pathway, and reduce cell apoptosis. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
