| 曹志华,田蜜,尚红亮.毛兰素抑制 IκB激酶 /核因子 κB通路促进脂多糖诱导大鼠心肌细胞的增殖作用[J].安徽医药,2026,30(5):901-905. |
| 毛兰素抑制 IκB激酶 /核因子 κB通路促进脂多糖诱导大鼠心肌细胞的增殖作用 |
| Erianin inhibits IKK/NF-κB pathway to promote cardiomyocyte viability in LPS environment |
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| DOI：10.3969/j.issn.1009-6469.2026.05.011 |
| 中文关键词: 石斛属 心力衰竭 毛兰素 IκB激酶 /核因子 κB信号通路 增殖 凋亡 |
| 英文关键词: Dendrobium Heart failure Erianin IκB kinase/nuclear factor-κB signaling pathway Proliferation Apoptosis |
| 基金项目:保定市科技计划项目( 2341ZF255) |
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| 摘要点击次数: 226 |
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| 中文摘要: |
| 目的探究毛兰素对脂多糖( LPS)诱导的大鼠心肌细胞活力、增殖、凋亡及 IκB激酶 /核因子 κB(IKK/NF-κB)信号通路的调控作用。方法 研究时间为 2024年 1―3月，体外培养大鼠心肌 H9C2细胞，分组包括对照组(不做干预)、脂多糖组( 1 mg/ L脂多糖)、实验组( 1 mg/L脂多糖 +40、80、160 nmol/L毛兰素)、脂多糖 +80+抑制剂组( 1 mg/L脂多糖 +80 nmol/L毛兰素 +10 μmol/L IKK/NF-κB通路抑制 BAY11-7082)、脂多糖 +抑制剂组( 1 mg/L脂多糖 +10 μmol/L BAY11-7082)和脂多糖 +80+激活剂组(1 mg/L脂多糖 +80 nmol/L毛兰素 +1 μmol/L IKK/NF-κB通路激活剂 Prostratin)。干预 24 h。分别采用酶联免疫吸附分析、细胞计数试剂盒( CCK-8)、 5-乙炔基 -2'脱氧尿嘧啶核苷、 Hoechst 33258染色法、蛋白质印迹法检测白细胞介素( IL)-6、肿瘤坏死因子-α(TNF-α)、细胞活力、增殖率、凋亡率和 IKK/NF-κB通路、细胞周期蛋白 D1(cyclin D1)、半胱氨酸天冬氨酸蛋白酶 -3(cas. pase-3)蛋白水平。结果 脂多糖组较对照组炎症因子 IL-6［(16.33±0.76)ng/L比( 5.50±0.87)ng/L］、 TNF-α［(17.00±1.00)ng/L比(6.17±0.76)ng/L］表达水平上升( P<0.05)细胞活力下降［( 51.33±2.31)%比( 100.00±3.00)%，P<0.05］；脂多糖 +40组、脂多糖 +80组和脂多糖 +160组较脂多糖组炎症IL-6、TNF-α下降( P<0.05)，脂多糖 +80组和脂多糖 +160组细胞活力显著升高( P<0.05)。选择 80 nmol/L浓度进行后续实验。脂多糖组细胞增殖率、 cyclin D1蛋白水平较对照组下降( P<0.05)，细胞凋亡率、 cas. pase-3、磷酸化( p)-IKK和 p-NF-κB蛋白水平上升( P<0.05)；脂多糖 +80组和脂多糖 +抑制剂组较脂多糖组显著扭转了上述指标变化(P<0.05)；与脂多糖 +80组相比，加入 IKK/NF-κB通路抑制剂后，上述指标变化更为显著( P<0.05)脂多糖 +80+激活剂组则与脂多糖 +80+抑制剂组相反( P<0.05)。结论 毛兰素或可通过调控 IKK/NF-κB通路信号转导促多糖诱导的大鼠心肌 进脂，H9C2细胞活力、增殖，抑制其凋亡。 |
| 英文摘要: |
| Objective To explore the regulatory effect of erianin on lipopolysaccharide (LPS) -induced myocardial cell viability and IκB kinase/nuclear factor-κB (IKK/NF-κB) signaling pathway in rats.Methods Myocardial H9C2 cells were cultured in vitro and di.vided into control group (without intervention), LPS group (1 mg/L LPS), experimental group (LPS group supplemented with 40, 80, 160nmol/L erianin) and LPS+80+inhibitor group (LPS group supplemented with 80 nmol/L erianin and 10 μmol/L IKK/NF-κB pathway in. hibitor BAY11-7082), LPS+ inhibitor group (add 10 μmol/L BAY11-7082 on the basis of LPS group) and LPS+80+activator group (add 80 nmol/L erianin and 1μmol/L IKK/NF-κB pathway activator Prostratin on the basis of LPS group). Intervention for 24 h. Enzyme-linked immunosorbent assay, cell counting kit (CCK-8), 5-acetylidene-2 'deoxyuracil riboside, Hoechst 33258 staining and Western blotting (WB) were used to detect interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), cell viability, proliferation rate, apoptosis rate, IKK/NF-κB pathway, cyclin D1, and cysteine aspartate protease-3 (caspase-3) protein levels, respectively.Results Compared with the control group, the expression levels of inflammatory cytokines IL-6 [(16.33±0.76)ng/L vs. (5.50±0.87)ng/L] and TNF-α [(17.00±1.00)ng/ L vs. (6.17±0.76)ng/L] in LPS group were significantly increased (P<0.05), and the cell viability was significantly decreased [(51.33± 2.31)% vs. (100.00±3.00)%, P<0.05]. Compared with LPS group, inflammatory cytokines IL-6 and TNF-α were significantly decreased in LPS+40, LPS+80 and LPS+160 groups (P<0.05), and cell viability was significantly increased in LPS+80 and LPS+160 groups (P< 0.05). 80 nmol/L maolan was selected for follow-up experiment. Compared with control group, cell proliferation rate and cyclin D1 pro.tein expression level in LPS group were significantly decreased (P<0.05), while cell apoptosis rate, caspase-3, phosphorylation (p) -IKK and p-NF-κB protein expression were significantly increased (P<0.05). Compared with LPS group, LPS+80 group and LPS+ inhibitor group significantly reversed the changes of the above indexes (P<0.05). Compared with LPS+80 group, adding IKK/NF-κB pathway in. hibitor significantly changed the above indexes (P<0.05), and LPS+80+ activator group significantly reversed the above indexes (P< 0.05).Conclusion Maolanin may promote the viability and proliferation of LPS-induced H9C2 cells and inhibit their apoptosis by reg. ulating IKK/NF-κB pathway signaling. |
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