| 王廷科,杨国青,顾建争,等.红景天苷对脂多糖诱导的心肌细胞炎症反应及增殖、凋亡的作用机制研究[J].安徽医药,2025,29(12):2348-2353. |
| 红景天苷对脂多糖诱导的心肌细胞炎症反应及增殖、凋亡的作用机制研究 |
| Mechanism of salidroside on lipopolysaccharide-induced inflammatory response, proliferation and apoptosis of cardiomyocytes |
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| DOI：10.3969/j.issn.1009-6469.2025.12.004 |
| 中文关键词: 红景天属 脂多糖类 大鼠心肌细胞 H9C2 心力衰竭 核因子 κB信号通路 凋亡 炎症反应 |
| 英文关键词: Rhodiola Lipopolysaccharides Rats cardiac muscle cell H9C2 Heart failure Nuclear transcription factor-κB sig-naling pathway Apoptosis Inflammatory response |
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| 中文摘要: |
| 目的探究红景天苷对脂多糖( LPS)诱导的大鼠心肌细胞增殖凋亡、炎症及核因子 κB(NF-κB)信号通路的调控作用。方法 2022年 1月至 2023年 1月将体外培养的大鼠心肌细胞 H9C2按随机数字表法分为对照组(不做干预)、 LPS组( 10 mg/L LPS)、 LPS+10、LPS+20、LPS+40和 LPS+80组( 10 mg/L LPS+10、20、40、80 μmol/L红景天苷)，红景天苷最佳浓度确定后，又补充红景天苷 +抑制剂( Y)组( 10 mg/L LPS+20 μmol/L红景天苷 +10 μmol/L NF-κB通路抑制剂 BAY11-7082)、抑制剂组( 10 mg/L LPS+10 μmol/L BAY11-7082)和红景天苷 +激活剂( A)组( 10 mg/L LPS+20 μmol/L红景天苷 +1 μmol/L NF-κB通路激活剂 Pros.tratin)，干预 24 h。用细胞计数试剂盒 -8(CCK-8)测定细胞活力；酶联免疫吸附分析检测白细胞介素( IL)-6、IL-10及肿瘤坏死因子 α(TNF-α)含量； Hoechst33258染色法测定细胞凋亡率；蛋白质印迹法测定 NF-κB相关蛋白、细胞周期蛋白 D1(cyclin D1)、胱天蛋白酶( caspase)-3、caspase-1、斑点样蛋白( ASC)和核苷酸寡聚化结构域( NOD)样受体蛋白 3(NLRP3)蛋白表达水平。结果 LPS组细胞活力显著低于对照组( P<0.05)LPS+20组细胞活力显著高于 LPS组( P<0.05)因此选择 LPS+20组进行后续试验。LPS组IL-10［(76.36±3.56)ng/L比(184.54±7.，70)ng/L］、 cyclin D1蛋白水平( 0.13±0.01比 0.9，3±0.01)低于对照组( P<0.05)， IL-6、TNF-α、细胞凋亡率、 caspase-3、p-NF-κBp65、ASC、NLRP3和 caspase-1蛋白水平［( 54.11±4.41)ng/L比( 19.94±2.91)ng/L(253.57±7.17)ng/L比( 69.86±5.06)ng/L、(46.33±2.08)%比(2.00±1.00)%、1.20±0.01比 0.11±0.01、0.81±0.03比 0.11±0.01、1.02±0.01比 0.10±0.01、0.55±0.02比 0.10±0.01、0.87±0.02比 0.11±0.01］高于对照组( P<0.05)； LPS+20组和抑制剂组逆转了 LPS组上述指标变化趋势(P<0.05)；与 LPS+20组相比， BAY11-7082加强了 Prostratin扭转了红景天苷对 H9C2细胞的作用(P<0.05)。结论红景天苷可通过阻断 NF-κB通路的信号转导抑制 LPS诱导的大鼠心肌 H9C2细胞的凋亡及炎症反应。 |
| 英文摘要: |
| Objective To investigate the regulatory effects of salidroside on proliferation, apoptosis, inflammation and nuclear tran-scription factor κB (NF-κB) signaling pathway induced by lipopolysaccharide (LPS) in rat cardiomyocytes. Methods From January 2022 to January 2023. Rat H9C2 cardiomyocytes cultured in vitro were randomly divided into control group (no intervention), LPSgroup (10 mg/L LPS), LPS+10, LPS+20, LPS+40 and LPS+80 groups (10 mg/L LPS+10, 20, 40 and 80 μmol/L salidroside). After theoptimal concentration of salidroside was determined, the salidroside+inhibitor (Y) group (10 mg/L LPS+20 μmol/L salidroside+10μmol/L NF-κB pathway inhibitor BAY11-7082), inhibitor group (10 mg/L LPS+10 μmol/L BAY11-7082) and salidroside+activator (A) group (10 mg/L LPS+20 μmol/L salidroside+1 μmol/L activator of NF-κB pathway Prostratin) were treated for 24 h. Cell viability was measured with cell counting kit -8 (CCK-8). The levels of interleukin (IL) -6, IL-10 and tumor necrosis factor (TNF) -ɑ were detected byenzyme linked immunosorbent assay. The apoptosis rate was determined by Hoechst33258 staining. The expression levels of NF-κB-re-lated proteins, cyclin D1, caspase-3, caspase-1, speck-like protein (ASC) and nucleotide oligomerization domain (NOD) -like receptor protein 3 (NLRP3) were determined by western blotting.Results The cell viability in LPS group was significantly lower than that in control group (P<0.05), and the cell viability in LPS+20 group was significantly higher than that in LPS group (P<0.05). LPS+20 group was selected for follow-up experiment. The levels of IL-10 [(76.36±3.56) ng/L vs. (184.54±7.70) ng/L] and cyclin D1(0.13±0.01 vs. 0.93±0.01) protein in LPS group were lower than those in control group (P<0.05). The levels of IL-6, TNF-ɑ, apoptosis rate and caspase-3, p-NF-κB p65, ASC, NLRP3, caspase-1 protein were [(54.11±4.41) ng/L vs. (19.94±2.91) ng/L, (253.57±7.17) ng/L vs. (69.86±5.06) ng/L, (46.33±2.08) % vs. (2.00±1.00) % , 1.20±0.01 vs. 0.11±0.01, 0.81±0.03 vs. 0.11±0.01, 1.02±0.01 vs. 0.10±0.01, 0.55±0.02 vs. 0.10±0.01, 0.87±0.02 vs. 0.11±0.01], which were higher than those in control group (P<0.05). The LPS+20 group and the inhibitor group reversed the trend of changes in the above indicators in the LPS group (P<0.05). Compared with LPS+20 group, BAY11-7082 en-hanced and Prostratin reversed the effect of salidroside on H9C2 cells (P<0.05).Conclusion Salidroside can inhibit the apoptosis and inflammatory response of H9C2 cells induced by LPS by blocking the signal transduction of NF-κB pathway. |
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