二氢杨梅素对高糖诱导的H9C2心肌细胞损伤的影响

目的探讨二氢杨梅素（DHM）对高糖（HG）诱导的心肌细胞H9C2损伤的影响及机制。 方法细胞处理分为对照组、35 mmol/L HG组、35mmol/L HG+50 μmol/L DHM组及50 μmol/L DHM组。CCK-8法检测细胞活力，化学比色法检测丙二醛（MDA）、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）水平，流式细胞术检测ROS水平；荧光定量PCR法及Elisa法分别检测TNFα、IL1β、IL6 mRNA和含量，Western Blotting检测p-IκBα、IκBα蛋白及核蛋白NF-κB p65的表达水平。采用单因素方差分析进行组间比较。 结果对照组、35mmol/?L HG组、35?mmol/L HG+50?μmol/L DHM组、35?mmol/L HG+100?μmol/L DHM组的细胞活力分别是（100±0.00） ﹪、（52.23±5.69） ﹪、（74.58±6.12） ﹪和（86.04±3.76）﹪，差异具有统计学意义（F?= 40.61，P?< 0.01）。对照组、35?mmol/L HG组和35?mmol/L HG+100?μmol/L DHM组的MDA和ROS水平，SOD和CAT活性分别是（0.44±0.06）?nmol/?ml，（2.33±0.40）?nmol/?ml，（1.48±0.41）?nmol/ml、（156.0±9.00）U/ml，（325.3±10.69）U/ml，（244.0±9.54）?U/ml，（10.62± 1.59）?U/?ml，（5.18±0.34）U/ml，（7.75±0.53）U/ml，（11.31±0.98）?U/ml，（5.20±1.12）?U/?ml和（8.06±0.66）U/ml，差异具有统计学意义（F?= 30.34，29.75，14.72，P均< 0.01）。DHM预处理可明显拮抗HG对H9C2心肌细胞TNFα、IL1β和IL6 mRNA及含量的上调作用，差异存在统计学意义（P?均< 0.01）。DHM可抑制HG对H9C2心肌细胞p-IκBα/?IκBα蛋白和核蛋白NF-κB p65表达的增加作用，差异存在统计学意义（P均< 0.01）。 结论DHM可拮抗HG诱导的H9C2心肌细胞损伤，这可能与其抑制NF-κB信号通路有关。

Effect of dihydrobayberry on high glucose-caused injury of H9C2 myocardial cell

ObjectiveTo investigate the influence of dihydrobayberry (DHM) on high glucose (HG) -induced cardiomyocytes H9c2 cells damage and its poteintial mechanism. MethodsCells were divided into the following groups: control group, 35 mmol/L HG group, 35?mmol/L HG+50?μmol/L DHM group and 50?μmol/L DHM group. CCk-8 assay was used to detect cell viability. The levels of malondialdehyde (MDA) , superoxide dismutase (SOD) and catalase (CAT) were determined by chemical colorimetry. ROS levels were measured by flow cytometry. TNFα, IL1β and IL6 mRNA expression and contents were determined by fluorescence quantitative PCR and Elisa assays respectively. The expression levels of p-IκBα and IκBα proteins, and nucleoprotein NF-κB p65 were detected by Western Blot. Univariate analysis of variance was used for comparison between groups. ResultsPretreatment with 50 and 100?μmol/L DHM significantly inhibited the reduced cell viability of H9C2 myocardial cells caused by 35?mmol/L HG: The cell viability of the control group, 35?mmol/L HG group, 35?mmol/L HG+50?μmol/L DHM group, 35?mmol/L HG+100?μmol/L DHM group were (100±0.00) ﹪, (52.23±5.69) ﹪, (74.58±6.12) ﹪ and (86.04±3.76) ﹪, respectively (F?= 40.61, P < 0.001) . We also found that pretreatment with DHM (50?μmol/L) significantly inhibited the enhanced MDA and ROS levels, and decreased SOD and CAT activity of H9C2 myocardial cells induced by HG (35?mmol/?L) . The MDA level, SOD and CAT activity of the control group, HG group and HG+ DHM group were (0.44±0.06) ?nmol/?ml, (2.33±0.40) nmol/ml, (1.48±0.41) nmol/ml, (156.00±9.00) U/ml, (325.3±10.69) U/?ml, (244.0±9.54) U/ml, (10.62±1.59) U/ml, (5.18±0.34) U/ml, (7.75±0.53) ?U/?ml and (11.31±0.98) ?U/?ml , (5.20±1.12) U/ml, (8.06±0.66) U/ml, respectively. (F?= 30.34, 29.75, 14.72, P?all < 0.001) . Pretreatment with DHM significantly inhibited the increased expression levels of TNFα, IL1β and IL6 mRNA and their contents caused by HG in H9C2 myocardial cells (P all < 0.001) . DHM significantly inhibited the increased expression of p-IκBα/IκBα and nucleoprotein NF-κB p65 in H9C2 myocardial cells caused by HG (P all < 0.001) . ConclusionDHM can antagonize HG-induced H9C2 myocardial cell injury, which may be related to its inhibition of NF-κB signaling pathway.