摘要
目的 探讨萝卜硫素对脂多糖（lipopolysaccharide, LPS）诱导心肌细胞肥大的影响及其作用机制。方法 体外原代培养新生大鼠心肌细胞，将心肌细胞按随机数字表法分为对照组，LPS诱导组，JAK2抑制剂组，萝卜硫素低、中、高剂量组。除对照组外，其余各组细胞加入1 mg/L的LPS进行干预，低、中、高剂量组加入10、20、40 μg/ml萝卜硫素进行干预，JAK2抑制剂组加入JAK2抑制剂10 nmol/L干预24 h。采用计算机图像分析系统测定心肌细胞体积，BCA法测定心肌细胞中总蛋白含量，ELISA法检测细胞培养基上清液中IL-6、TNF-a水平，WB法检测酪氨酸激酶/信号转导子和转录激活子（janus kinase/signal transducer and activator of transcription, JAK/STAT）信号通路相关蛋白表达水平。结果 与LPS诱导组比较，低、中、高剂量组细胞体积[（1 635.71±154.84）μm3、（1 450.06±140.13）μm3、（1 194.51±134.76）μm3比（1 854.28±181.37）μm3]和蛋白[（20.14±2.11）μg、（17.59±1.64）μg、（14.27±1.47）μg比（23.17±2.56）μg]含量降低（P＜0.05）；细胞培养基上清中IL-6[（1 410.08±255.17）pg/ml、（1 065.61±210.37）pg/ml、（790.09±140.28）pg/ml比（1 804.07±275.34）pg/ml]、TNF-a[（164.16±27.51）pg/ml、（130.13±22.08）pg/ml、（92.27±12.16）pg/ml比（182.42±30.37） pg/ml]水平降低（P＜0.05）；细胞p-JAK2/JAK2[（0.39±0.05）、（0.27±0.04）、（0.21±0.03）比（0.54±0.07）]、p-STAT3[（0.47±0.05）、（0.25±0.03）、（0.18±0.03）比（0.53±0.06）]表达降低（P＜0.05）。结论 萝卜硫素对LPS诱导的心肌细胞肥大具有保护作用，其机制可能与抑制JAK2/STAT3信号通路活化有关。
Objective To investigate the effects of sulforaphane on lipopolysaccharide （LPS）- induced cardiac myocytes hypertrophy of rats and study its possible mechanism. Methods The hypertrophic primary cardiac cells of neuonatal rats were divided into control group, LPS-induced group, JAK2 inhibitor group, low-, middle-, and high-dose sulforaphane groups. The cells in all groups, except for control group, were intervened by LPS （1 mg/L）. The low-, middle-, and high-dose sulforaphane groups were treated with 10, 20, 40 μg/ml sulforaphane respectively. The JAK2 inhibitor group was treated with 10 nmol/L of JAK2 inhibitor for 24 h. Computer photograph analysis system was used to determine the cardiomyocyte volume, BCA kit was used to analyze the total protein concentration, ELISA kit was used to observe the expression levels of inflammatory cytokine （including IL-6 and TNF-α）, and the Western Blot technology was used to analyze the expression levels of the related proteins in JAK2/STAT3 signaling pathway. Results Compared with control group, the cell volume （1 635.71 ± 154.84 μm3, 1 450.06 ± 140.13 μm3, 1 194.51 ± 134.76 μm3 vs. 1 854.28 ± 181.37 μm3） and the levels of protein （20.14 ± 2.11 μg, 17.59 ± 1.64 μg, 14.27 ± 1.47 μg vs. 23.17 ± 2.56 μg） in low-, medium-, high- dose of sulforaphane groups were significantly decreased （P〈0.05）. The levels of IL-6 （1 410.08 ± 255.17 pg/ml, 1 065.61 ± 210.37 pg/ml, 790.09 ± 140.28 pg/ml vs. 1 804.07 ± 275.34 pg/ml） and TNF-α （164.16 ± 27.51 pg/ml, 130.13± 22.08 pg/ml, 92.27 ±12.16 pg/ml vs. 182.42 ± 30.37 pg/ml） in low-, medium-, high- dose of sulforaphane groups were significantly decreased （P〈0.05）. The expression levels of p-JAK2/JAK2 （0.39 ± 0.05, 0.27 ± 0.04, 0.21 ± 0.03 vs. 0.54 ± 0.07） and p-STAT3 （0.47 ± 0.05, 0.25 ± 0.03, 0.18 ± 0.03 vs. 0.53 ± 0.06） in low-, medium-, high- dose of sulforaphane groups were also significantly decreased （P〈0.05）. Conclusions Sulforaphane has a protective e
作者
李玉慈
王玲
罗丹
周龙友
Li Yuci;Wang Ling;Luo Dan;Zhou Longyou(Cardiovascular Medicine Center,Central Hospital of Enshi Autonomous Prefecture,Enshi 445000,China)
出处
《国际中医中药杂志》
2018年第8期733-737,共5页
International Journal of Traditional Chinese Medicine
