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贵州医科大学 药学院 天然资源有效利用重点实验室,贵阳 550025
[第一作者] 甘诗泉,博士,讲师,从事民族药和心血管药物药理研究,E-mail:503888243@qq.com
*沈祥春,博士,教授,从事心血管系统药物药理、功能天然产物化学生物学研究,E-mail:shenxiangchun@126.com
收稿日期:2019-06-20,
网络出版日期:2019-11-07,
纸质出版日期:2020-02-20
移动端阅览
甘诗泉, 王声全, 张光琼, 等. 艳山姜挥发油通过调控巨噬细胞CD36和ABCA1表达抑制泡沫细胞的形成[J]. 中国实验方剂学杂志, 2020,26(4):64-69.
Shi-quan GAN, Sheng-quan WANG, Guang-qiong ZHANG, et al. Essential Oil from Alpinia zerumbet Rhizome Inhibits Macrophage-derived Foam Cell Formation Via Modulating Expression of CD36 and ABCA1[J]. Chinese journal of experimental traditional medical formulae, 2020, 26(4): 64-69.
甘诗泉, 王声全, 张光琼, 等. 艳山姜挥发油通过调控巨噬细胞CD36和ABCA1表达抑制泡沫细胞的形成[J]. 中国实验方剂学杂志, 2020,26(4):64-69. DOI: 10.13422/j.cnki.syfjx.20200438.
Shi-quan GAN, Sheng-quan WANG, Guang-qiong ZHANG, et al. Essential Oil from Alpinia zerumbet Rhizome Inhibits Macrophage-derived Foam Cell Formation Via Modulating Expression of CD36 and ABCA1[J]. Chinese journal of experimental traditional medical formulae, 2020, 26(4): 64-69. DOI: 10.13422/j.cnki.syfjx.20200438.
目的:
2
观察艳山姜挥发油对氧化低密度脂蛋白(ox-LDL)诱导巨噬细胞转化为泡沫细胞的抑制作用,并探索其机制。
方法:
2
使用佛波酯(PMA,100 μg·L
-1
)诱导人白血病单核细胞(THP-1)24 h后形成巨噬细胞,实验分为4组,分别为空白组(无血清RPMI 1640),模型组(80 mg·L
-1
ox-LDL),艳山姜挥发油低剂量组(80 mg·L
-1
ox-LDL+ 4 μg·L
-1
艳山姜挥发油),艳山姜挥发油高剂量组(80 g·L
-1
ox-LDL+ 20 μg·L
-1
艳山姜挥发油)。噻唑蓝(MTT)比色法检测艳山姜挥发油对巨噬细胞的活性的影响,蛋白免疫印迹法(Western blot)检测巨噬细胞中白细胞分化抗原36(CD36)和三磷酸腺苷结合盒转运体A1(ABCA1)的表达,酶联免疫吸附测定(ELISA)检测巨噬细胞内胆固醇酯含量,油红O染色法检测巨噬细胞中脂质小滴的含量。
结果:
2
艳山姜挥发油对巨噬细胞无毒性。与空白组比较,模型组的巨噬细胞内脂滴和胆固醇酯的含量显著增加(
P
<
0.01),CD36蛋白表达显著上升(
P
<
0.01),ABCA1蛋白表达无显著变化;与模型组比较,艳山姜挥发油显著抑制巨噬细胞中脂滴和胆固醇酯的含量(
P
<
0.01),下调CD36的蛋白表达(
P
<
0.01),上调ABCA1蛋白的表达(
P
<
0.01),艳山姜挥发油可抑制巨噬细胞向泡沫细胞的转化。
结论:
2
艳山姜挥发油对ox-LDL诱导的巨噬细胞向泡沫细胞的形成具有抑制作用,该药理作用与艳山姜挥发油下调巨噬细胞CD36和上调ABCA1蛋白的表达有关。
Objective:
2
To clarify the inhibitory effect of essential oil from
Alpinia zerumbet
rhizome (EOFAZ) on oxidized low-density lipoprotein (ox-LDL)-induced transformation of macrophage into foam cell and explore its possible mechanism.
Method:
2
THP-1 monocyte was incubated with 100 μg·L
-1
phorbol myristate acetate (PMA) to grow into macrophage
experiment was divided into 4 groups as follows
control group
model group (80 mg·L
-1
ox-LDL)
EOFAZ at low dose (80 mg·L
-1
ox-LDL+ 4 μg·L
-1
EOFAZ)and EOFAZ at high dose (80 g·L
-1
ox-LDL+ 20 μg·L
-1
EOFAZ). Mathye thiazolye telrazliurn (MTT) method was employed to examine the influence of EOFAZ on macrophage viability. Western blot was used to analyze the expression level of cluster of differentiation 36(CD36) and ATP-binding cassette transporter A1(ABCA1) protein in macrophage. Enzyme-linked immunosorbent assay (ELISA) was used to detect cholesteryl ester contents in macrophage. Oil red O staining was applied to determine the accumulation of lipids in macrophage.
Result:
2
EOFAZ showed non-toxic effect on macrophage. Compared to control group
macrophage in model group displayed higher level of cholesteryl ester and lipid droplet(
P
<
0.01)
as well as significant increasing of CD36 expression (
P
<
0.01)
but no effect on ABCA1 expression. EOFAZ notably reduced the contents of lipids and cholesteryl ester(
P
<
0.01)
down-regulated expression of CD36 and up-regulated expression of ABCA1 in macrophage in comparison with the model group(
P
<
0.01)
indicating that EOFAZ inhibited transformation of macrophage into foam cell.
Conclusion:
2
EOFAZ could inhibit ox-LDL-induced transformation of macrophage into foam cell
the underlying mechanism may involves its ability to increase CD36 expression and decrease ABCA1 expression in macrophage.
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