Role of CD36 in palmitate acid-induced inflammation of HepG2 cells

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Role of CD36 in palmitate acid-induced inflammation of HepG2 cells

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- Role of CD36 in palmitate acid-induced inflammation of HepG2 cells
- Journal of Chongqing Medical University Vol. 42, Issue 7, Pages: 864-869(2017)
- 作者机构：
  
  重庆医科大学脂糖代谢性疾病重庆市重点实验室脂质研究中心
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.001350
  CLC： R575
- Published：2017，
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Wei Li, Yang Ping, Chen Yaxi, et al. Role of CD36 in palmitate acid-induced inflammation of HepG2 cells. [J]. Journal of Chongqing Medical University 42(7):864-869(2017)
DOI：

Wei Li, Yang Ping, Chen Yaxi, et al. Role of CD36 in palmitate acid-induced inflammation of HepG2 cells. [J]. Journal of Chongqing Medical University 42(7):864-869(2017) DOI： 10.13406/j.cnki.cyxb.001350.

摘要

目的:探讨白细胞分化抗原36(cluster of differentiation 36

CD36)是否参与了棕榈酸诱导的HepG2细胞炎症反应。方法:给予HepG2细胞不同浓度的棕榈酸(0.00、0.08、0.16、0.32、0.64 mmol/L)处理24 h

使用实时荧光定量PCR方法检测CD36和炎症因子的mRNA表达水平

Western blot检测CD36蛋白表达水平。然后利用小RNA干扰技术

构建低表达CD36的HepG2细胞(CD36RNAi HepG2)和对照细胞(NCi HepG2)模型。通过实时荧光定量PCR检测棕榈酸负荷的NCi HepG2和CD36RNAi HepG2中炎症因子的表达情况

荧光探针DCFH DA法检测细胞内活性氧含量

Western blot检测细胞核内的核转录因子-κB的蛋白表达水平。结果:棕榈酸能够上调HepG2细胞中CD36及炎症因子——肿瘤坏死因子-α(tumor necrosis factor-α

TNF-α)和白介素-6(interleukin-6

IL-6)的表达。棕榈酸浓度分别为0.00、0.08、0.16、0.32及0.64 mmol/L时

CD36的mRNA表达相对值分别为(1.001±0.078)、(1.510±0.341)(q=4.763

P=0.007)、(1.780±0.070)(q=7.301

P=0.000)、(2.510±0.141)(q=14.16

P=0.000)及(2.103±0.150)(q=10.34

P=0.000)。TNF-α的mRNA表达相对值分别为(1.000±0.098)、(1.571±0.177)(q=1.598

P=0.141)、(1.725±0.274)(q=2.016

P=0.071)、(2.113±0.341)(q=3.102

P=0.011)及(5.282±0.855)(q=11.940

P=0.000)。IL-6的mRNA表达相对值分别为(0.999±0.047)、(1.791±0.596)(q=1.486

P=0.168)、(2.119±0.294)(q=2.107

P=0.061)、(2.808±0.147)(q=3.398

P=0.007)及(6.916±1.284)(q=11.130

P=0.000)。抑制HepG2细胞中CD36表达

可以显著降低棕榈酸所诱导的细胞内活性氧(reactive oxygen species

ROS)增加和核转录因子-κB在核内分布的增强

降低HepG2细胞内炎症因子表达水平。NCi HepG2、NCi HepG2+棕榈酸组及CD36 RNAi HepG2+棕榈酸组的ROS相对含量分别为(1.000±0.113)、(1.968±0.293)(与NCi组相比

t=6.888

P=0.000)、(0.519±0.129)(与NCi+棕榈酸组相比

t=10.106

P=0.000)。NCi HepG2、NCi HepG2+棕榈酸组及CD36 RNAi HepG2+棕榈酸组的核转录因子-κB的蛋白相对值分别为(0.997±0.093)、(2.443±0.085)(与NC相比

t=19.892

P=0.000)、(1.607±0.107)(与NCi+棕榈酸组相比

t=10.607

P=0.000)。抑制HepG2细胞中CD36表达后

棕榈酸浓度分别为0.08、0.16、0.32及0.64 mmol/L时

NCi HepG2及CD36 RNAi HepG2组的TNF-α的表达水平分别为(1.004±0.113)和(0.185±0.071)(t=10.716

P=0.000);(1.009±0.160)和(0.221±0.028)(t=8.389

P=0.001);(1.008±0.163)和(0.173±0.011)(t=8.780

P=0.001);(1.009±0.163)和(0.147±0.013)(t=9.013

P=0.000)。抑制HepG2细胞中CD36表达后

棕榈酸浓度分别为0.08、0.16、0.32及0.64 mmol/L时

NCi HepG2及CD36 RNAi HepG2组的IL-6的表达水平分别为(1.044±0.347)和(0.207±0.033)(t=4.121

P=0.015);(1.006±0.139)和(0.198±0.007)(t=10.110

P=0.001);(1.001±0.052)和(0.125±0.006)(t=28.443

P=0.000);(1.012±0.188)和(0.114±0.015)(t=8.367

P=0.001)。结论:棕榈酸能够上调HepG2细胞CD36表达

促进HepG2炎症反应;抑制CD36可能通过减少氧化应激、抑制核转录因子-κB信号通路

进而改善棕榈酸诱导的HepG2细胞炎症。

Abstract

Objective:To investigate whether cluster of differentiation 36（CD36）is involved in the palmitic acid induced inflammation of HepG2 cells. Methods:HepG2 cells were treated with different concentrations of palmitic acid（0.00

0.08

0.16

0.32 and 0.64mmol/L）for 24 h. Protein and mRNA levels of CD36 were detect ed respectively by Western blot and real-time PCR. The mRNA expression of inflammatory cytokines was detected by real-time PCR. Small RNA interference was used to inhibit CD36 expression in HepG2 cells（CD36RNAi HepG2）. Intracellular reactive oxygen species（ROS）was detected by fluorescent probe DCFH DA（2’

7’-dichlorofluorescin diacetate）. P65-nuclear transcription factor κB protein expression in nuclear was detected by Western blot. Results:Palmitic acids upregulated CD36

tumor necrosis factor-alpha（TNF-α）and interleukin-6（IL-6）expression in HepG2 cells. When HepG2 cells were treated with different concentrations of palmitic acid（0.00

0.08

0.16

0.32 and 0.64 mmol/L）

CD36 mRNA levels in HepG2 cells were（1.001±0.078）

（1.223±0.294）（q=4.763

P=0.007）

（1.510±0.341）（q=7.301

P=0.000）

（1.780±0.070）（q=14.16

P=0.000）and（2.510±0.141）（q=10.34

P=0.000）. TNF-α mRNA levels were（1.000±0.098）

（1.571±0.177）（q=1.598

P=0.141）

（1.725±0.274）（q=2.016

P=0.071）

（2.113±0.341）（q=3.102

P=0.011）

（5.282±0.855）（q=11.940

P=0.000）. IL-6 mRNA levels were（0.999±0.047）;（1.791±0.596）（q=1.486

P=0.168）;（2.119±0.294）（q=2.107

P=0.061）;（2.808±0.147）（q=3.398

P=0.007）;（6.916±1.284）（q=11.130

P=0.000）. When CD36 was inhibited

intracellular ROS levels and P65-nuclear transcription factor κB expressions in nuclear were significantly reduced

compared with those of negative control HepG2 cells（NCi HepG2）. The levels of inflammatory cytokines in CD36 RNAi HepG2 cells were also significantly lower than those in NCi HepG2 cells. In NCi HepG2 group

NCi HepG2+palmitic acid group and CD36 RNAi HepG2+palmitic acid group

the ROS levels were（1.000±0.113）

（1.968±0.293）（compared with those of NCi HepG2 cells

t =6.888

P =0.000）

（0.519 ±0.129）（compared with those of NCi + palmitic acid HepG2 cells

t=10.106

P=0.000）. In NCi HepG2 group

NCi HepG2 +palmitic acid group and CD36 RNAi HepG2 +palmitic acid group

the P65-nuclear transcription factor κB levels were（0.997±0.093）

（0.443±0.085）（compared with those of NCi HepG2 cells

t=19.892

P=0.000）

（1.607±0.107）（compared with those of NCi+ palmitic acid HepG2 cells

t=10.607

P=0.000）. When NCi and CD36 RNAi HepG2 cells were treated with different concentrations of palmitic acid（0.08

0.16

0.32 and 0.64 mmol/L）

TNF-αmRNA levels in NCi and CD36 RNAi HepG2 cells were（1.004±0.113） and（0.185±0.071）（t=10.716

P=0.000）

（1.009±0.160）and（0.221 ±0.028）（t=8.389

P =0.001）

（1.008 ±0.163） and（0.173 ±0.011）（t=8.780

P =0.001）;（1.009 ±0.163） and（0.147 ±0.013）（t=9.013

P=0.001）. In NCi and CD36 RNAi HepG2 cells

which were treated with different concentrations of palmitic acid（0.08

0.16

0.32 and 0.64 mmol/L）

IL-6 mRNA levels were（1.044±0.347）and（0.207±0.033）（t=4.121

P=0.015）;（1.006±0.139）and（0.198±0.007）（t=10.110

P=0.001）;（1.001±0.052）and（0.125±0.006）（t=28.443

P=0.000）;（1.012±0.188）and（0.114±0.015）（t=8.367

P=0.001）. Conclusion:Palmitate increases CD36 expression and induces inflammation in HepG2 cells. Inhibition of CD36 reduces oxidative stress and prevents NF-κB signaling pathway activation

resulting in attenuation of inflammation stress in the presence of palmitate in HepG2 cells.

关键词

CD36棕榈酸HepG2炎症

Keywords

CD36palmitate acidHepG2 cellsinflammation

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