TAT-NBD exerts anti-inflammatory effect in rat cortical astrocytes by inhibiting bilirubin-induced nuclear factor-κB activation

李胜君; 李梦文; 张燕; 冯洁; 华子瑜

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TAT-NBD exerts anti-inflammatory effect in rat cortical astrocytes by inhibiting bilirubin-induced nuclear factor-κB activation

更新时间：2026-01-09

- TAT-NBD exerts anti-inflammatory effect in rat cortical astrocytes by inhibiting bilirubin-induced nuclear factor-κB activation
- Journal of Army Medical University Vol. 37, Issue 21, Pages: 2131-2136(2015)
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  CLC： R392.32;R742.89;R977.6
- Published：2015
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李胜君,李梦文,张燕,冯洁,华子瑜.反式激活蛋白-NEMO结合域抑制胆红素诱导的大鼠皮层星形胶质细胞NF-κB活化[J].陆军军医大学学报(原第三军医大学学报),2015,37(21):2131-2136.

　Li Shengjun,Li Mengwen,Zhang Yan,Feng Jie,Hua Ziyu.TAT-NBD exerts anti-inflammatory effect in rat cortical astrocytes by inhibiting bilirubin-induced nuclear factor-κB activation[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(21):2131-2136.
李胜君,李梦文,张燕,冯洁,华子瑜.反式激活蛋白-NEMO结合域抑制胆红素诱导的大鼠皮层星形胶质细胞NF-κB活化[J].陆军军医大学学报(原第三军医大学学报),2015,37(21):2131-2136. DOI：

　Li Shengjun,Li Mengwen,Zhang Yan,Feng Jie,Hua Ziyu.TAT-NBD exerts anti-inflammatory effect in rat cortical astrocytes by inhibiting bilirubin-induced nuclear factor-κB activation[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(21):2131-2136. DOI：

摘要

目的明确反式激活蛋白-NEMO结合域（TAT-NBD）对胆红素诱导的大鼠皮层星形胶质细胞核因子-κB(NF-κB)活化及炎症反应的作用。方法分离并鉴定新生SD大鼠大脑皮质星形胶质细胞，随机分为对照组、胆红素组、TAT-NBD干预组。免疫荧光观察各组细胞形态，改良MTT检测细胞相对存活率。Western blot检测NF-κB p65表达，EMSA检测NF-κB的入核、活化。ELISA法检测培养基上清炎症因子IL-1β、TNF-α、IL-6水平。结果胆红素组NF-κB p65蛋白灰度比值明显高于对照组(P0.01)，2、12 h达高峰(P0.05)；TAT-NBD干预组NF-κB p65蛋白表达明显低于胆红素组（P0.01）。IL-1β、TNF-α、IL-6的释放与胆红素诱导的NF-κB p65表达有时间相关性，于12 h达高峰，且TAT-NBD干预2、12 h的IL-1β、TNF-α、IL-6 浓度均低于胆红素组(P0.01)。星形胶质细胞的存活率与胆红素作用时间呈负相关，TAT-NBD干预2、12 h的相对存活率均高于胆红素组(P0.05)。结论胆红素可诱导原代培养的大鼠星形胶质细胞NF-κB激活、过表达，TAT-NBD抑制NF-κB的活化高峰、减少炎症因子释放产生抗炎作用，可用于预防胆红素脑损伤。

Abstract

Objective To determine the effect of trans-activator of transcription-NEMO binding domain (TAT-NBD) on bilirubin-induced activation of nuclear factor-κB (NF-κB) and neuroinflammation in rat cortical astrocytes. Methods Astrocytes were freshly separated from the cortex of newborn SD rats. After identification and purification

the astrocytes at passage 2 were randomly divided into control group

bilirubin group and TAT-NBD intervention group. Cellular morphology were observed by immunofluorescence assay

the survival rate were assessed with a modified MTT assay

the expression and activity of NF-κB p65 protein was detected by Western blotting and electrophoretic mobility shift assay (EMSA)

and the contents of IL-1β

TNF-α and IL-6 in the supernatants were measured with ELISA. Results Compared with the astrocytes in the control group

the expression of NF-κB p65 protein was significantly increased in bilirurin-treated cells (P0.01)

reaching the peak at 2 and 12 h (P0.05). Consistent with the expression of NF-κB

the contents of IL-1β

TNF-α and IL-6 were in a time-dependent manner. TAT-NBD intervention dramatically inhibited bilirubin-induced NF-κB p65 activation as well as the release of IL-1β

TNF-α and IL-6 (P0.01). The viability of astrocyte cells was decreased after bilirubin exposure

whereas the survival rate of TAT-NBD intervention group was significantly higher than that of bilirubin group but lower than that of the control group (P0.01). Conclusion In in vitro model

bilirubin-induced cortical astrocytes inflammation is obviously related to the over-expression and activation of NF-κB. TAT-NBD does show strong anti-inflammatory effects by inhibiting the activation of NF-κB and release of inflammatory cytokines

which might be useful in prophylaxis of bilirubin-induced brain injury.

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Related Institution

Department of Pediatric Research Institute，Children’s Hospital of Chongqing Medical University， National Clinical Research Center for Child Health and Disorders， Ministry of Education Key Laboratory of Child Development and Disorders

Department of Dermatology， Children’s Hospital of Chongqing Medical University

Graduate School， Guizhou University of Traditional Chinese Medicine

Department of Critical Care Medicine， Qingzhen First People’s Hospital

Graduate School， Zunyi Medical University

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