Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice

Context: Researchers in a variety of fields have extensively focused on histone deacetylase 6 (HDAC6) due to its aggravation of inflammatory reaction. However, relevant studies examining whether HDAC6 could exacerbate lipopolysaccharide (LPS)-induced inflammation are still lacking. Objective: We ass...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Yuanjian Song, Li Qin, Rongli Yang, Fan Yang, Nwobodo Alexander Kenechukwu, Xiaofang Zhao, Xiaoyan Zhou, Xiangru Wen, Lei Li
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2019
Materias:	histone deacetylase 6 tubastatin a inflammation phosphorylated p38mapk Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/f1709d849667425f8095138a7bb6b442
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:f1709d849667425f8095138a7bb6b442
record_format	dspace
spelling	oai:doaj.org-article:f1709d849667425f8095138a7bb6b4422021-11-17T14:21:55ZInhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice1388-02091744-511610.1080/13880209.2018.1563620https://doaj.org/article/f1709d849667425f8095138a7bb6b4422019-01-01T00:00:00Zhttp://dx.doi.org/10.1080/13880209.2018.1563620https://doaj.org/toc/1388-0209https://doaj.org/toc/1744-5116Context: Researchers in a variety of fields have extensively focused on histone deacetylase 6 (HDAC6) due to its aggravation of inflammatory reaction. However, relevant studies examining whether HDAC6 could exacerbate lipopolysaccharide (LPS)-induced inflammation are still lacking. Objective: We assessed the role of HDAC6 in LPS-induced brain inflammation and used the HDAC6-selective inhibitor Tubastatin A (TBSA) to investigate the potential mechanisms further. Materials and methods: Brain inflammation was induced in Kunming (KM) mice via intraperitoneal (I.P.), injection of Lipopolysaccharide (LPS) (1 mg/kg), the TBSA (0.5 mg/kg) was delivered via intraperitoneal. The phosphorylated p38 (p-p38) Mitogen-activated protein kinases (MAPK) and expression of typical inflammatory mediators, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in both the hippocampus and cortex, were examined by immunoblotting. Nissl staining was used to detect the neuronal damage in the hippocampus and the cortex. Results: About 1 mg/kg LPS via daily intraperitoneal (I.P.) injections for 12 days significantly increased p38 MAPK phosphorylation, TNF-α and IL-6 expression, and neuronal loss. However, 0.5 mg/kg TBSA (three days before LPS treatment) by I.P. injections for 15 days could reverse the above results. Conclusions: This present study provided evidence that TBSA significantly suppressed LPS-induced neuroinflammation and the expression of p-p38. Results derived from our study might help reveal the effective targeting strategies of LPS-induced brain inflammation through inhibiting HDAC6.Yuanjian SongLi QinRongli YangFan YangNwobodo Alexander KenechukwuXiaofang ZhaoXiaoyan ZhouXiangru WenLei LiTaylor & Francis Grouparticlehistone deacetylase 6tubastatin ainflammationphosphorylated p38mapkTherapeutics. PharmacologyRM1-950ENPharmaceutical Biology, Vol 57, Iss 1, Pp 263-268 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	histone deacetylase 6 tubastatin a inflammation phosphorylated p38mapk Therapeutics. Pharmacology RM1-950
spellingShingle	histone deacetylase 6 tubastatin a inflammation phosphorylated p38mapk Therapeutics. Pharmacology RM1-950 Yuanjian Song Li Qin Rongli Yang Fan Yang Nwobodo Alexander Kenechukwu Xiaofang Zhao Xiaoyan Zhou Xiangru Wen Lei Li Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice
description	Context: Researchers in a variety of fields have extensively focused on histone deacetylase 6 (HDAC6) due to its aggravation of inflammatory reaction. However, relevant studies examining whether HDAC6 could exacerbate lipopolysaccharide (LPS)-induced inflammation are still lacking. Objective: We assessed the role of HDAC6 in LPS-induced brain inflammation and used the HDAC6-selective inhibitor Tubastatin A (TBSA) to investigate the potential mechanisms further. Materials and methods: Brain inflammation was induced in Kunming (KM) mice via intraperitoneal (I.P.), injection of Lipopolysaccharide (LPS) (1 mg/kg), the TBSA (0.5 mg/kg) was delivered via intraperitoneal. The phosphorylated p38 (p-p38) Mitogen-activated protein kinases (MAPK) and expression of typical inflammatory mediators, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in both the hippocampus and cortex, were examined by immunoblotting. Nissl staining was used to detect the neuronal damage in the hippocampus and the cortex. Results: About 1 mg/kg LPS via daily intraperitoneal (I.P.) injections for 12 days significantly increased p38 MAPK phosphorylation, TNF-α and IL-6 expression, and neuronal loss. However, 0.5 mg/kg TBSA (three days before LPS treatment) by I.P. injections for 15 days could reverse the above results. Conclusions: This present study provided evidence that TBSA significantly suppressed LPS-induced neuroinflammation and the expression of p-p38. Results derived from our study might help reveal the effective targeting strategies of LPS-induced brain inflammation through inhibiting HDAC6.
format	article
author	Yuanjian Song Li Qin Rongli Yang Fan Yang Nwobodo Alexander Kenechukwu Xiaofang Zhao Xiaoyan Zhou Xiangru Wen Lei Li
author_facet	Yuanjian Song Li Qin Rongli Yang Fan Yang Nwobodo Alexander Kenechukwu Xiaofang Zhao Xiaoyan Zhou Xiangru Wen Lei Li
author_sort	Yuanjian Song
title	Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice
title_short	Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice
title_full	Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice
title_fullStr	Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice
title_full_unstemmed	Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice
title_sort	inhibition of hdac6 alleviating lipopolysaccharide-induced p38mapk phosphorylation and neuroinflammation in mice
publisher	Taylor & Francis Group
publishDate	2019
url	https://doaj.org/article/f1709d849667425f8095138a7bb6b442
work_keys_str_mv	AT yuanjiansong inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT liqin inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT rongliyang inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT fanyang inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT nwobodoalexanderkenechukwu inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT xiaofangzhao inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT xiaoyanzhou inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT xiangruwen inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice AT leili inhibitionofhdac6alleviatinglipopolysaccharideinducedp38mapkphosphorylationandneuroinflammationinmice
_version_	1718425520293543936

Inhibition of HDAC6 alleviating lipopolysaccharide-induced p38MAPK phosphorylation and neuroinflammation in mice

Ejemplares similares