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Mangiferin regulates interleukin-6 and cystathionine-b-synthase in lipopolysaccharide-induced brain injury.
Fu, Yan-Yan; Zhang, Fang; Zhang, Lei; Liu, Hong-Zhi; Zhao, Zi-Ming; Wen, Xiang-Ru; Wu, Jian; Qi, Da-Shi; Sun, Ying; Du, Yang; Dong, Hong-Yan; Liu, Yong-Hai; Song, Yuan-Jian.
Afiliación
  • Fu YY; Research Center for Neurobiology, Department of Neurobiology, Xuzhou Medical College, 209 Tongshan Road, Xuzhou, Jiangsu, 221004, People's Republic of China.
Cell Mol Neurobiol ; 34(5): 651-7, 2014 Jul.
Article en En | MEDLINE | ID: mdl-24794713
ABSTRACT
Mangiferin has been extensively applied in different fields due to its anti-inflammatory properties. However, the precise mechanism used by mangiferin on lipopolysaccharide (LPS)-induced inflammation has not been elucidated. Here, we discuss the potential mechanism of mangiferin during a LPS-induced brain injury. Brain injury was induced in ICR mice via intraperitoneal LPS injection (5 mg/kg). Open- and closed-field tests were used to detect the behaviors of mice, while immunoblotting was performed to measure the expression of interleukin-6 (IL-6) and cystathionine-b-synthase (CBS) in the hippocampus after mangiferin was orally administered (p.o.). Mangiferin relieved LPS-induced sickness 6 and 24 h after LPS injection; in addition, this compound suppressed LPS-induced IL-6 production after 24 h of LPS induction as well as the downregulation of LPS-induced CBS expression after 6 and 24 h of LPS treatment in the hippocampus. Therefore, mangiferin attenuated sickness behavior by regulating the expression of IL-6 and CBS.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Lesiones Encefálicas / Lipopolisacáridos / Interleucina-6 / Cistationina betasintasa / Xantonas Límite: Animals Idioma: En Revista: Cell Mol Neurobiol Año: 2014 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Lesiones Encefálicas / Lipopolisacáridos / Interleucina-6 / Cistationina betasintasa / Xantonas Límite: Animals Idioma: En Revista: Cell Mol Neurobiol Año: 2014 Tipo del documento: Article