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L-F001, a multifunctional fasudil-lipoic acid dimer, antagonizes hypoxic-ischemic brain damage by inhibiting the TLR4/MyD88 signaling pathway.
Zhou, Ruiyu; Wu, Liqiang; Jin, Ni; Sha, Sha; Ouyang, Ying.
Afiliación
  • Zhou R; Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
  • Wu L; The Affiliated Kashi Hospital, Sun Yat-sen University, Kashi, China.
  • Jin N; Guangdong Provincial Emergency Hospital, Guangzhou, China.
  • Sha S; Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
  • Ouyang Y; Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Brain Behav ; 13(12): e3280, 2023 12.
Article en En | MEDLINE | ID: mdl-37822185
INTRODUCTION: Neonatal hypoxic-ischemic brain damage (HIBD) is a serious inflammatory injury. At present, the standard treatment for this disease is hypothermia therapy, and the effect of drug intervention is still limited. L-F001 is a compound of fasudil and lipoic acid. Previous in vitro experiments have confirmed that L-F001 has anti-inflammatory neuroprotective functions. However, its therapeutic effect on neonates with HIBD remains unknown. This study was aimed at exploring the therapeutic effect of L-F001 on HIBD rats. METHODS: The newborn rats were divided into three groups: Sham operation group, HIBD group, and HIBD + L-F001 group. HE staining, Nissil staining, the immunofluorescence of iNOS and COX-2, ELISA (IL-1ß, IL-6, TNF-α, and IL-10), and western blotting analyses were performed to determine the therapeutic effect of L-F001. Finally, we evaluated the growth and development of each group by measuring body weight. RESULTS: The hippocampal structure of HIBD rats was disordered, and the Nissil body was small and shallow. The expressions of iNOS and COX-2 in HIBD rats were increased, whereas the expressions of IL-1ß, IL-6, and TNF-α in plasma were upregulated, and the expression of IL-10 was decreased. L-F001 could improve the tissue structure and reduce the expression of iNOS and COX-2 in HIBD rats. Meanwhile, L-F001 could also reduce the expression of pro-inflammatory cytokines and restore the content of anti-inflammatory cytokines in plasma. We further found that the TLR4 pathway was activated after hypoxic-ischemia in neonatal rats. L-F001 could inhibit the activation of TLR4 pathway. Finally, we found that after L-F001 treatment, the body weight of HIBD rats increased significantly compared with the untreated group. CONCLUSIONS: L-F001 antagonizes the inflammatory response after hypoxic-ischemia by inhibiting the activation of the TLR4 signaling pathway, thus playing a neuroprotective role. L-F001 may be a potential therapeutic agent for neonatal HIBD.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Ácido Tióctico / Hipoxia-Isquemia Encefálica Límite: Animals Idioma: En Revista: Brain Behav Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Ácido Tióctico / Hipoxia-Isquemia Encefálica Límite: Animals Idioma: En Revista: Brain Behav Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos