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Lonicerin alleviates intestinal myenteric neuron injury induced by hypoxia/reoxygenation treated macrophages by downregulating EZH2.
Yao, Zhiguang; Liang, Yuan; Pan, Chunyan; Zeng, Kun; Qu, Zhibo.
Afiliación
  • Yao Z; Department of Surgical District 2, Eighth People's Hospital of Dongguan City, Dongguan, China.
  • Liang Y; Department of Pediatrics, Eighth People's Hospital of Dongguan City, Dongguan, China.
  • Pan C; Department of Health Management, Eighth People's Hospital of Dongguan City, Dongguan, China.
  • Zeng K; Department of Science and Education, Eighth People's Hospital of Dongguan City, Dongguan, China.
  • Qu Z; Department of Surgical District 2, Eighth People's Hospital of Dongguan City, Dongguan, China.
J Biochem Mol Toxicol ; 38(9): e23810, 2024 Sep.
Article en En | MEDLINE | ID: mdl-39163614
ABSTRACT
Intestinal ischemia-reperfusion (IR) injury is a common gastrointestinal disease that induces severe intestinal dysfunction. Intestinal myenteric neurons participate in maintaining the intestinal function, which will be severely injured by IR. Macrophages are widely reported to be involved in the pathogenesis of organ IR injury, including intestine, which is activated by NLRP3 signaling. Lonicerin (LCR) is a natural extracted monomer with inhibitory efficacy against the NLRP3 pathway in macrophages. The present study aims to explore the potential protective function of LCR in intestinal IR injury. Myenteric neurons were extracted from mice. RAW 264.7 cells were stimulated by H/R with or without 10 µM and 30 µM LCR. Remarkable increased release of IL-6, MCP-1, and TNF-α were observed in H/R treated RAW 264.7 cells, along with an upregulation of NLRP3, cleaved-caspase-1, IL-1ß, and EZH2, which were sharply repressed by LCR. Myenteric neurons were cultured with the supernatant collected from each group. Markedly decreased neuron number and shortened length of neuron axon were observed in the H/R group, which were signally reversed by LCR. RAW 264.7 cells were stimulated by H/R, followed by incubated with 30 µM LCR with or without pcDNA3.1-EZH2. The inhibition of LCR on NLRP3 signaling in H/R treated RAW 264.7 cells was abolished by EZH2 overexpression. Furthermore, the impact of LCR on neuron number and neuron axon length in myenteric neurons in the H/R group was abated by EZH2 overexpression. Collectively, LCR alleviated intestinal myenteric neuron injury induced by H/R treated macrophages via downregulating EZH2.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Regulación hacia Abajo / Proteína Potenciadora del Homólogo Zeste 2 / Macrófagos / Neuronas Límite: Animals Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Regulación hacia Abajo / Proteína Potenciadora del Homólogo Zeste 2 / Macrófagos / Neuronas Límite: Animals Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos