Scholarlink

<p>Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social interaction and repetitive behaviors, with increasing evidence implicating immune dysregulation, oxidative stress, and altered transcriptional regulation. This study investigated the pharmacological effects of Rannasangpei (RNSP), a classical Tibetan formulation, and its active constituent crocin-1 in a valproic acid (VPA)-induced mouse model of ASD. Behavioral tests demonstrated that RNSP and crocin-1 markedly reduced VPA-induced repetitive behaviors and improved social interaction. Biochemical analyses revealed that these effects were associated with restoration of redox balance, characterized by increased activities of catalase and superoxide dismutase and decreased levels of malondialdehyde, together with improvement of the GSH/GSSG ratio. Both treatments also attenuated neuroinflammation, as indicated by reduced expression of IL-6, IL-17A, TNF-α, and Lepr, together with recovery of IL-10 in the prefrontal cortex and cerebellum. Transcriptomic profiling further revealed that RNSP and crocin-1 were associated with widespread transcriptional reorganization in the prefrontal cortex (PFC) and cerebellum. In the PFC, these changes involved pathways related to cell-cell adhesion, morphogenesis, and MAPK signaling. In the cerebellum, the dominant enrichment pattern centered on membrane trafficking and cytoskeleton-related processes, with additional enrichment of oxidative stress response pathways. Integration of pathway analysis and representative gene changes indicated region-specific but functionally related alterations in programs linked to intracellular transport, neuronal structure, and synaptic function. Safety evaluation further showed that neither RNSP nor crocin-1 produced obvious systemic toxicity under the present experimental conditions, as indicated by no consistent treatment-related abnormalities in serum biochemical parameters and histological features of major peripheral organs. These findings indicate that RNSP and crocin-1 were associated with changes in oxidative stress, neuroinflammation, and transcriptional regulation across multiple brain regions, supporting their potential therapeutic relevance in ASD.</p><p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Rannasangpei and its constituent crocin-1 ameliorate valproic acid–induced autism-like behaviors accompanied by reduced oxidative stress and neuroinflammation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月18日

查看全文
  • Rui Qiu,
  • Liguo Li,
  • Tongtong Yao,
  • Quan Tang,
  • Lei Chen,
  • Qiang Fu,
  • Jingkun Yu,
  • Linyu Jiang,
  • Yinqi Xue,
  • Xiaoya Yu,
  • Yong Cheng,
  • Hui Zhou

摘要

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social interaction and repetitive behaviors, with increasing evidence implicating immune dysregulation, oxidative stress, and altered transcriptional regulation. This study investigated the pharmacological effects of Rannasangpei (RNSP), a classical Tibetan formulation, and its active constituent crocin-1 in a valproic acid (VPA)-induced mouse model of ASD. Behavioral tests demonstrated that RNSP and crocin-1 markedly reduced VPA-induced repetitive behaviors and improved social interaction. Biochemical analyses revealed that these effects were associated with restoration of redox balance, characterized by increased activities of catalase and superoxide dismutase and decreased levels of malondialdehyde, together with improvement of the GSH/GSSG ratio. Both treatments also attenuated neuroinflammation, as indicated by reduced expression of IL-6, IL-17A, TNF-α, and Lepr, together with recovery of IL-10 in the prefrontal cortex and cerebellum. Transcriptomic profiling further revealed that RNSP and crocin-1 were associated with widespread transcriptional reorganization in the prefrontal cortex (PFC) and cerebellum. In the PFC, these changes involved pathways related to cell-cell adhesion, morphogenesis, and MAPK signaling. In the cerebellum, the dominant enrichment pattern centered on membrane trafficking and cytoskeleton-related processes, with additional enrichment of oxidative stress response pathways. Integration of pathway analysis and representative gene changes indicated region-specific but functionally related alterations in programs linked to intracellular transport, neuronal structure, and synaptic function. Safety evaluation further showed that neither RNSP nor crocin-1 produced obvious systemic toxicity under the present experimental conditions, as indicated by no consistent treatment-related abnormalities in serum biochemical parameters and histological features of major peripheral organs. These findings indicate that RNSP and crocin-1 were associated with changes in oxidative stress, neuroinflammation, and transcriptional regulation across multiple brain regions, supporting their potential therapeutic relevance in ASD.