自噬
体内
PI3K/AKT/mTOR通路
体外
汤剂
药理学
疾病
医学
化学
细胞凋亡
神经科学
生物
信号转导
细胞生物学
传统医学
内科学
生物化学
遗传学
作者
Xiaojing Chen,Q. Tian,Min Gao,Xibin Zhou,Chunxiang Zhou
标识
DOI:10.3389/fnagi.2025.1478199
摘要
Introduction Lingguizhugan decoction (LGZG) has been reported to treat Alzheimer’s disease (AD) by anti-inflammatory and transporting amyloid-β (Aβ). Methods Using APP/PS1 transgenic mice as in vivo model and gave LGZG decoction by oral gavage. Using Aβ 25-35 -induced SH-SY5Y cells as in vitro model and then added LGZG medicated serum (LMS) to observe the regulatory effect of LGZG on AD autophagy-related pathways. Morris water maze (MWM) was used to evaluate the mice’s learning and memory ability. Mice’s hippocampus tissue sections were stained immunohistochemically to observe hippocampal Aβ deposition. Transmission electron microscopy monitored autophagosomes and autolysosomes. Western blot analysis measured protein expression levels of beclin-1, p62 and light chain 3II (LC3 II) and mTOR signaling. Results: LGZG could greatly improve learning and memory ability of APP/PS1 mice, and enhance autophagy in vitro and in vivo . LGZG increased the levels of beclin-1 and LC3 II and decreased the levels of p62. Conclusion LGZG enhanced autophagy and showed therapeutic potential in AD by inhibiting mTOR/p70s6K signaling.
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