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来自琼斯的富含环烯醚萜的组分通过激活PI3K/Akt信号通路促进脊髓损伤后的轴突再生和运动功能恢复。

Iridoids rich fraction from Jones promotes axonal regeneration and motor functional recovery after spinal cord injury through activation of the PI3K/Akt signaling pathway.

作者信息

Wang Yunyun, Lu Jiachun, Xiao Hua, Ding Lijuan, He Yongzhi, Chang Cong, Wang Wenchun

机构信息

Department of Rehabilitation Medicine, The General Hospital of Western Theater Command, Affiliated Hospital of Southwest Jiaotong University, Chengdu, Sichuan, China.

Chengdu Eighth People's Hospital (Geriatric Hospital of Chengdu Medical College), Chengdu, Sichuan, China.

出版信息

Front Mol Neurosci. 2024 May 2;17:1400927. doi: 10.3389/fnmol.2024.1400927. eCollection 2024.

DOI:10.3389/fnmol.2024.1400927
PMID:38756705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11097773/
Abstract

Jones (VJJ), renowned for its extensive history in traditional Chinese medicine and ethnomedicine within China, is prevalently utilized to alleviate ailments such as epigastric distension and pain, gastrointestinal disturbances including food accumulation, diarrhea, and dysentery, as well as insomnia and other diseases. Moreover, the Iridoid-rich fraction derived from Jones (IRFV) has demonstrated efficacy in facilitating the recuperation of motor functions after spinal cord injury (SCI). This study is aimed to investigate the therapeutic effect of IRFV on SCI and its underlying mechanism. Initially, a rat model of SCI was developed to assess the impact of IRFV on axonal regeneration. Subsequently, employing the PC12 cell model of oxidative damage, the role and mechanism of IRFV in enhancing axonal regeneration were explored using the phosphoinositide-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway inhibitor LY294002. Ultimately, the same inhibitor was administered to SCI rats to confirm the molecular mechanism through which IRFV promotes axonal regeneration by activating the PI3K/Akt signaling pathway. The results showed that IRFV significantly enhanced motor function recovery, reduced pathological injury, and facilitated axonal regeneration in SCI rats. experiments revealed that IRFV improved PC12 cell viability, augmented axonal regeneration, and activated the PI3K/Akt signaling pathway. Notably, the inhibition of this pathway negated the therapeutic benefits of IRFV in SCI rats. In conclusion, IRFV promote promotes axonal regeneration and recovery of motor function after SCI through activation of the PI3K/Akt signaling pathway.

摘要

在中国,Jones(VJJ)以其在传统中医和民族医学方面的悠久历史而闻名,常用于缓解诸如胃脘胀满疼痛、包括食积、腹泻和痢疾在内的胃肠道紊乱,以及失眠等疾病。此外,从Jones中提取的富含环烯醚萜的部分(IRFV)已证明在促进脊髓损伤(SCI)后运动功能恢复方面具有功效。本研究旨在探讨IRFV对SCI的治疗作用及其潜在机制。首先,建立SCI大鼠模型以评估IRFV对轴突再生的影响。随后,利用氧化损伤的PC12细胞模型,使用磷酸肌醇-3-激酶(PI3K)/蛋白激酶B(Akt)信号通路抑制剂LY294002探索IRFV在增强轴突再生中的作用和机制。最终,将相同的抑制剂给予SCI大鼠,以确认IRFV通过激活PI3K/Akt信号通路促进轴突再生的分子机制。结果表明,IRFV显著增强了SCI大鼠的运动功能恢复,减轻了病理损伤,并促进了轴突再生。实验表明,IRFV提高了PC12细胞活力,增强了轴突再生,并激活了PI3K/Akt信号通路。值得注意的是,该信号通路的抑制消除了IRFV对SCI大鼠的治疗益处。总之,IRFV通过激活PI3K/Akt信号通路促进SCI后轴突再生和运动功能恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/544c53d7bb7e/fnmol-17-1400927-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/a8c4a06aac34/fnmol-17-1400927-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/f25197b99372/fnmol-17-1400927-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/d53051353abd/fnmol-17-1400927-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/98a48992b228/fnmol-17-1400927-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/107bfffc7e23/fnmol-17-1400927-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/544c53d7bb7e/fnmol-17-1400927-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/a8c4a06aac34/fnmol-17-1400927-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/f25197b99372/fnmol-17-1400927-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/d53051353abd/fnmol-17-1400927-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/98a48992b228/fnmol-17-1400927-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/107bfffc7e23/fnmol-17-1400927-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1037/11097773/544c53d7bb7e/fnmol-17-1400927-g006.jpg

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11-Ethoxyviburtinal improves chronic restraint stress-induced anxiety-like behaviors in gender-specific mice via PI3K/Akt and E /ERβ signaling pathways.
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