Calycosin ameliorates spinal cord injury by targeting Hsp90 to inhibit oxidative stress and apoptosis of nerve cells

Li, Mingdong; Hasiqiqige,; Huan, Yanqiang; Wang, Xiaolei; Tao, Mingkai; Jiang, Tianqi; Xie, Hongbin; Jisiguleng, Wu; Wang, Xing; Zhu, Zhibo; Wang, Aitao; He, Yongxiong

doi:10.1016/j.jchemneu.2022.102190

Cited by 6 publications

(3 citation statements)

References 62 publications

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“…Mechanistically, MiR-495 downregulates the expression of STAT3, while MiR-122-5p represses CPEB1, targeting the PI3K/AKT signaling pathway ( 26 , 27 ). Another study on traditional Chinese medicine suggests that calycosin promotes the expression level of p-AKT by up-regulating heat shock protein 90 (HSP90), while inhibiting the expression levels of p-ASK1 (pThr845) and p-p38, thereby alleviating ROS, oxidative stress, and apoptosis in neurons ( 28 ). In contrast to what was mentioned above ( 26 ), the role of AKT phosphorylation in promoting or inhibiting ROS generation and apoptosis is still controversial.…”

Section: Ros In Apoptosismentioning

confidence: 99%

ROS: Executioner of regulating cell death in spinal cord injury

Yin,

Wan,

Gong

et al. 2024

Front. Immunol.

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The damage to the central nervous system and dysfunction of the body caused by spinal cord injury (SCI) are extremely severe. The pathological process of SCI is accompanied by inflammation and injury to nerve cells. Current evidence suggests that oxidative stress, resulting from an increase in the production of reactive oxygen species (ROS) and an imbalance in its clearance, plays a significant role in the secondary damage during SCI. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial regulatory molecule for cellular redox. This review summarizes recent advancements in the regulation of ROS-Nrf2 signaling and focuses on the interaction between ROS and the regulation of different modes of neuronal cell death after SCI, such as apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, we highlight the pathways through which materials science, including exosomes, hydrogels, and nanomaterials, can alleviate SCI by modulating ROS production and clearance. This review provides valuable insights and directions for reducing neuronal cell death and alleviating SCI through the regulation of ROS and oxidative stress.

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Section: Ros In Apoptosismentioning

confidence: 99%

ROS: Executioner of regulating cell death in spinal cord injury

Yin,

Wan,

Gong

et al. 2024

Front. Immunol.

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“…Many studies have reported that secondary injury is an important stage in the treatment of SCI. , Timely therapeutic intervention can inhibit the progression of secondary injury and have a significant impact on long-term neurological and functional recovery . The spinal cord microenvironment in the secondary injury phase produces large amounts of reactive oxygen species (ROS) (e.g., H 2 O 2 ). , The ROS cannot be metabolized in a timely manner and form accumulation, leading to local ischemia, hypoxia, and inflammatory cascade response . This further results in axonal degeneration, demyelination, and neuronal apoptosis. , Therefore, inhibiting the hyperaccumulation of ROS and alleviating the hypoxic environment are effective strategies in the treatment of SCI.…”

Section: Introductionmentioning

confidence: 99%

“…9,10 The ROS cannot be metabolized in a timely manner and form accumulation, leading to local ischemia, hypoxia, and inflammatory cascade response. 11 This further results in axonal degeneration, demyelination, and neuronal apoptosis. 12,13 Therefore, inhibiting the hyperaccumulation of ROS and alleviating the hypoxic environment are effective strategies in the treatment of SCI.…”

Section: Introductionmentioning

confidence: 99%

Macrophage Membrane-Coated MnO₂ Nanoparticles Provide Neuroprotection by Reducing Oxidative Stress after Spinal Cord Injury

An,

Jiang,

et al. 2023

ACS Appl. Nano Mater.

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Secondary injury following spinal cord injury (SCI) results in a large production of reactive oxygen species (ROS) (e.g., H 2 O 2 ) in the spinal cord microenvironment, which then leads to an excessive burst of inflammation and ultimately neuronal death. In this study, we prepared manganese dioxide (MnO 2 ) nanoparticles coated by macrophage membranes, named M@MnO 2 , to cope with early ROS bursts in the SCI microenvironment. The biosafety and targeting ability of the MnO 2 nanoparticles were improved through the macrophage membranes. Successful preparation of M@MnO 2 was verified by transmission electron microscopy, Western blot, and dynamic light scattering. Small animal imaging showed that M@MnO 2 accumulated in large quantities at the site of SCI. In the early stages of SCI, M@MnO 2 effectively reduced the ROS content, as well as the hypoxia-inducible factor 1α (HIF-1α) content, malondialdehyde content, and superoxide anion content caused by ROS, further leading to a decrease in some of the proteins associated with inflammation at the site of SCI (CD11b, CD86, COX2, IL-1β, and iNOS), ultimately achieving neuroprotection and recovery of motor function.

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Calycosin promotes axon growth by inhibiting PTPRS and alleviates spinal cord injury

Jiang,

Wang,

Wen

et al. 2024

J Mol Neurosci

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Calycosin ameliorates spinal cord injury by targeting Hsp90 to inhibit oxidative stress and apoptosis of nerve cells

Cited by 6 publications

References 62 publications

ROS: Executioner of regulating cell death in spinal cord injury

ROS: Executioner of regulating cell death in spinal cord injury

Macrophage Membrane-Coated MnO₂ Nanoparticles Provide Neuroprotection by Reducing Oxidative Stress after Spinal Cord Injury

Calycosin promotes axon growth by inhibiting PTPRS and alleviates spinal cord injury

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Calycosin ameliorates spinal cord injury by targeting Hsp90 to inhibit oxidative stress and apoptosis of nerve cells

Cited by 6 publications

References 62 publications

ROS: Executioner of regulating cell death in spinal cord injury

ROS: Executioner of regulating cell death in spinal cord injury

Macrophage Membrane-Coated MnO2 Nanoparticles Provide Neuroprotection by Reducing Oxidative Stress after Spinal Cord Injury

Calycosin promotes axon growth by inhibiting PTPRS and alleviates spinal cord injury

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Macrophage Membrane-Coated MnO₂ Nanoparticles Provide Neuroprotection by Reducing Oxidative Stress after Spinal Cord Injury