Icariin Inhibits Endoplasmic Reticulum Stress-induced Neuronal Apoptosis after Spinal Cord Injury through Modulating the PI3K/AKT Signaling Pathway

Int. J. Biol. Sci., 2019 · DOI: 10.7150/ijbs.30348 · Published: January 1, 2019

Simple Explanation

Spinal cord injury (SCI) can lead to neuronal apoptosis, a process where nerve cells die due to stress in the endoplasmic reticulum (ER). This study explores how icariin (ICA), a natural compound, might protect against this damage. The researchers used a mouse model of SCI and treated some mice with ICA. They also conducted experiments on cultured cells to understand how ICA affects ER stress and cell survival. The findings suggest that ICA can reduce ER stress and promote nerve cell survival after SCI by influencing a specific signaling pathway called PI3K/AKT.

Study Duration

8 weeks

Participants

Adult C57BL/6 male mice

Evidence Level

Not specified

Key Findings

1
ICA administration significantly enhanced motor recovery and protected spinal cord tissues against infraction and hemorrhage post injury.
2
ICA significantly inhibited the expression of ER stress apoptotic proteins caspase-12, CHOP, Bax/Bcl-2, caspase-9 and caspase-3.
3
The neuroprotective effect of ICA on motor recovery and neuronal survival was related to attenuating ER stress via PI3K/AKT signaling pathway after SCI.

Research Summary

This study investigates the neuroprotective effects of icariin (ICA) on spinal cord injury (SCI) by attenuating endoplasmic reticulum (ER) stress through the PI3K/AKT signaling pathway. The results demonstrate that ICA administration enhances motor recovery, protects spinal cord tissues, and reduces the expression of ER stress markers and apoptotic proteins in a mouse model of SCI. In vitro experiments further confirm that ICA inhibits neuronal apoptosis induced by ER stress, and this effect is associated with the PI3K/AKT pathway, suggesting a potential therapeutic strategy for SCI.

Practical Implications

Therapeutic Potential

Targeting ER stress with compounds like ICA may offer a promising approach for treating CNS injuries.

Signaling Pathway Modulation

Modulating the PI3K/AKT pathway could be crucial for neuroprotection in SCI.

Drug Development

ICA or its derivatives could be further explored as potential therapeutic agents for SCI.

Study Limitations

1
Additional potential mechanisms due to the relationships between ER and other organelles or signaling pathways.
2
The analysis of difference in temporal and specific cellular activation in ER stress remains unclear.
3
the precise mechanisms associated with apoptosis and ER stress may be cell specific in SCI

Your Feedback

Was this summary helpful?

Back to Spinal Cord Injury