Maltol Promotes Mitophagy and Inhibits Oxidative Stress via the Nrf2/PINK1/Parkin Pathway after Spinal Cord Injury.
Yuqin MaoJiqing DuXianghang ChenAbdullah Al MamunLin CaoYanhong YangJoana MubwandarikwaMuhammad ZaeemWanying ZhangYan ChenYusen DaiZhou-Guang WangKeyong YePublished in: Oxidative medicine and cellular longevity (2022)
Spinal cord injury (SCI), a fatal disease in the central nervous system, is characteristic of weak neuronal regeneration ability and complex pathological progress. Activation of oxidative stress (OS) and apoptosis-mediated cell death significantly contributes to the progression of SCI. Current evidence suggests that maltol exerts natural antioxidative properties via obstructing OS and apoptosis. However, the significant effect of maltol on SCI treatment has never been evaluated yet. In our current study, we explored maltol administration that could trigger the expression of Nrf2 and promote the retranslocation of Nrf2 from the cytosol to the nucleus, which can subsequently obstruct OS signal and apoptosis-mediated neuronal cell death after SCI. Furthermore, we found that maltol treatment enhances PINK1/Parkin-mediated mitophagy in PC12 cells, facilitating the recovery of mitochondrial functions. Our findings propose that maltol could be a promising therapeutic candidate for the treatment and management of SCI.
Keyphrases
- oxidative stress
- spinal cord injury
- cell death
- cell cycle arrest
- diabetic rats
- dna damage
- induced apoptosis
- ischemia reperfusion injury
- endoplasmic reticulum stress
- spinal cord
- neuropathic pain
- cell proliferation
- blood brain barrier
- long non coding rna
- nlrp inflammasome
- signaling pathway
- brain injury
- cerebrospinal fluid