Betulin ameliorates neuronal apoptosis and oxidative injury via DJ-1/Akt/Nrf2 signaling pathway after subarachnoid hemorrhage.
Xiaoyang LuShu YangQixiong LuYuansheng ZhangZaihong ChaWei HuangTao LiPublished in: CNS neuroscience & therapeutics (2024)
Betulin which was a potent agonist of DJ-1 had the ability to induce its expression in brain tissue. DJ-1 had neuroprotective effect on EBI through comprehensive mechanisms, including facilitating intrinsic and extrinsic antiapoptotic pathway, and reducing oxidative injury by upregulating the expression of redox proteins. Betulin as an inexpensive drug showed the potential for SAH treatment.
Keyphrases
- cerebral ischemia
- subarachnoid hemorrhage
- signaling pathway
- poor prognosis
- brain injury
- oxidative stress
- blood brain barrier
- pi k akt
- endoplasmic reticulum stress
- cell proliferation
- binding protein
- epithelial mesenchymal transition
- long non coding rna
- cell death
- white matter
- cell cycle arrest
- induced apoptosis
- emergency department
- mouse model
- multiple sclerosis
- risk assessment
- replacement therapy
- human health