Apelin-13/APJ system attenuates early brain injury via suppression of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation and oxidative stress in a AMPK-dependent manner after subarachnoid hemorrhage in rats.
Weilin XuTao LiLiansheng GaoJingwei ZhengJun YanJianmin ZhangAnwen ShaoPublished in: Journal of neuroinflammation (2019)
Exogenous apelin-13 binding to APJ attenuates early brain injury by reducing ER stress-mediated oxidative stress and neuroinflammation, which is at least partly mediated by the AMPK/TXNIP/NLRP3 signaling pathway.
Keyphrases
- nlrp inflammasome
- brain injury
- subarachnoid hemorrhage
- cerebral ischemia
- endoplasmic reticulum stress
- induced apoptosis
- oxidative stress
- signaling pathway
- skeletal muscle
- dna damage
- ischemia reperfusion injury
- multiple sclerosis
- epithelial mesenchymal transition
- diabetic rats
- white matter
- resting state
- protein kinase
- inflammatory response