Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that the ischemic injury of brain leads to the injury of brain cells, and ischemic injury is further aggravated after the recovery of blood reperfusion. In this study, we first constructed Oxygen and glucose deprivation/reoxygenation
(OGD/R) injury model of PC12 cells, we found that the expression of LncRNA AK139328 in model cells was significantly increased through RT-qPCR. Subsequently, we interfered LncRNA AK139328 in model cells by plasmid transfection and found that interfering LncRNA AK139328 could significantly
reduce the expression of inflammatory factors, including TNF a, IL-1β, IL-6, McP-1, and oxidative stress-related factors, including ROS, MDA, LDH, while the expressions of SOD and GSHPx were significantly increased. Flow cytometry was used to detect cell apoptosis, and apoptosisrelated
proteins bcl-2, Bax, cleaved-caspase3 and cleaved PARP-1 were detected by western blot. Results show that interfering LncRNA AK139328 could reduce the apoptosis rate of OGD/R cells and the expression of Bax, cleaved caspase3 and cleaved PARP-1, while increasing the expression of bcl-2. Meanwhile,
we found that after interfering LncRNA AK139328, the expressions of Nrf2, HO-1, NQO-1 and phosphorylated-P65 increased, while P65 showed no significant changes. This may be related to Nrf2/HO-1 and NF-κB signaling pathways. In a word, our study showed that interfering with LncRNA
AK139328 can reduce cell inflammation and apoptosis in CIRI.
Protective Effects of Chlorogenic Acid on Cerebral Ischemia/Reperfusion Injury Rats by Regulating Oxidative Stress-Related Nrf2 Pathway
