Theaflavin attenuates cerebral ischemia/reperfusion injury by abolishing miRNA ‑128‑3p‑mediated Nrf2 inhibition and reducing oxidative stress.

Theaflavin attenuates cerebral ischemia/reperfusion injury by abolishing miRNA‑128‑3p‑mediated Nrf2 inhibition and reducing oxidative stress. Mol Med Rep. 2019 Oct 17;: Authors: Li R, Li X, Wu H, Yang Z, Fei L, Zhu J Abstract Theaflavin has been proven to own strong antioxidative capacity; however, the molecular mechanism underlying its protective effect against cerebral ischemia‑reperfusion (I/R) injury remains unclear. Therefore, the present study was designed to elucidate the neuroprotective effects of theaflavin on cerebral I/R injury and its underlying molecular mechanisms. To investigate the effects of theaflavin on neurological function, neurogenesis, and oxidative stress, experiments were performed using a cerebral I/R injury rat model, and neural stem cells (NSCs) were subjected to oxygen‑glucose deprivation and reoxygenation (OGD/R). Further, the expression profiles of miRNA‑128‑3p and the regulatory function of nuclear factor (erythroid‑derived 2)‑related factor 2 (Nrf2) were evaluated in these models. We found that theaflavin treatment significantly reduced infarct volume and neuronal injury, and thus improved the impaired memory and learning ability. Furthermore, theaflavin treatment significantly enhanced the increase in NSC proliferation, reduction in the apoptotic rate and inhibition of oxidative stress. Mechanistically, theaflavin targeted miRNA‑128‑3p and further activated the Nrf2 pathway to r...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research