Area of research
Complementary and alternative medicine · Neurology
Research interest
Research topics from publications: Edaravone Attenuates Aβ 1-42-Induced Inflammatory Damage and Ferroptosis in HT22 Cells; Mfn2-Mediated Preservation of Mitochondrial Function Contributes to the Protective Effects of BHAPI in Response to Ischemia; Ape1 protects against MPP+-induced neurotoxicity through ERK1/2 signaling in PC12 cells; Che-1 inhibits oxygen–glucose deprivation/reoxygenation-induced neuronal apoptosis associated with inhibition of the p53-mediated proapoptotic signaling pathway; IGFBP5 Promotes Neuronal Apoptosis in a 6-OHDA-Toxicant Model of Parkinson’s Disease by Inhibiting the Sonic Hedgehog Signaling Pathway; Sinigrin improves cerebral ischaemia‐reperfusion injury by inhibiting the TLR4 pathway‐mediated oxidative stress. Representative work: Oxidative stress, induced by reactive oxygen species (ROS), is an apoptosis activator. Oxidative stress causes dopaminergic neuron loss and plays a pivotal role in the pathogenesis of Parkinson's disease (PD). A recent study showed that apurinic/apyrimidinic endonuclease 1 (Ape1) decreases cytotoxicity and promotes neuron survival under oxidative stress. Furthermore, it has been proven that Ape1 is involved in the pathogenesis of PD. However, little is known about the contribution of Ape1 toward the development of PD. Thus, the present study was designed to define a critical pathway by which Ape1 mediates neurotoxicity in a model of PD. The results show that Ape1 was upregulated in MPP-treat Accumulating evidence suggests that Che-1 is a strong antiapoptotic protein and can protect cells against various insults. However, whether Che-1 is involved in the protection of neurons against cerebral ischemia/reperfusion injury remains unclear. In this study, we aimed to investigate the potential role of Che-1 in regulating cerebral ischemia/reperfusion injury-induced neuronal injury using the oxygen–glucose deprivation and reoxygenation (OGD/R) model in vitro. We found that Che-1 expression was induced in neurons following OGD/R treatment. Functional experiments showed that Che-1 knockdown aggravated OGD/R-induced neuronal apoptosis. In contrast, Che-1 overexpression exerted a protectiv
IGFBP5 Promotes Neuronal Apoptosis in a 6-OHDA-Toxicant Model of Parkinson’s Disease by Inhibiting the Sonic Hedgehog Signaling Pathway
Sinigrin improves cerebral ischaemia‐reperfusion injury by inhibiting the <scp>TLR4</scp> pathway‐mediated oxidative stress
Edaravone Attenuates Aβ 1-42-Induced Inflammatory Damage and Ferroptosis in HT22 Cells
Che-1 inhibits oxygen–glucose deprivation/reoxygenation-induced neuronal apoptosis associated with inhibition of the p53-mediated proapoptotic signaling pathway
Mfn2-Mediated Preservation of Mitochondrial Function Contributes to the Protective Effects of BHAPI in Response to Ischemia
Ape1 protects against MPP+-induced neurotoxicity through ERK1/2 signaling in PC12 cells