Tectorigenin, an isoflavone aglycone from the rhizome of Belamcanda chinensis, induces neuronal expression of erythropoietin via accumulation of hypoxia-inducible factor-1α.
Etta Y LiuZoey X ZhengBrody Z ZhengYingjie XiaMaggie S GuoTina T DongKarl Wah-Keung TsimPublished in: Phytotherapy research : PTR (2019)
Traditional Chinese medicines (TCMs) have been demonstrated as an important source for potential drug discovery. Flavonoids are regarded as the most common active components in TCMs because of their beneficial functions in the brain and erythropoietic system. Erythropoietin (EPO), a glycoprotein hormone, has been well-studied for its neuroprotective function. The blood circulating EPO is not able to cross the blood brain barrier, and thus there is mounting demand to search for compounds that can induce endogenous cerebral EPO. Here, tectorigenin, an active compound in the rhizome of Belamcanda chinensis (L.) DC., significantly induced the expression of EPO mRNA via accumulation of hypoxia-inducible factor (HIF)-1α in cultured neuron-like NT2/D1 cells and rat cortical neurons. Furthermore, tectorigenin induced transcription of HIF-1α and reduced degradation of HIF-1α-OH, a hydroxylated form of HIF-1α, in the culture. Thus, the upregulation of HIF-1α was assumed to play a significant role in regulating EPO during the treatment of tectorigenin in cultured neurons. Hence, we reported the neuroprotective function of tectorigenin through upregulation of EPO in neurons, which could be a good candidate in developing drugs or food supplements for the treatment of brain disorders.
Keyphrases
- smoking cessation
- endothelial cells
- poor prognosis
- cerebral ischemia
- high glucose
- drug discovery
- spinal cord
- cell proliferation
- diabetic rats
- white matter
- long non coding rna
- subarachnoid hemorrhage
- induced apoptosis
- binding protein
- resting state
- drug induced
- signaling pathway
- oxidative stress
- blood brain barrier
- dendritic cells
- risk assessment
- brain injury
- functional connectivity
- cell death
- multiple sclerosis
- immune response
- cell cycle arrest
- stress induced