| First Author | Zhou L | Year | 2020 |
| Journal | Neurosci Lett | Volume | 729 |
| Pages | 135007 | PubMed ID | 32371156 |
| Mgi Jnum | J:289393 | Mgi Id | MGI:6432588 |
| Doi | 10.1016/j.neulet.2020.135007 | Citation | Zhou L, et al. (2020) Compound K induces neurogenesis of neural stem cells in thrombin induced nerve injury through LXRalpha signaling in mice. Neurosci Lett 729:135007 |
| abstractText | Intracerebral hemorrhage (ICH) causes neurological function deficit due to the loss of neurons surrounding the hematoma. Increased neurogenesis of endogenous neural stem cells (EnNSCs) is believed to increase cell proliferation and differentiation, thereby improving the neurological deficit. However, there are still limited drugs that are effective for treating neurological deficit. So, the effects of compound K (CK) in EnNSCs were measured after thrombin-induced mice models both in vivo and in vitro, and investigated the probable mechanisms of CK during pro-neurogenesis. The results revealed that 10 muM CK promotes neurogenesis, proliferation and reduces apoptosis of EnNSCs after induction by thrombin. After that, CK treatment increased the neurogenesis of EnNSCs through liver X receptor alpha (LXRalpha) signaling pathway using adeno-associated virus knockdown and knocked out mice of LXRalpha gene. Finally, intraperitoneal injection of 10 mg/kg CK improved the neurogenesis of subventricular zone (SVZ), myelin repair and behavioral deficit after stereotaxic injection of thrombin in the basal ganglia of mice, and this process involved LXRalpha. These observations provided evidence regarding the effect of CK in pro-neurogenesis via LXRalpha activation, and suggested further evaluation of it due to its potential role as an effective modulator in the treatment of ICH. |
