Transient receptor potential vanilloid-1 antagonist AMG517 playing a neuroprotective role in cerebral ischemia / reperfusion injury in mice by regulating the release of inflammatory factors
10.16098/j.issn.0529-1356.2020.02.003
- Author:
Zhi-Feng PENG
1
;
Ying LIU
1
;
Chun-Hong NIU
2
Author Information
1. Department of Physiology, Medical College of Shanxi Datong University
2. Department of Pathophysiology, Medical College of Shanxi Datong University
- Publication Type:Journal Article
- Keywords:
AMG517;
Enzyme inked immunosorbent assay;
Ischemia/ reperfusion injury;
Mouse;
Neurobehavioral score;
Real-time PCR;
Transient receptor potential vanilloid-1
- From:
Acta Anatomica Sinica
2020;51(2):167-171
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of transient receptor potential vanilloid-1 (TRPV1) antagonist AMG517 on cerebral ischemic / reperfusion injury in mice. Methods Forty male C57BL / 6 mice were assigned to the following groups: sham group, vehicle + ischemia / reperfusion group (vehicle), capsaicin + ischemia / reperfusion group (capsaicin), and AMG517 + ischemia / reperfusion group (AMG517) . Ischemic / reperfusion injury was induced by permanent middle cerebral artery occlusion(MCAO) and neurological deficits were evaluated 72 hours after MCAO. Then, infarct volume, brain edema, mRNA expression of TRPV1 and serum concentrations of tumor necrosis factor α(TNF-α) and interleukin-10 (IL-10) were measured. Results Compared with the vehicle group, AMG517 significantly decreased the infarct volume (P < 0. 01) . Neurobehavioral score significantly decreased following administration of AMG517 (P < 0. 01) 72 hours after MCAO. Compared with the sham group, the mRNA expression of TRPV1 significantly increased in vehicle group (P < 0. 01) . AMG517 significantly increased the anti-inflammatory cytokine IL-10 and decreased the inflammatory cytokine TNF-α (P<0. 05) . Conclusion AMG517 can improve ischemia / reperfusion injury in mice and may play a neuroprotective effect by alleviating inflammation.
