Chun-Yan Li1, Wei Ma2, Kuang-Pin Liu3, Jin-Wei Yang4, Xian-Bin Wang5, Zhen Wu6, Tong Zhang7, Jia-Wei Wang8, Wei Liu9, Jie Liu10, Yu Liang11, Xing-Kui Zhang12, Jun-Jun Li13, Jian-Hui Guo14, Li-Yan Li15. 1. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 578010447@qq.com. 2. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 343897745@qq.com. 3. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 924948924@qq.com. 4. Second Department of General Surgery, First People's Hospital of Yunnan Province, Yunnan, Kunming 650032, China. Electronic address: caohede@163.com. 5. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 1115489960@qq.com. 6. Second Department of General Surgery, First People's Hospital of Yunnan Province, Yunnan, Kunming 650032, China. Electronic address: 1169541576@qq.com. 7. Second Department of General Surgery, First People's Hospital of Yunnan Province, Yunnan, Kunming 650032, China. Electronic address: 295328958@qq.com. 8. Second Department of General Surgery, First People's Hospital of Yunnan Province, Yunnan, Kunming 650032, China. Electronic address: 1289317457@qq.com. 9. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 1326170352@qq.com. 10. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 3030850652@qq.com. 11. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 2272200492@qq.com. 12. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 344744824@qq.com. 13. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: 58739749@qq.com. 14. Second Department of General Surgery, First People's Hospital of Yunnan Province, Yunnan, Kunming 650032, China. Electronic address: guojianhuikm@163.com. 15. Institute of Neuroscience, Kunming Medical University, Yunnan, Kunming, 650500, China. Electronic address: kmliyanl@163.com.
Abstract
BACKGROUND: Many studies have confirmed that "in situ ischemia postconditioning" (ISPostC) and "remote ischemic postconditioning" (RIPostC) can reduce cerebral ischemia/reperfusion injury, but there is no comparison was made on the consistency of neuroprotection in ISPostC and RIPostC to different ischemic duration and number of cycles. NEW METHOD: We used a transient middle cerebral artery occlusion model to compare the neuroprotection of ISPostC and RIPostC. We conducted ISPostC and RIPostC via brief and repeated MCA and Femoral artery occlusion followed by different ischemic duration and number of cycles. Infarct volume, brain edema, Neurological deficit scores and Apoptosis were evaluated. RESULTS: First, the ISPostC with three cycles of 10-s occlusion/30-s release of both carotid arteries and the RIPostC with three cycles of 10-min occlusion/10-min release of the left and right femoral arteries can obviously reduce cerebral infarction size, brain edema, apoptosis, and improve behavioral deficits than other approaches. Second, three cycles of ischemia/reperfusion may be the best for RIPostC. COMPARISON WITH EXISTING METHOD(S): In this paper, we compared different ischemic duration and frequency of ISPostC and RIPostC models to determine the best method. This conclusion helps to unify the experimental methods. CONCLUSIONS: Different ischemic duration and frequency of ischemic postconditioning affect neuroprotection. three cycles of 10-s occlusion/30-s release of both carotid arteries and three cycles of 10-min occlusion/10-min release of both femoral arteries could be the first choice to study mechanisms of ischemic postconditioning and be conducive to the unification of research results.
BACKGROUND: Many studies have confirmed that "in situ ischemia postconditioning" (ISPostC) and "remote ischemic postconditioning" (RIPostC) can reduce cerebral ischemia/reperfusion injury, but there is no comparison was made on the consistency of neuroprotection in ISPostC and RIPostC to different ischemic duration and number of cycles. NEW METHOD: We used a transient middle cerebral artery occlusion model to compare the neuroprotection of ISPostC and RIPostC. We conducted ISPostC and RIPostC via brief and repeated MCA and Femoral artery occlusion followed by different ischemic duration and number of cycles. Infarct volume, brain edema, Neurological deficit scores and Apoptosis were evaluated. RESULTS: First, the ISPostC with three cycles of 10-s occlusion/30-s release of both carotid arteries and the RIPostC with three cycles of 10-min occlusion/10-min release of the left and right femoral arteries can obviously reduce cerebral infarction size, brain edema, apoptosis, and improve behavioral deficits than other approaches. Second, three cycles of ischemia/reperfusion may be the best for RIPostC. COMPARISON WITH EXISTING METHOD(S): In this paper, we compared different ischemic duration and frequency of ISPostC and RIPostC models to determine the best method. This conclusion helps to unify the experimental methods. CONCLUSIONS: Different ischemic duration and frequency of ischemic postconditioning affect neuroprotection. three cycles of 10-s occlusion/30-s release of both carotid arteries and three cycles of 10-min occlusion/10-min release of both femoral arteries could be the first choice to study mechanisms of ischemic postconditioning and be conducive to the unification of research results.