The protective effect of melatonin on brain ischemia and reperfusion in rats and humans: In vivo assessment and a randomized controlled trial. Issue 4 (30th September 2018)

• Record Type: Journal Article
• Authors: Zhao, Zhewei; Lu, Chengran; Li, Tianjia; Wang, Wenda; Ye, Wei; Zeng, Rong; Ni, Leng; Lai, Zhichao; Wang, Xuebin; Liu, Changwei
• Is Part Of: Journal of pineal research. Volume 65:Issue 4(2018)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2018-09-30
• Subjects: brain -- carotid endarterectomy -- ischemia and reperfusion -- melatonin -- randomized controlled trial; Pineal gland -- Periodicals; Pineal Gland -- Periodicals; Épiphyse (Glande); Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 612.492
• DOI: 10.1111/jpi.12521
• Languages: English
• ISSNs: 0742-3098

Abstract

Abstract: Carotid endarterectomy (CEA) is the treatment of choice for carotid stenosis. Some patients develop ischemia and reperfusion (I/R) injury after CEA. This study was designed to investigate the neuroprotective effects of melatonin on I/R injury in both rats and humans. To this end, 36 male rats were evaluated, and a double‐blind randomized controlled trial (RCT) including 60 patients was performed. A rat model of middle cerebral artery occlusion was used to mimic cerebral I/R. After 2 hour of occlusion and 24 hour of reperfusion, blood samples and brain tissues were harvested for further assessments. Compared with the vehicle treatment, melatonin decreased the expression of nuclear factor κ light‐chain‐enhancer of activated B cells (NF‐κB) and S100 calcium‐binding protein β (S100β) ( P < 0.05) and markedly increased the expression of nuclear erythroid 2‐related factor 2 (Nrf2), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) ( P < 0.05). The participants in the RCT took 6 mg/d melatonin orally from 3 days before surgery to 3 days after surgery. Blood samples were drawn at the following times: baseline; pre‐anesthesia; carotid reconstruction completion; and 6, 24, and 72 hour after CEA. Compared with the oral placebo treatment, melatonin decreased the expression of NF‐κB, tumor necrosis factor‐α, interleukin‐6 (IL‐6), and S100β ( P < 0.05) and increased the expression of Nrf2, SOD, CAT, and GPx ( P < 0.05) in patients after CEA. Our findings suggested that melatonin could ameliorate brain I/R injury after CEA and that this outcome was essentially due to the antioxidant and anti‐inflammatory effects of melatonin.