Whole body hypoxic preconditioning-mediated multiorgan protection in db/db mice  via  nitric oxide-BDNF-GSK-3β-Nrf2 signaling pathway

Yuefang Li; Yan Huang; Xi Cheng; Youjun He; Xin Hu

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자료유형: 학술저널

저자정보: Yuefang Li (Cadre Ward the No.901 Hospital of the Joint Logistics Support Unit of the Chinese People's Liberati) Yan Huang (Cadre Ward the No.901 Hospital of the Joint Logistics Support Unit of the Chinese People's Liberati) Xi Cheng (Cadre Ward the No.901 Hospital of the Joint Logistics Support Unit of the Chinese People's Liberati) Youjun He (Cadre Ward the No.901 Hospital of the Joint Logistics Support Unit of the Chinese People's Liberati) Xin Hu (Cadre Ward the No.901 Hospital of the Joint Logistics Support Unit of the Chinese People's Liberati)

저널정보: 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제25권 제4호

발행연도: 2021.1

수록면: 281 - 296 (16page)

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The beneficial effects of hypoxic preconditioning are abolished in the diabetes. The present study was designed to investigate the protective effects and mechanisms of repeated episodes of whole body hypoxic preconditioning (WBHP) in db/db mice. The protective effects of preconditioning were explored on diabetesinduced vascular dysfunction, cognitive impairment and ischemia-reperfusion (IR)-induced increase in myocardial injury. Sixteen-week old db/db (diabetic) and C57BL/6 (non-diabetic) mice were employed. There was a significant impairment in cognitive function (Morris Water Maze test), endothelial function (acetylcholineinduced relaxation in aortic rings) and a significant increase in IR-induced heart injury (Langendorff apparatus) in db/db mice. WBHP stimulus was given by exposing mice to four alternate cycles of low (8%) and normal air O2 for 10 min each. A single episode of WBHP failed to produce protection; however, two and three episodes of WBHP significantly produced beneficial effects on the heart, brain and blood vessels. There was a significant increase in the levels of brain-derived neurotrophic factor (BDNF) and nitric oxide (NO) in response to 3 episodes of WBHP. Moreover, pretreatment with the BDNF receptor, TrkB antagonist (ANA-12) and NO synthase inhibitor (LNAME) attenuated the protective effects imparted by three episodes of WBHP. These pharmacological agents abolished WBHP-induced restoration of p-GSK-3?/GSK-3? ratio and Nrf2 levels in IR-subjected hearts. It is concluded that repeated episodes of WHBP attenuate cognitive impairment, vascular dysfunction and enhancement in IRinduced myocardial injury in diabetic mice be due to increase in NO and BDNF levels that may eventually activate GSK-3? and Nrf2 signaling pathway to confer protection

#Brain-derived neurotrophic factor #Dementia #Heart #Ischemia #Myocardial infarction #Nitric oxide

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