卒中患者的睡眠障碍呈现多样性,包括睡眠呼吸障碍、失眠、睡眠时间过长/过短、睡眠中周期性肢体运动(periodic limbmovements during sleep,PLMS)、快动眼睡眠期行为障碍(rapid eye movement sleepbehavior disorder,RBD)和昼夜节律失...卒中患者的睡眠障碍呈现多样性,包括睡眠呼吸障碍、失眠、睡眠时间过长/过短、睡眠中周期性肢体运动(periodic limbmovements during sleep,PLMS)、快动眼睡眠期行为障碍(rapid eye movement sleepbehavior disorder,RBD)和昼夜节律失调性睡眠-觉醒障碍等。并且已有研究证实了睡眠障碍与脑血管病的发生、发展及预后之间存在着错综复杂的关系,互为影响。近几年,脑血管病患者的睡眠障碍问题受到了神经科诸多学者的关注,但是目前关于脑血管病患者的睡眠障碍防治仍然未得到足够重视。展开更多
The integrity and function dysfunction of the blood brain barrier(BBB)is considered to be an early event in the pathogenesis of a variety of neurological diseases in old patients and dysfunction of BBB could be induce...The integrity and function dysfunction of the blood brain barrier(BBB)is considered to be an early event in the pathogenesis of a variety of neurological diseases in old patients and dysfunction of BBB could be induced bycommon stress that old people often face,such as sepsis during which lipopolysaccharide(LPS)is released into circulation and BBB is damaged.Since decreased melatonin level had been shown in the serum and brain of old people and mice,we aim to investigate whether supplement with melatonin could alleviate LPSinduced BBB damage in old mice.Mice(24-28 months old)received one week melatonin(10 mg·kg-1·d-1,intraperitoneally,ip)or saline before challenge with LPS(1 mg·kg-1,ip).Evan′s blue(EB)and immunoglobulin G(Ig G)leakage were used to assess the BBB permeability.Immunofluoresence and Western blotting were used to detect the protein expression and distribution.Our results showed that LPS significantly increased BBB permeability in old mice accompanied by tight junction protein occludin and claudin-5 degradation,inhibition of AMP-activated protein kinase(AMPK)activation and increase of gp91phox protein expression.Interestingly,one week of melatonin treatment significantly decreased LPS-induced BBB hyperpermeability,activated AMPK and inhibited gp91phox expression upregualtion.Moreover,activation of AMPK by metformin significantly inhibited LPS-induced gp91phox expression upregualtion in endothelial cells.Taken together,our findings demonstrate that melatonin alleviates LPS-impaired integrity of BBB by activation of AMPK and inhibition of gp91phox expression in old mice.展开更多
文摘卒中患者的睡眠障碍呈现多样性,包括睡眠呼吸障碍、失眠、睡眠时间过长/过短、睡眠中周期性肢体运动(periodic limbmovements during sleep,PLMS)、快动眼睡眠期行为障碍(rapid eye movement sleepbehavior disorder,RBD)和昼夜节律失调性睡眠-觉醒障碍等。并且已有研究证实了睡眠障碍与脑血管病的发生、发展及预后之间存在着错综复杂的关系,互为影响。近几年,脑血管病患者的睡眠障碍问题受到了神经科诸多学者的关注,但是目前关于脑血管病患者的睡眠障碍防治仍然未得到足够重视。
文摘The integrity and function dysfunction of the blood brain barrier(BBB)is considered to be an early event in the pathogenesis of a variety of neurological diseases in old patients and dysfunction of BBB could be induced bycommon stress that old people often face,such as sepsis during which lipopolysaccharide(LPS)is released into circulation and BBB is damaged.Since decreased melatonin level had been shown in the serum and brain of old people and mice,we aim to investigate whether supplement with melatonin could alleviate LPSinduced BBB damage in old mice.Mice(24-28 months old)received one week melatonin(10 mg·kg-1·d-1,intraperitoneally,ip)or saline before challenge with LPS(1 mg·kg-1,ip).Evan′s blue(EB)and immunoglobulin G(Ig G)leakage were used to assess the BBB permeability.Immunofluoresence and Western blotting were used to detect the protein expression and distribution.Our results showed that LPS significantly increased BBB permeability in old mice accompanied by tight junction protein occludin and claudin-5 degradation,inhibition of AMP-activated protein kinase(AMPK)activation and increase of gp91phox protein expression.Interestingly,one week of melatonin treatment significantly decreased LPS-induced BBB hyperpermeability,activated AMPK and inhibited gp91phox expression upregualtion.Moreover,activation of AMPK by metformin significantly inhibited LPS-induced gp91phox expression upregualtion in endothelial cells.Taken together,our findings demonstrate that melatonin alleviates LPS-impaired integrity of BBB by activation of AMPK and inhibition of gp91phox expression in old mice.
