2018Zhonghua mazuixue zazhiRequires access

Effect of electroacupuncture preconditioning on hippocampal IκB-α/NF-κB/ICAM-1 signaling pathway during cerebral ischemia-reperfusion in mice

Chuanlin Mu, Yan Wang, Wenjie Li, Lin Yang, Xiaomei Wan

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Abstract

Objective To evaluate the effect of electroacupuncture (EA) preconditioning on hippocampal I-kappa B-α (IκB-α)/nuclear factor κB (NF-κB)/intercellular adhesion molecule-1 (ICAM-1) signaling pathway during cerebral ischemia-reperfusion (I/R)in mice. Methods A total of 120 healthy male C57BL/6 mice, aged 10-12 weeks, weighing 20-25 g, were divided into 4 groups (n=30 each)using a random number table method: control group (group C), cerebral I/R group (group I/R), preconditioning with EA at non-acupoint + cerebral I/R group (group S+ I/R) and preconditioning with EA at Baihui acupoint + cerebral I/R group (group E+ I/R). The cerebral I/R injury model was established by occlusion of bilateral common carotid arteries followed by reperfusion for 72 h in mice anesthetized with halothane or chloral hydrate in group I/R.Group S+ I/R received EA at the points 2 mm lateral to the acupoints of Baihui for 5 consecutive days, and then the cerebral I/R injury model was established.Group E+ I/R received EA at Baihui acupoints with a sparse-dense wave at an intensity of 1 mA and a frequency of 2 Hz/15 Hz for 30 min once a day for 5 consecutive days, and then the cerebral I/R injury model was established.Neurobehavioral score was assessed at 24 and 48 h of reperfusion.Then 5 mice in each group were sacrificed, and the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the pathological changes in hippocampal CA1 region and for determination of the expression of IκB-α, NF-κB, ICAM-1, interleukin-6 (IL-6), IL-1β protein and mRNA by Western blot and real-time polymerase chain reaction, respectively. Results Compared with group C, neurobehavioral score was significantly increased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was up-regulated in I/R, S+ I/R and E+ I/R groups (P 0.05). Compared with group S+ I/R, neurobehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+ I/R (P<0.05). Conclusion The mechanism by which EA preconditioning attenuates cerebral I/R injury may be related to inhibiting activation of hippocampal IκB-α/NF-κB/ICAM-1 signaling pathway in mice. Key words: Electroacupuncture; Ischemia preconditioning; Brain ischemia; Reperfusion injury; I-kappa B proteins; NF-kappa B; Intercellular adhesion molecule-1

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Objective To evaluate the effect of electroacupuncture (EA) preconditioning on hippocampal I-kappa B-α (IκB-α)/nuclear factor κB (NF-κB)/intercellular adhesion molecule-1 (ICAM-1) signaling pathway during cerebral ischemia-reperfusion (I/R)in mice. Methods A total of 120 healthy male C57BL/6 mice, aged 10-12 weeks, weighing 20-25 g, were divided into 4 groups (n=30 each)using a random number table method: control group (group C), cerebral I/R group (group I/R), preconditioning with EA at non-acupoint + cerebral I/R group (group S+ I/R) and preconditioning with EA at Baihui acupoint + cerebral I/R group (group E+ I/R). The cerebral I/R injury model was established by occlusion of bilateral common carotid arteries followed by reperfusion for 72 h in mice anesthetized with halothane or chloral hydrate in group I/R.Group S+ I/R received EA at the points 2 mm lateral to the acupoints of Baihui for 5 consecutive days, and then the cerebral I/R injury model was established.Group E+ I/R received EA at Baihui acupoints with a sparse-dense wave at an intensity of 1 mA and a frequency of 2 Hz/15 Hz for 30 min once a day for 5 consecutive days, and then the cerebral I/R injury model was established.Neurobehavioral score was assessed at 24 and 48 h of reperfusion.Then 5 mice in each group were sacrificed, and the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the pathological changes in hippocampal CA1 region and for determination of the expression of IκB-α, NF-κB, ICAM-1, interleukin-6 (IL-6), IL-1β protein and mRNA by Western blot and real-time polymerase chain reaction, respectively. Results Compared with group C, neurobehavioral score was significantly increased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was up-regulated in I/R, S+ I/R and E+ I/R groups (P 0.05). Compared with group S+ I/R, neurobehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+ I/R (P<0.05). Conclusion The mechanism by which EA preconditioning attenuates cerebral I/R injury may be related to inhibiting activation of hippocampal IκB-α/NF-κB/ICAM-1 signaling pathway in mice. Key words: Electroacupuncture; Ischemia preconditioning; Brain ischemia; Reperfusion injury; I-kappa B proteins; NF-kappa B; Intercellular adhesion molecule-1

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Available abstract

Objective To evaluate the effect of electroacupuncture (EA) preconditioning on hippocampal I-kappa B-α (IκB-α)/nuclear factor κB (NF-κB)/intercellular adhesion molecule-1 (ICAM-1) signaling pathway during cerebral ischemia-reperfusion (I/R)in mice. Methods A total of 120 healthy male C57BL/6 mice, aged 10-12 weeks, weighing 20-25 g, were divided into 4 groups (n=30 each)using a random number table method: control group (group C), cerebral I/R group (group I/R), preconditioning with EA at non-acupoint + cerebral I/R group (group S+ I/R) and preconditioning with EA at Baihui acupoint + cerebral I/R group (group E+ I/R). The cerebral I/R injury model was established by occlusion of bilateral common carotid arteries followed by reperfusion for 72 h in mice anesthetized with halothane or chloral hydrate in group I/R.Group S+ I/R received EA at the points 2 mm lateral to the acupoints of Baihui for 5 consecutive days, and then the cerebral I/R injury model was established.Group E+ I/R received EA at Baihui acupoints with a sparse-dense wave at an intensity of 1 mA and a frequency of 2 Hz/15 Hz for 30 min once a day for 5 consecutive days, and then the cerebral I/R injury model was established.Neurobehavioral score was assessed at 24 and 48 h of reperfusion.Then 5 mice in each group were sacrificed, and the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the pathological changes in hippocampal CA1 region and for determination of the expression of IκB-α, NF-κB, ICAM-1, interleukin-6 (IL-6), IL-1β protein and mRNA by Western blot and real-time polymerase chain reaction, respectively. Results Compared with group C, neurobehavioral score was significantly increased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was up-regulated in I/R, S+ I/R and E+ I/R groups (P 0.05). Compared with group S+ I/R, neurobehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+ I/R (P<0.05). Conclusion The mechanism by which EA preconditioning attenuates cerebral I/R injury may be related to inhibiting activation of hippocampal IκB-α/NF-κB/ICAM-1 signaling pathway in mice. Key words: Electroacupuncture; Ischemia preconditioning; Brain ischemia; Reperfusion injury; I-kappa B proteins; NF-kappa B; Intercellular adhesion molecule-1

Key concepts: Electroacupuncture, Medicine, Chloral hydrate, Hippocampal formation, Ischemia, Anesthesia, Reperfusion injury, Internal medicine

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Effect of electroacupuncture preconditioning on hippocampal IκB-α/NF-κB/ICAM-1 signaling pathway during cerebral ischemia-reperfusion in mice — Research Paper | ScholarLens