Neuroprotective Effect of Acupuncture against Single Prolonged Stress-Induced Memory Impairments and Inflammation in Rat Brain via Modulation of Brain-Derived Neurotrophic Factor Expression.

Bombi Lee,Weidong Pan

doi:10.1155/2022/4430484

Abstract

Posttraumatic stress disorder (PTSD) is a serious mental disorder that can appear after exposure to extreme stress. Acupuncture is an alternative therapy that is widely used to treat various neurodegenerative diseases, as well as cognitive and memory impairments. The aim of this study was to examine whether acupuncture stimulation at a specific acupoint (Shenmen or heart meridian, HT7) could improve memory defects caused by single prolonged stress (SPS) in rats. After exposure to SPS, acupuncture on the HT7 acupoint in male rats was performed, once daily for 21 days. We confirmed that this treatment improved fear memory, cognitive function, and spatial memory by modulating the neuroinflammation and expression of brain-derived neurotrophic factor (BDNF) mRNA in the brain. It also significantly inhibited the activation of proinflammatory cytokines, such as tumor necrosis factor-α and interleukin-1β and the enzyme cyclooxygenase-2 in the brain; it increased the expression of BDNF mRNA in the hippocampus. Our findings provide valuable information concerning the clinical usefulness of acupuncture in the treatment of PTSD.

Highlights

Posttraumatic stress disorder (PTSD) is a mental disorder in which fear memory and anxiety reactions appear after exposure to a previously experienced traumatic event [1]
A high concentration of CORT caused by a response to traumatic stress causes increased levels of proinflammatory cytokines, failure to extinguish fear memories, and behavioral changes related to memory dysfunction [12]. erefore, the reduction of serum CORT from acupuncture focused on the HT7 acupoint suggests the possibility of recovery from the behavioral response and neuroinflammation caused by memory impairment
To determine whether the single prolonged stress (SPS)-induced cognitive memory and spatial memory impairments in rats were clearly linked to a decrease in movement caused by motor dysfunction, we assessed locomotor activity in all rats in the open field test (OFT); the results showed no significant differences among groups. ese mean swimming speeds of rats in the Morris water maze (MWM) test were consistent across groups. erefore, the findings indicate that the additional time needed for rats to reach the platform and explore new objects was related to behavioral changes caused by memory impairment

Summary

Introduction

Posttraumatic stress disorder (PTSD) is a mental disorder in which fear memory and anxiety reactions appear after exposure to a previously experienced traumatic event (e.g., a car accident, disaster, abuse, or extreme stress) [1]. PTSD causes fear memory disorders to appear even in safe situations when the traumatic event has disappeared; it can cause serious pathological changes such as anxiety disorders, depression, flashbacks, and cognitive memory dysfunction [3]. PTSD is caused by excessive stress-related dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and neurophysiological imbalance in the fear circuit region of the brain [2, 4]. Erefore, in PTSD patients, proinflammatory cytokines (e.g., interleukin-1β (IL-1β) and tumor necrosis factorα (TNF-α)) accumulate in large amounts in the fear circuit region of the brain, such as the medial prefrontal cortex (mPFC), hippocampus (Hipp), and amygdala (Amg) [9, 10] PTSD causes a breakdown of the immune system and excessive secretion of the stress hormone, corticosterone (CORT), by excessive release of proinflammatory cytokines by a neuroinflammatory response [5,6,7,8]. erefore, in PTSD patients, proinflammatory cytokines (e.g., interleukin-1β (IL-1β) and tumor necrosis factorα (TNF-α)) accumulate in large amounts in the fear circuit region of the brain, such as the medial prefrontal cortex (mPFC), hippocampus (Hipp), and amygdala (Amg) [9, 10]

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Discussion

Conclusion