Ischemic stroke causes severe neuronal damage. Chlorogenic acid is a phenolic substance present in fruits and coffee. It also exerts neuroprotective effects against various brain injuries. The 14-3-3 family protein perform a variety of functions including metabolism, signal transduction, cell differentiation, and apoptosis. The purpose of this study is to investigate whether chlorogenic acid regulates the expression of 14-3-3 protein in stroke animal models. Ischemic stroke was induced by middle cerebral artery occlusion (MCAO) surgery. Phosphate buffered saline (PBS) or chlorogenic acid (30 mg/kg) were intraperitoneally injected to adult male rats 2 h before MCAO surgery. Adhesive-removal test was performed 24 h after MCAO surgery and cerebral cortical tissues were collected for further study. MCAO damage caused severe neurological impairment and chlorogenic acid treatment ameliorated this disorder. Our proteomic approach showed a decrease in 14-3-3 expression in MCAO animals with PBS. The decrease in 14-3-3 expression alleviated in MCAO animal with chlorogenic acid. We confirmed changes in various 14-3-3 protein isoforms, including beta/alpha, zeta/delta, gamma, epsilon, eta, and tau through reverse transcription-PCR. These results explained that chlorogenic acid regulates the expression of 14-3-3 protein in MCAO-induced cerebral ischemia. 14-3-3 is considered to be an important protein for cell survival through binding to pro-apoptotic proteins. The maintenance of 14-3-3 levels is an important event in neuroprotection against ischemic injury. Therefore, we can demonstrate that the 14-3-3 protein contributes to the neuroprotective effect of chlorogenic acid in stroke animal models.

The majority of strokes are caused by ischemia and result in brain tissue damage, leading to problems of the central nervous system including hemiparesis, dysfunction of language and consciousness, and dysfunction of perception. The purpose of this study was to investigate the effects of Poly(ADP-ribose) polymerase(PARP) on necrosis in neuronal cells that have undergone needle electrode electrical stimulation(NEES) prior to induction of ischemia. Ischemia was induced in male SD rats(body weight 300g) by occlusion of the common carotid artery for 5 min, after which the blood was reperfused. After induction of brain ischemia, NEES was applied to Zusanli(ST 36), at 12, 24 and 48 hours. Protein expression was investigated using immuno-reactive cells, which react to PARP antibodies in cerebral nerve cells, and Western blotting. The results were as follows: In the cerebral cortex, the number of PARP reactive cells after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. PARP expression after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. As a result, NEES showed the greatest effect on necrosis- related PARP immuno-reactive cells 24 hours after ischemia, indicating necrosis inhibition, blocking of neural cell death, and protection of neural cells. Based on the results of this study, NEES can be an effective method of treating dysfunction and improving function of neuronal cells in brain damage caused by ischemia.

본 연구는 경도인지장애가 동반된 환자를 대상으로 뇌 자기공명영상에서 인지 영역에 대한 대뇌 피질 두께를 측정하고 신경심리검사 결과와 비교하여 신경해부학적 상관관계를 규명하고자 하였다. 이를 위하여 파킨슨병으로 최초 진단 받고 신경심리검사를 시행한 78명(경도인지장애군: 39명; 비인지장애군: 39명)과 정상인 그룹 32명을 선정하였다. 신경심리검사에서 경도인지장애군과 비인지장애군의 상관관계와 신경심리검사와 뇌 자기공명영상에서 대뇌 피질 두께의 상관관계는 독립표본 T 검증 또는 피어슨 상관분석을 실시하였으며 수집된 자료의 유의 수준은 p<0.05에서 검증하였다. 결론적으로 경도인지장애를 동반한 파킨슨병 환자는 뇌 자기공명영상에서 양측 쐐기압소엽과 우하측두엽의 대뇌 피질 두께가 통계적으로 유의하게 감소하였으며 인지 기능 평가를 위한 신경심리검사에서 시공간 기능, 언어 및 시각 기억력 기능이 저하되었다. 특히 언어 및 시각 기억력 영역에 대한 신경심리검사와 신경해부학적으로 좌측 쐐기앞소엽에서 상관관계가 있었다.