| 30431067 |
'Governor vessel-unblocking and mind-regulating' acupuncture therapy ameliorates cognitive dysfunction in a rat model of middle cerebral artery occlusion. |
Int J Mol Med. 2019 Jan;43(1):221-232. doi: 10.3892/ijmm.2018.3981. Epub 2018 Nov 6. |
2019 Jan |
Acupuncture is a traditional Chinese medicinal therapy, which is used for the amelioration of cognitive dysfunction. The aim of this study was to investigate the effectiveness and relevancy mechanisms of 'governor vessel鈥憉nblocking and mind鈥憆egulating' acupuncture therapy for cognitive dysfunction in rats with ischemia. For this purpose, we used the middle cerebral artery occlusion (MCAO) method to induce cognitive dysfunction in rats. The behavioral changes in the rats were examined using the Morris water maze (MWM) test. The effects of the treatment on oxidative stress response and the function of the mitochondria in brain tissues were also assessed. The results revealed that 'governor vessel鈥憉nblocking and mind鈥憆egulating' acupuncture therapy markedly improved the cognitive ability of the rats with cognitive dysfunction. The production of pro鈥憃xidative stress factors, including nitric oxide (NO) and inducible nitric oxide synthase (iNOS), was also blocked along with the amelioration of cognitive function, while the production of adenosine triphosphate (ATP), superoxide dismutase (SOD) and cyclooxygenase (COX) was restored. At the molecular level, the accumulation of amyloid beta (Abeta) in the mitochondria was suppressed by 'governor vessel鈥憉nblocking and mind鈥憆egulating' acupuncture therapy, which may be attributed to the inhibition of the function of translocase of outer mitochondrial membrane 40 (TOMM40) and translocase of inner mitochondrial membrane 17A (TIMM17A). On the whole, the findings of the present study confirm the effects of 'governor vessel鈥憉nblocking and mind鈥憆egulating' acupuncture therapy on cognitive dysfunction induced by brain ischemia in rats, and that the mechanisms underlying the effects of this treatment might be mediated through the inhibition of TOMM40 and TIMM17A synthesis, which can relieve mitochondrial dysfunction from the accumulation of Abeta."
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