Abstract

To study the effect of scalp acupuncture (SA) on the mitophagy signaling pathway in the caudate nucleus of Sprague-Dawley rats following intracerebral hemorrhage (ICH). An ICH model was established by injecting autologous arterial blood into the caudate nucleus in 200 male Sprague-Dawley rats, which were divided into five groups: sham, ICH, 3-methyladenine group (3-MA, 30 mg/kg), SA, and SA+3-MA. Animals were analyzed at 6 and 24 h as well as at 3 and 7 days. Composite neurological scale score was significantly higher in the SA group than in the ICH group. Transmission electron microscopy showed less structural damage and more autophagic vacuoles within brain in the SA group than in the ICH group. SA group showed higher levels of Beclin1, Parkin, PINK1, NIX protein, and a lower level of Caspase-9 in brain tissue. These animals consequently showed less neural cell apoptosis. Compared with the SA group, however, the neural function score and levels of mitophagy protein in the SA+3-MA group were decreased, neural cell apoptosis was increased with more severe structural damage, which suggested that 3-MA may antagonize the protective effect of SA on brain in rats with ICH. SA may mitigate the neurologic impairment after ICH by enhancing mitophagy and reducing apoptosis.

Highlights

  • Intracerebral hemorrhage (ICH) remains the most serious and intractable type of stroke in the world

  • If mitochondria can be preserved through the specific form of autophagy called mitophagy, this secondary damage may be ameliorated

  • The inflammatory reaction and coagulation cascade caused by hematoma can lead to edema of the surrounding brain tissue, which causes the more serious and lasting damage, and has a negative impact on the prognosis of intracerebral hemorrhage

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Summary

Introduction

Intracerebral hemorrhage (ICH) remains the most serious and intractable type of stroke in the world. Primary brain damage after ICH includes physical damage such as hematoma, which can lead to secondary brain damage that is propagated by mitochondrial dysfunction, activation of microglia, and release of neurotransmitters and inflammatory mediators. SA Attenuates Damage Through Mitophagy (Fan et al, 2019). These responses lead to apoptosis and necrosis of the brain tissue, two strong determinants of neurological deterioration and poor prognosis (Bobinger et al, 2018). One study showed that inhibiting autophagy helped reduce the severity of brain damage after iron-induced ICH (Chen et al, 2012), whereas another study showed that promoting autophagy decreased early brain injury in subarachnoid hemorrhage (Jing et al, 2012)

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